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From organizing your movie collection to deciding to buy a house, problem-solving makes up a large part of daily life. Problems can range from small (solving a single math equation on your homework assignment) to very large (planning your future career).

In cognitive psychology, the term problem-solving refers to the mental process that people go through to discover, analyze, and solve problems. This involves all of the steps in the problem process, including the discovery of the problem, the decision to tackle the issue, understanding the problem, researching the available options and taking actions to achieve your goals. Before problem-solving can occur, it is important to first understand the exact nature of the problem itself. If your understanding of the issue is faulty, your attempts to resolve it will also be incorrect or flawed.

There are a number of mental processes at work during problem-solving. These include:

Perceptually recognizing a problem

Representing the problem in memory

Considering relevant information that applies to the current problem

Identify different aspects of the problem

Labeling and describing the problem

Algorithms: An algorithm is a step-by-step procedure that will always produce a correct solution. A mathematical formula is a good example of a problem-solving algorithm. While an algorithm guarantees an accurate answer, it is not always the best approach to problem-solving. This strategy is not practical for many situations because it can be so time-consuming. For example, if you were trying to figure out all of the possible number combinations to a lock using an algorithm, it would take a very long time!

Heuristics: A heuristic is a mental rule-of-thumb strategy that may or may not work in certain situations. Unlike algorithms, heuristics do not always guarantee a correct solution. However, using this problem-solving strategy does allow people to simplify complex problems and reduce the total number of possible solutions to a more manageable set.

Trial and Error: A trial-and-error approach to problem-solving involves trying a number of different solutions and ruling out those that do not work. This approach can be a good option if you have a very limited number of options available. If there are many different choices, you are better off narrowing down the possible options using another problem-solving technique before attempting trial-and-error.

Insight: In some cases, the solution to a problem can appear as a sudden insight. According to researchers, insight can occur because you realize that the problem is actually similar to something that you have dealt with in the past, but in most cases, the underlying mental processes that lead to insight happen outside of awareness.

Of course, problem-solving is not a flawless process. There are a number of different obstacles that can interfere with our ability to solve a problem quickly and efficiently. Researchers have described a number of these mental obstacles, which include functional fixedness, irrelevant information, and assumptions.

Functional Fixedness: This term refers to the tendency to view problems only in their customary manner. Functional fixedness prevents people from fully seeing all of the different options that might be available to find a solution.

Irrelevant or Misleading Information: When you are trying to solve a problem, it is important to distinguish between information that is relevant to the issue and irrelevant data that can lead to faulty solutions. When a problem is very complex, the easier it becomes to focus on misleading or irrelevant information.

Assumptions: When dealing with a problem, people often make assumptions about the constraints and obstacles that prevent certain solutions.

Mental Set: Another common problem-solving obstacle is known as a mental set, which is the tendency people have to only use solutions that have worked in the past rather than looking for alternative ideas. A mental set can often work as a heuristic, making it a useful problem-solving tool. However, mental sets can also lead to inflexibility, making it more difficult to find effective solutions.

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Effective Problem-Solving Strategies and Common Obstacles

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From organizing your movie collection to deciding to buy a house, problem-solving makes up a large part of daily life. Problems can range from small (solving a single math equation on your homework assignment) to very large (planning your future career).

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This summary was written and compiled by Karin Kirk, SERC, and contains an overview of motivation research and pertinent references.

Self efficacy is commonly defined as the belief in one's capabilities to achieve a goal or an outcome. Students with a strong sense of efficacy are more likely to challenge themselves with difficult tasks and be intrinsically motivated. These students will put forth a high degree of effort in order to meet their commitments, and attribute failure to things which are in their control, rather than blaming external factors. Self-efficacious students also recover quickly from setbacks, and ultimately are likely to achieve their personal goals. Students with low self-efficacy, on the other hand, believe they cannot be successful and thus are less likely to make a concerted, extended effort and may consider challenging tasks as threats that are to be avoided. Thus, students with poor self-efficacy have low aspirations which may result in disappointing academic performances becoming part of a self-fulfilling feedback cycle. ( Bandura ) [Margolis and McCabe, 2006]

How can students gain self-efficacy?

There are four sources of self-efficacy. Teachers can use strategies to build self-efficacy in various ways.

Mastery experiences - Students' successful experiences boost self-efficacy, while failures erode it. This is the most robust source of self-efficacy.
Vicarious experience - Observing a peer succeed at a task can strengthen beliefs in one's own abilities.
Verbal persuasion - Teachers can boost self-efficacy with credible communication and feedback to guide the student through the task or motivate them to make their best effort.
Emotional state -A positive mood can boost one's beliefs in self-efficacy, while anxiety can undermine it. A certain level of emotional stimulation can create an energizing feeling that can contribute to strong performances. Teachers can help by reducing stressful situations and lowering anxiety surrounding events like exams or presentations.
[Margolis and McCabe, 2006] and ( Bandura )

Pedagogic strategies that foster self-efficacy

It is particularly exciting to note that teaching strategies used in the classroom can and do make a difference to students' self-efficacy. (Fencl and Scheel, 2005)

Research shows that the type of learning environment and teaching method can improve self efficacy in the classroom ( Bandura ). A similar result was reported by Fencl and Scheel . They describe a required, nonmajors' physics course where the effects of different teaching methods on the classroom climate and self-efficacy were measured. The students' response indicated that a question and answer format, inquiry-based lab activities and conceptual (rather than quantitative) problems had a significant effect on creating a positive climate in the classroom. In addition to those pedagogies, collaborative learning and the use of electronic applications showed a positive correlation with increased self-efficacy in their student sample. Fencl and Scheel point out that the teaching methods that showed a measurable positive effect share the common feature of engaging students in a comfortable or creative manner. Moreover, pedagogies such as collaborative learning and inquiry-based activities have also been shown to have a strong correlation with how well students learn physics [Fencl and Scheel, 2005] .

Bandura also concludes that cooperative learning strategies have the dual outcome of improving both self-efficacy and academic achievement. "Cooperative learning structures, in which students work together and help one another also tend to promote more positive self-evaluations of capability and higher academic attainments than do individualistic or competitive ones." ( Bandura )
Other pedagogies for improving self-efficacy include:

Establish specific, short-term goals that will challenge the students, yet are still viewed as attainable. [Schunk and Pajares, 2002]

Help students lay out a specific learning strategy and have them verbalize their plan. As students proceed through the task, ask students to note their progress and verbalize the next steps. [Schunk and Pajares, 2002]

Compare student performance to the goals set for that student, rather than comparing one student against another or comparing one student to the rest of the class(Bandura ).

Teaching Practices to Avoid

In his 1994 textbook chapter, Albert Bandura notes that certain well-worn pedagogical practices may have the unintended effect of diminishing the self-efficacy of students who do not reside at the top of the class academically. These include:

Generalized, "lock-step" instruction that is inflexible and does not allow for student input. A formulaic type of instructional setting makes it harder for students to ask questions or become involved in the process. The result may be that if a student becomes confused or discouraged, they are likely to remain so.

Statements or teaching practices that compare students' performance against each other. This may raise the self-efficacy of the top students, but is likely to lower the self-efficacy of the rest of the class. (Bandura )

Tips to improve self-efficacy for struggling students

(from Margolis and McCabe, 2006 )

Use moderately- difficult tasks
If the task is too easy will be boring or embarrassing and may communicate the feeling that the teacher doubts their abilities; a too-difficult task will re-enforce low self-efficacy. The target for difficulty is slightly above the students' current ability level.

Use peer models
Students can learn by watching a peer succeed at a task. Peers may be drawn from groups as defined by gender, ethnicity, social circles, interests, achievement level, clothing, or age.

Teach specific learning strategies
Give students a concrete plan of attack for working on an assignment, rather than simply turning them loose. This may apply to overall study skills, such as preparing for an exam, or to a specific assignment or project.

Capitalize on students' interests
Tie the course material or concepts to student interests such as sports, pop culture, movies or technology.

Allow students to make their own choices
Set up some areas of the course that allow students to make their own decisions, such as with flexible grading, assignment options or self-determined due dates.

Encourage students to try
Give them consistent, credible and specific encouragement, such as, "You can do this. We've set up an outline for how to write a lab report and a schedule for what to do each week - now follow the plan and you will be successful."

Give frequent, focused feedback
Giving praise and encouragement is very important, however it must be credible. Use praise when earned and avoid hyperbole. When giving feedback on student performance, compare to past performances by the same student, don't make comparisons between students.

Encourage accurate attributions
Help students understand that they don't fail because they're dumb, they fail because they didn't follow instructions, they didn't spend enough time on the task, or they didn't follow through on the learning strategy.

Teachers need high self-efficacy too

Teachers with a high sense of efficacy about their teaching capabilities may have an easier time motivating their students and enhancing their cognitive development. These teachers may also be able to rebound from setbacks and more willing to experiment with new ideas or techniques. Low efficacious teachers may rely more on a controlling teaching style and may be more critical of students. [Woolfolk Hoy, 2003] and ( Bandura )

"Schools in which staff members collectively judge themselves capable of promoting academic success imbue their schools with a positive atmosphere for development that promotes academic attainments regardless of whether they serve predominantly advantaged or disadvantaged students."( Bandura )

Further reading

Web sites

by Albert Bandura, Stanford University

This is a comprehensive summary of the topic written by one of its pioneers. The site provides a definition of self-efficacy, characteristics of efficacious people, and a description of how self-efficacy can be developed or undermined. The author describes self-efficacy in social, family and school settings and in various stages of life.

by Frank Pajares, Emory University

This site contains an extensive historical overview about self-efficacy and its place in education. Topics include the origins of the theory, current research and educational applications. One of the author's conclusions is that the educational system would benefit from additional focus on self-efficacy in students.

Information on Self-Efficacy: A Community of Scholars
This is a clearinghouse of information about self-efficacy, hosted by the Division of Educational Studies at Emory University.

Journal Articles

Improving Self-Efficacy and Motivation: What to Do, What to Say
by Howard Margolis and Patrick P McCabe
citation and bibliographic information
This article suggests practical solutions to improve the motivation of struggling learners. Specifically, the authors present strategies such as using peers as role models, teaching specific learning strategies, presenting the students with options and choices, communicating recent success, and more. These tactics can strengthen struggling learners' beliefs in their academic abilities and increase their willingness to engage in academic tasks.

Engaging Students: An Examination of the Effects of Teaching Strategies on Self-Efficacy and Course Climate in a Nonmajors Physics Course
by Heidi Fencl and Karen Scheel
citation and bibliographic information
Self-efficacy is a key predictor of achievement and retention in most academic areas, including the sciences. In this study, the effects of teaching strategies on self-efficacy and course climate were examined. The teaching methods that made significant contributions to self efficacy were question and answer, collaborative learning, conceptual problems, electronic applications and inquiry lab activities.

The Development of Academic Self-Efficacy
by Dale Schunk and Pajares, Frank Pajares
This textbook chapter provides a synthesis of educational psychology research as it relates to students' beliefs in their own abilities. The authors describe self-efficacy and its relation to other motivation constructs and explain the role of various sources of and influences on self-efficacy. The effects of various pedagogical practices are discussed, including a description of specific methods that improve self-efficacy. The role of gender and ethnicity on self-efficacy are also discussed.

Self-Efficacy in College Teaching
by Anita Woolfolk Hoy, The Ohio State University
This essay examines the topic of self-efficacy in the context of teachers' self-efficacy and how that translates into their performance. The author asserts that highly efficacious teachers tend to be more open to new ideas, more willing to experiment with new methods to better meet the needs of their students, and more committed to teaching. They persist when things do not go smoothly and are more resilient in the face of setbacks. And they tend to be less critical of students who make errors and to work longer with a student who is struggling.

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teach the earth enhancing your teaching affective domain

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Self efficacy is commonly defined as the belief in one's capabilities to achieve a goal or an outcome. Students with a strong sense of efficacy are more likely to challenge themselves with difficult tasks and ...

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What is Emotional Learning?

Social and Emotional Learning has emerged as a field thanks to a new understanding of science, nature, child development, and biology, based on the subjective goals of increasing the potential for success and happiness. Social and emotional learning increase a child's emotional intelligence quotient, known colloquially as people-smarts, providing children with an opportunity to excel at more than just academics. Teachers and parents must intentionally teach literacy and academic skills, and according to social and emotional learning theorists, they should be just as intentional about providing instruction in social and emotional skills.

For nearly a hundred years, IQ was the standard by which we measured the relative intelligence of people. A paradigm shift occurred when studies in the 1980s by Howard Gardner showed that EQ is a better predictor of success than IQ. The responsible handling of emotions leads to fewer incidences of acting out and bad behavior and lowers incidences of violence, depression, and low motivation. It creates better perception of emotion in faces and pictures, including in one's own image. When children don't have these skills, they often exhibit challenging or confrontational behavior or become quiet and withdrawn.

Educators have a duty to teach students to manage their emotions, resolve conflicts peacefully, and be responsible for their actions. Effective teaching of emotional intelligence requires, first and foremost, good teacher and parent role models. By creating an environment of emotional acceptance and encouraging children to work through their emotions in a positive way, children will learn that certain behaviors are allowed and others are not. It's also important to look for teachable moments in your everyday life. For example, if a child hits another child, discipline must be accompanied by teaching, for example, telling children that hitting is not okay and to get an adult if they need help resolving a dispute. However, there are two reasons this is not the most effective way to teach social behavior. First, the incident has already occurred, and both children are upset and will not be receptive to learning. Second, the child might find the teacher's attention reinforcing and hit children just to get the teacher's attention again. Instead, social skills should be taught like any other part of the curriculum, with lessons as part of the daily schedule.

Parents, how can you help your children improve their emotional intelligence? According to specialists, emotional learning starts at home at an early age. By being attentive to your young child's emotional needs, you can find opportunities to teach emotional learning in your day-to-day life. An easy way to begin is by discussing moods and asking questions like "What makes you angry?" It's important to teach children that emotions are normal, but that they should be able to regulate them.

Educators, want some tips on providing social and emotional education to your students? There are several emotional education programs for teachers, including "The Resolving Conflicts Creatively Program". Integrating these programs into the daily curriculum and lesson plans will help your students understand how to behave with their peers. Your students will realize that you value their emotional maturity as much as their academic success. You should encourage your students to keep a journal about their feelings. Self-awareness and self-reflection is a large part of emotional maturity. Students can be taught strategies to remain calm and in a positive mood.

Teaching children how to handle their emotions is an important part of learning. Good parents and teachers have a duty to provide instruction in dealing with emotions constructively.

For More On Emotional Learning

1. Consortium for Research on Emotional Intelligence in Organizations - Cutting edge research and information related to emotional intelligence in the workplace. Visitors can download the latest research findings, learn of training opportunities, and access reference materials.

2. Emotional Literacy Education - How to make the world a better place through emotional literacy education and self-knowledge.

3. The EQ Institute - Practical information on emotional intelligence and its importance to society; including reports on the progress of the EQI Montessori primary school, the first school in the world designed specifically to teach Emotional Intelligence to children.

4. LouElla Jackson- DiSC distributor (Carlson Learning) offering assessment tools that help develop emotional intelligence.

5. The Institute for Emotionally Intelligent Learning- Presents programs on assessing and promoting emotional health, humor in the workplace and violence prevention.

6. Special Needs Education- Dedicated to providing a service that encompasses the educational, physical, cognitive and emotional needs of students with learning problems.

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Social and Emotional Learning has emerged as a field thanks to a new understanding of science, nature, child development, and biology, based on the subjective goals of increasing the potential for success and happiness. Social and emotional learning increase a child's emotional intelligence quotient, known colloquially as people-smarts, providing children with an opportunity to excel at more than just academics.

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If you've ever noticed that you tend to feel energized and drowsy around the same times every day, you have your circadian rhythm to thank. What is it, exactly? Your circadian rhythm is basically a 24-hour internal clock that is running in the background of your brain and cycles between sleepiness and alertness at regular intervals. It's also known as your sleep/wake cycle.

For most adults, the biggest dip in energy happens in the middle of the night (somewhere between 2:00am and 4:00am, when they're usually fast asleep) and just after lunchtime (around 1:00pm to 3:00pm, when they tend to crave a post-lunch nap). Those times can be different if you're naturally a night owl or a morning person. You also won't feel the dips and rises of your circadian rhythm as strongly if you're all caught up on sleep. It's when you're sleep-deprived that you'll notice bigger swings of sleepiness and alertness.

A part of your hypothalamus (a portion of your brain) controls your circadian rhythm. That said, outside factors like lightness and darkness can also impact it. When it's dark at night, your eyes send a signal to the hypothalamus that it's time to feel tired. Your brain, in turn, sends a signal to your body to release melatonin, which makes your body tired. That's why your circadian rhythm tends to coincide with the cycle of daytime and nighttime (and why it's so hard for shift workers to sleep during the day and stay awake at night).

Your circadian rhythm works best when you have regular sleep habits, like going to bed at night and waking up in the morning around the same times from day to day (including weekends). When things get in the way, like jet lag, daylight savings time, or a compelling sporting event on TV that keeps you up into the wee hours of the morning, you can disrupt your circadian rhythm, which makes you feel out of sorts and can make it harder to pay attention .

Interestingly, your circadian rhythm will likely change as you get older. And you may not have the same sleep/wake cycle as your partner, child or parents. But the more you pay attention to your body and notice feelings of alertness and drowsiness, and the more time you spend developing good sleep hygiene habits, the better your slumber will be and the better you'll feel.

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What is Circadian Rhythm? - National Sleep Foundation

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If you've ever noticed that you tend to feel energized and drowsy around the same times every day, you have your circadian rhythm to thank. What is it, exactly? Your circadian rhythm is basically a 24-hour internal clock that is running in the background of your brain and cycles between sleepiness and alertness at regular intervals.

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Olds and Milner's experiments were significant because they appeared to verify the existence of brain structures that are devoted to mediating rewarding experiences. For, if the rats were lever-pressing repeatedly to receive stimulation to these areas, it suggested they were enjoying the experience. Subsequent studies attempted to more thoroughly map out these "reward areas," and it was discovered that some of the most sensitive areas are situated along the medial forebrain bundle. The medial forebrain bundle is a large collection of nerve fibers that travels between the VTA and the lateral hypothalamus, making many other connections along the way. Some areas of the medial forebrain bundle were found to be so sensitive that rats would choose receiving stimulation to them over food or sex.

Eventually it was recognized that dopamine neurons are activated during this type of rewarding brain stimulation, and researchers found that they could cause rats to stop lever pressing by administering a dopamine antagonist (a drug that blocks the effects of dopamine). In other words, without the activity of dopamine the rats were less likely to find brain stimulation reinforcing, and so they stopped pressing the lever altogether. Other evidence, such as the discovery that dopamine antagonists seemed to reduce the rewarding qualities of drugs like amphetamines, further supported the importance of dopamine's role in reward.

Based on brain stimulation experiments and the increasingly recognized importance of dopamine in reward, attention began to turn toward major dopamine pathways as playing an important part in mediating rewarding experiences. The medial forebrain bundle connects the dopamine-rich VTA with the nucleus accumbens and is considered part of the mesolimbic dopamine pathway. It eventually became recognized that, when we use an addictive drug or experience something otherwise rewarding, dopamine neurons in the VTA are activated. These neurons project to the nucleus accumbens via the mesolimbic dopamine pathway, and their activation causes dopamine levels in the nucleus accumbens to rise. Furthermore, disrupting this pathway in rodents that had become addicted to pressing a lever for brain stimulation or a drug reward caused them to stop lever-pressing, suggesting these areas are crucially important to the occurrence of addictive behavior.

As the mesolimbic dopamine pathway is activated whenever we use an addictive drug, it has come to be considered the primary pathway of the reward system. However, dopaminergic projections from the VTA travel to the frontal cortex as well; they comprise the mesocortical dopamine pathway. These fibers are also thought to be involved in reward and motivation, although their contribution to rewarding experiences is less clear than that of the mesolimbic pathway.

It's important to note that since the earliest research on the reward system our perspective on dopamine's role in reward has changed slightly. At one time dopamine was considered to be the neurotransmitter responsible for causing the experience of pleasure, but it is now thought to be involved with aspects of reward other than the direct experience of enjoyment. While the details are still being worked out, some have suggested dopamine is involved in encoding memories about a reward (e.g. how to get it, where it was obtained) and attributing importance to environmental stimuli that are associated with the reward.

While the reward system is implicated in pleasurable and potentially addictive behaviors, the substrates of pleasure are not confined to the structures mentioned above and dopamine is not the only neurotransmitter involved. The reward system refers to a group of structures that seem to be frequently involved in mediating rewarding experiences, but the actual network dedicated to creating the feelings we associate with these experiences is likely more complex.

References (in addition to linked text above):

Wise RA (1998). Drug-activation of brain reward pathways. Drug and alcohol dependence, 51(1-2): 13-22.
Learn more:
Watch this 2-Minute Neuroscience video to learn more about the ventral tegmental area and this 2-Minute Neuroscience video to learn more about the nucleus accumbens.

Related articles:
Know your brain: Nucleus accumbens Know your brain: Ventral tegmental area

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Know your brain: Reward system - Neuroscientifically Challenged

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Where is the reward system? The term reward system refers to a group of structures that are activated by rewarding or reinforcing stimuli (e.g. addictive drugs). When exposed to a rewarding stimulus, the brain responds by increasing release of the neurotransmitter dopamine and thus the structur

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"The hypothalamus, the anterior thalamic nucleus, the cingulate gyrus, the hippocampus and their interconnections, constitute a harmonious mechanism which may elaborate the functions of central emotion as well as participate in the emotional expression."
James Papez, 1937

The limbic system consists of the phylogenetically old limbic lobe and other subcortical structures and their connections. Although not empirically proven, the limbic system is a functional concept which may be employed to explain various brain functions.[ 1]

HISTORY

Paul Pierre Broca in 1878 spoke of ' le grand lobe limbique' or the great limbic lobe and applied the term "limbic" (from the Latin limbus for border) to the curved rim of the cortex which incudes the cingulate and the parahippocampal gyri. However, its putative role in emotion was elaborated by the American physician, James Papez in 1937 in the seminal paper titled 'A proposed mechanism of emotion'. This anatomical model is referred to as the Papez circuit.[ 2] Yakovlev in 1948 proposed Yakovlev's circuit in the control of emotion involving the orbitofrontal, insular and anterior temporal lobe cortex, the amygdala and the dorsomedial nucleus of thalamus.[ 3] In 1952, Paul D. MacLean coined the term "limbic system" to describe Broca's limbic lobe and related subcortical nuclei as the collective neural substrate for emotion.[ 1] MacLean was also instrumental in proposing and defining the Triune concept of the brain. MacLean's evolutionary "Triune brain theory" proposed that the human brain was in reality three brains in one: the R-complex (reptilian complex), the limbic system and the neocortex.[ 4] The concept of the limbic system has since been further expanded and developed by Nauta, Heimer and others.

COMPONENTS OF THE LIMBIC SYSTEM

There is no universal agreement on the total list of structures, which comprise the limbic system. The brain regions that constitute the limbic system are:

These structures form a complex network for controlling emotion.[ 5]

Limbic lobe

The limbic lobe situated at the inferomedial aspect of the cerebral hemispheres, consists of two concentric gyri surrounding the corpus callosum. Broca proposed that the larger outer gyrus be named "limbic gyrus" and the smaller inner one "the intralimbic gyrus". The limbic gyrus (limbic lobe) consists of the isthmus of the cingulate gyrus, the parahippocampal gyrus (both of which are continuous via a bundle of white matter called "cingulum") and the subcallosal area.[ 6]

The cingulate gyrus (Latin = Belt ridge) dorsal to the corpus callosum is heavily interconnected with the association areas of the cerebral cortex. The parahippocampal gyrus in the medial temporal lobe contains several distinct regions, the most important being the entorhinal cortex (ERC). The ERC funnels highly processed cortical information to the hippocampal formation and serves as its major output pathway.[ 5]

The hippocampal formation

Hippocampal formation in the temporal lobe has three distinct zones:

Embryologically, the hippocampal formation is an extension of the medial edge of the temporal lobe. The entire hippocampal formation has a length of about 5 cm from its anterior end at the amygdala to its tapering posterior end near the splenium of the corpus callosum.[ 5]

Dentate gyrus

The dentate gyrus is composed of three layers: an outer acellular molecular layer, a granular middle layer and an inner polymorphic layer.

Hippocampus

The word hippocampus means "Sea Horse" in Greek. Hippocampus is a trilaminate structure with an outer molecular layer, a middle pyramidal layer and an inner polymorphic layer. On the basis of differences in cytoarchitecture and connectivity, the hippocampus has four fields (named by Lorente de No in 1934): CA1, CA2, CA3 and CA4 (CA: Cornu Ammonis). To embryologic enthusiasts, CA4 is not part of the Cornu Ammonis but is a separate structure-the dentate hilus. The thin layer of fibers adjacent to the polymorphic layer of the hippocampus is known as the alveus. These fibres coalesce to form the fimbria and subsequently, the crura of the fornix (main efferent pathway of the hippocampal formation). The crura of the fornix converge to form the body of the fornix, which later forms the columns of the fornix and pass through the hypothalamus into the mammillary bodies.[ 5, 7]

Amygdala

Identified by Burdach in the early 19 th century, amygdala, an almond-shaped structure deep within the temporal lobe, is a collection of nuclei lying beneath the uncus. Lying at the anterior end of the hippocampal formation and the anterior tip of the inferior horn of the lateral ventricle, it merges with the periamygdaloid cortex, which forms part of the surface of the uncus. The amygdaloid complex is structurally diverse and comprises of approximately 13 nuclei. These are further divided into subdivisions that have extensive internuclear and intranuclear connections. The major groups are:

1. Basolateral nuclei

2. Cortical-like nuclei

3. Centromedial nuclei

4. Other amygdaloid nuclei

5. Extended Amygdala[ 8] (centromedial amygdala, sublenticular substantia innominata and bed nucleus of the stria terminalis)[ 9]

Hypothalamus

Table 1

FUNCTIONAL CIRCUITRY

Papez circuit

James Papez's delineation of a circuit after injecting rabies virus into a cat's hippocampus and monitoring its progression through the brain, unraveled the basis of cortical control of emotion. Further elaboration of the circuit has included the prefrontal cortex (PFC), amygdala and septum among other areas [].[ 1, 2]

Internal circuit

The intrinsic connections of the hippocampus involve fibers from the entorhinal area, dentate gyrus, Ammon's horn and the subiculum. The three primary pathways of this area are called the perforant pathway, mossy fibers and Schaffer collaterals. The existence of a fourth pathway, the alvear path from the entorhinal area to Ammon's horn through the alveus, has been questioned.

Circuits of amygdala

Amygdala serves to integrate information processing between prefrontal / temporal association cortices and the hypothalamus. The amygdala has two major output pathways:

Dorsal route via stria terminalis projects to the septal area and hypothalamus.

Ventral route via the ventral amygdalofugal pathway terminates in the septal area, hypothalamus and the medial dorsal thalamic nucleus [ Figure 4 ].

The amygdala has also got connections with the basal ganglia circuit via its projections to the ventral pallidum and ventral striatum, which is relayed back to the cortex via the dorsomedial nucleus of the thalamus [].

Basolateral circuit

This circuit is relayed via the basolateral amygdala. This circuit consists of the orbitofrontal and anterior temporal cortex, amygdala (especially the basolateral amygdala) and magnocellular division of the dorsomedial nucleus of the thalamus (frontothalamic pathway), which relays back to the orbitofrontal cortex.[ 11] This circuit encodes information about social signals and social plans for social acts. The circuit has been proposed as a substrate for the human ability to infer the intentions of others from their language, gaze and gestures (Theory of mind and social cognition)[].[ 12]

FUNCTIONS OF THE LIMBIC SYSTEM

The functions of the various structures of limbic system are outlined below [].

Table 2

Cingulate gyrus

Autonomic functions regulating heart rate and blood pressure as well as cognitive, attentional and emotional processing.

Parahippocampal gyrus

Spatial memory

Hippocampus

Long-term memory

Amygdala

Anxiety, aggression, fear conditioning; emotional memory and social cognition.

Hypothalamus

Regulates the autonomic nervous system via hormone production and release. Secondarily affects and regulates blood pressure, heart rate, hunger, thirst, sexual arousal and the circadian rhythm sleep/wake cycle.

Nucleus accumbens

Reward, Addiction

Sleep and dreams

Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) have shown that the limbic system is one of the most active brain areas during the process of dreaming. The limbic system probably interweaves unconscious primal emotions with our conscious cognitive thoughts and perceptions and thereby ties together emotions and memory during rapid eye movement (REM) sleep to form the content of dreams. The suprachiasmatic nucleus of hypothalamus is the circadian rhythm generator controlling the sleep-wake cycle.[ 15] The ventrolateral preoptic nucleus (VLPO) of the hypothalamus sends projections to the histaminergic tuberomamillary nucleus (TMN), the serotonergic dorsal and median raphe nucleus and the noradenergic locus coeruleus. It also sends axons that terminate within the cholinergic basal forebrain, the pedunculopontinethalamic nucleus (PPT) and lateral dorsal thalamic nucleus (LDT). The VLPO projections to these areas are inhibitory in nature as they are γ-aminobutyric acid-ergic (GABAergic) and galaninergic. The VLPO via its inhibition of the major arousal mechanisms, functions as a 'sleep switch', promoting sleep. Its reciprocal relationship with the major arousal areas helps it to function as one half of a 'flip-flop' circuit, the stable firing (flip-flop) of which prevents intermediate states of sleep and wakefulness. The VLPO by its disinhibition of the PPT-LDT also promotes REM sleep. The lateral hypothalamic area (LHA) contains orexinergic neurons that promote wakefulness. The orexinergic neurons inhibit the sleep-promoting VLPO and the REM sleep-promoting neurons in the PPT-LDT. The orexinergic neurons also increase the firing of the locus coeruleus, dorsal raphe and the TMN and in a way, act as a finger pressing the 'flip-flop' circuit switch into the wakefulness position.[ 16]

Emotional responses

Fear

Fear responses are produced by the stimulation of the hypothalamus and amygdala. Amygdalar destruction abolishes fear and its autonomic and endocrine responses. Amygdala is also involved in fear learning, which is blocked when long-term potentiation (LTP) is disrupted in pathways to the amygdala. Imaging studies have shown that viewing fearful faces activates the left amygdala.[ 14, 17]

Rage and placidity

Rage responses to minor stimuli are observed after removal of the neocortex. The destruction of the ventromedial hypothalamic nuclei and septal nuclei in animals with intact cerebral cortices may induce rage. Rage may also be generated by the stimulation of an area extending back through the lateral hypothalamus to the central gray matter of the midbrain. Bilateral destruction of the amygdala results in placidity. However, when the ventromedian nucleus is destroyed after the destruction of the amygdala, the placidity generated is converted to rage.[ 14]

Autonomic and endocrine responses to emotion

Limbic stimulation causes changes in respiration and blood pressure. The stimulation of the cingulate gyrus and hypothalamus can elicit autonomic responses. There is however little evidence for localization of autonomic responses in limbic circuitry.[ 14] Hypothalamic autonomic responses are triggered by a complex phenomenon mediated by the cortical and limbic structures processing drives and emotions. The fear and rage responses mediated by the limbic system cause stimulation of various parts of the hypothalamus, especially the lateral areas and produce diffuse sympathetic discharge. The massive sympathetic discharge during stress is called the "flight or fright response". Stress via cortical and limbic connections causes release of corticotropin-releasing hormone (CRH) from the paraventricular nuclei of the hypothalamus. CRH release mediates endocrine and immune responses [].[ 18]

Memory

Emotional memory

Emotion has powerful influence on learning and memory. Amygdala, in conjunction with prefrontal cortex and medial temporal lobe, is involved in consolidation and retrieval of emotional memories. Amygdala, prefrontal cortex and hippocampus are also involved in the acquisition, extinction and recovery of fears to cues and contexts. Hippocampus is critical for long-term, declarative memory storage.[ 22]

Medial temporal lobe memory system

The components include the hippocampus and adjacent cortex, the parahippocampal regions (PHG) and the entorhinal and perirhinal regions. This memory system is involved in the storage of new memories.[ 23]

Diencephalic memory system

The diencephalic memory circuit consists of the hypothalamus, mammillary body and the dorsomedial nucleus of thalamus. This circuit is important for the storage of recent memory; a dysfunction of this circuit results in Korsakoff's syndrome.[ 23]

CLINICAL IMPLICATIONS

Affective disorders

Studies have shown variation in the volumes of the frontal lobes, basal ganglia, amygdala and hippocampus in affective disorders. Functional studies have revealed decreased prefrontal and anterior cingulate activity in affective disorders. The anterior cingulate is the center for integration of attentional and emotional output and helps effortful control of emotional arousal.[ 29] Recently, researchers have posited that this spectrum of affective and cognitive symptomatology represents dysfunction within a single extended network-the anterior limbic network, which includes prefrontal regions and subcortical structures such as the thalamus, striatum and the amygdala. The dysfunction of this system (anterior limbic network) is suggested in bipolar disorder, but its role in depression is unclear [].[ 30]

CONCLUSION

The limbic system plays a pivotal role in behavior. The intricate functional neuroanatomy of limbic system with its diverse circuits may explain some of the manifestations of neuropsychiatric disorders. Relentless research has identified the role of the amygdala in various anxiety disorders and emotional memory. The monitoring role of anterior cingulate, the trisynaptic hippocampal circuitry underlying cognitive functioning and the significance of hypothalamus in various neurovegetative functions suggest the integral role of the limbic system in understanding human behavior and its aberrations.

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"The hypothalamus, the anterior thalamic nucleus, the cingulate gyrus, the hippocampus and their interconnections, constitute a harmonious mechanism which may elaborate the functions of central emotion as well as participate in the emotional expression." James Papez, 1937 The limbic system consists of the phylogenetically old limbic lobe and other subcortical structures and their connections.

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Broadening the Scope of Educational Neuroscience

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Broadening the Scope of Educational Neuroscience

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Dynamic Learning & Memory, Synaptic Plasticity & Neurogenesis

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Dynamic Learning & Memory, Synaptic Plasticity & Neurogenesis

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Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

Mammalian memory is the result of the interaction of millions of neurons in the brain and their coordinated activity. Candidate mechanisms for memory are synaptic plasticity changes, such as long-term potentiation (LTP). LTP is essentially an electrophysiological phenomenon manifested in hours-lasting increase on postsynaptic potentials after synapse tetanization. It is thought to ensure long-term changes in synaptic efficacy in distributed networks, leading to persistent changes in the behavioral patterns, actions and choices, which are often interpreted as the retention of information, i.e., memory. Interestingly, new neurons are born in the mammalian brain and adult hippocampal neurogenesis is proposed to provide a substrate for dynamic and flexible aspects of behavior such as pattern separation, prevention of interference, flexibility of behavior and memory resolution. This work provides a brief review on the memory and involvement of LTP and adult neurogenesis in memory phenomena.

Introduction

The brain, with billions of cells' connections and plethora of cell types in mutual interactions, is one of the most complicated organs in the human body and attracts attention of both scientific researchers and the public. This is underlined by the fact that we do not know the pathophysiology of many devastating brain disorders, which often affect memory and cognition (such as schizophrenia, Alzheimer's disease etc.). Notably, the brain definitely does not work as an "elevated supervisor"; indeed, researchers working in neuroscience have now started to appreciate the "systems-level" understanding of the human body function in health and disease ( Qureshi and Mehler, 2013).

Studying detailed physiology of any living system without evaluating its output (behavior), cannot give us enough information for understanding the function of the system. Vice versa, studying behavior without looking at the proximate mechanisms cannot provide sufficient insight, although striking exceptions from physiology exist such as ant navigation (e.g., Wohlgemuth et al., 2001), when scientists proceeded from studying behavioral outputs downstream to physiological mechanisms. Many scientists concerned with the integration of molecular and cellular views with systems-level and behavioral studies focus on the learning and memory. This particular function of nervous system in animals is well accessible by methods with different resolution (from spikes to molecules and cells to the whole organism).

In this review, I will try to provide a short update on integration of memory formation with a concept of synaptic plasticity ( Hebb, 1949) (mainly long-term potentiation (LTP; Bliss and Lomo, 1973)) and adult neurogenesis in the dentate gyrus (DG) of the hippocampus ( Altman, 1963; Altman and Das, 1965). My selection must obviously be subjective; there are excellent reviews on other issues related to this topic, such as the role of transcriptional factors and various kinases ( Kandel, 2012; Xia and Storm, 2012). The rationale for selecting these subtopics settles on prevailing view on synaptic plasticity processes as a "hotspot" of current research into basic mechanisms of learning and memory ( Glanzman, 2013). Focus on neurogenesis is based on the fact that despite many memory studies involve static settings, our world is endlessly dynamic and learning should be considered a highly dynamic process; neurogenesis may provide these flexible aspects of memory. These fields open ways for searching mechanisms of deficits in many neuropsychiatric disorders with enormous human and socioeconomic impact and suggest ways of novel causal therapies for depression, PTSD, Alzheimer's disease or schizophrenia ( Voineskos et al., 2013). Scientists relate both LTP and neurogenesis to memory ( Brown et al., 1990; Snyder et al., 2001), LTP as a candidate mechanism for long-term retention of information and hippocampal neurogenesis as a candidate mechanism for specific dynamic and flexible aspects of learning.

Learning and Memory

Memory refers to a capability of virtually any animal to encode, store and retrieve information, to guide behavioral output. Learning is viewed as acquisition or encoding the information to memory. It is an excellent example of model system allowing for multi-level analysis (again, note close relation of memory deficits to these pathological conditions). Absence/presence of a memory trace (engram) is often presented or even defined as a change of a particular behavior (such as a rat with lesions to the hippocampus may get lost in a spatial maze), or then, as a change of ability to learn/remember. The term engram was first coined by Richard Semon, a German biologist ( Semon, 1921). It usually refers to mechanisms (or tags) by which the memories are stored. The prevailing view today is that memory should leave physical (e.g., molecular) and often rather distributed changes in neuronal tissue ( Moser and Moser, 1998; Frey and Frey, 2008).

Another well-accepted opinion is that there is nothing like "universal memory"; instead, multiple memory systems exist ( Doeller et al., 2008; Lee et al., 2008; Schwabe, 2013) having their specific (partially competing but also shared) brain resources to fulfill their tasks ( Squire, 2004). Temptating is a concept that memory may be stored (at least in mammals) in distributed changes in synaptic weights, which may modulate synchronization and grouping of firing of neuronal assemblies ( Hebb, 1949; Harris et al., 2003). Further introspection of the engram and its nature also provokes many questions about stability, localization, time course of possible changes, and consolidation and transformation of a memory trace (reviewed in Dudai, 2004).

Importantly, complex and vulnerable mammalian memory types, i.e., declarative and spatial memory, depend on the medial temporal lobes (MTL) of the brain (reviewed in Eichenbaum, 2001). These are the hippocampus, subiculum and neighboring cortical areas such as entorhinal, perirhinal and postrhinal cortices ( Amaral and Witter, 1989). Many scientist today are convinced that the hottest candidates for neural correlate of a long-term memory trace are long-term changes in synaptic strengths ( Hebb, 1949), i.e., LTP and long-term depression (LTD). For the sake of simplicity, this minireview selects LTP out of the synaptic plasticity mechanisms, although there is a great evidence for LTD role in learning and memory as well (reviewed in Kemp and Manahan-Vaughan, 2007).

LTP, Protein Kinase Mzeta and Memory

Already in 1973, Terje Lomo a Timothy Bliss published a seminal study ( Bliss and Lomo, 1973) showing that tetanization of specific pathway in the hippocampal formation of anesthetized rabbit resulted in significant increase in the excitatory postsynaptic potentials in postsynaptic cells, which further supported Hebb's theories ( Hebb, 1949). Later on, this phenomenon was demonstrated in anesthetized and freely moving rats and mice. Today, LTP attracts many scientists, because it represents an intriguing but artificial model of long-term changes of the CNS function (more than 12,000 hits in PubMed on the term search). However, causal link between LTP and memory has been suspected but not settled for a long time, although supportive studies were provided earlier, in which interference with LTP affected learning and memory.

In 2006, two studies convincingly reported the link between LTP and learning and memory. Whitlock et al. (2006) examined the hypothesis that not only tetanization but also memory encoding per se may induce long-term plastic changes. The study showed that training rats to solve inhibitory avoidance, in which animal learns to avoid a preferred dark compartment punished by mild footshocks led to induction of the LTP in a subset of hippocampal synapses. Some synapses were unaffected, again supporting the concept of distributed memory trace. It is interesting to note that inhibitory avoidance learning, despite a simple paradigm, contains both operant and contextual fear conditioning component and involves highly coordinated recruitment of molecular and cellular machinery in the hippocampal formation ( Izquierdo et al., 2002). The paper by Whitlock and colleagues contributed much to the notion that memory encoding may produce LTP in some synapses and that memory acquisition could be analogized to electrical tetanization of the synapse. Other studies have strongly corroborated this view ( Cohen et al., 2011; Rodríguez-Durán et al., 2011; Kenney and Manahan-Vaughan, 2013).

Another paper in the same issue of Science ( Pastalkova et al., 2006) focused on the maintenance phase of LTP as a candidate mechanism for memory storage, based on previous robust evidence from the laboratory of Todd Sacktor that an atypical form of protein kinase C (PKMzeta) is necessary and sufficient for maintenance phase of the LTP ( Ling et al., 2002). The study employed so-called zeta-inhibiting peptide (ZIP), which was injected into hippocampi of rats that previously acquired the spatial active place avoidance task. Subsequently, memory retention was tested and it was found selectively impaired by ZIP injection. Interestingly, such microinjection failed to abolish novel learning in the same task, suggesting that PKMzeta erased previous memory trace but did not block encoding of novel information.

However, Volk et al. (2013) have recently generated constitutive and conditional PKMzeta-knockout mice and detected no impairment of either LTP maintenance or hippocampus-dependent memory ( Volk et al., 2013). Since the previous reports sometimes used pharmacological blockade of enzyme by ZIP, Volk et al. also applied ZIP to their transgenic mice lacking PKMzeta and detected LTP suppression. This suggests ZIP targets other enzymes required for LTP. Analogous results have been found by Lee et al. (2013) in PKMzeta-null mice. The role of PKMzeta has therefore been questioned ( Kwapis and Helmstetter, 2013).

Interestingly, another form of PKC named iota ( Selbie et al., 1993) was suggested to compensate for deficient PKMzeta in these experiments, suggesting that more diverse cascade can provide basis for memory maintenance rather than a single "memory molecule" ( Glanzman, 2013). In any case, scientists appear to be on the track of interesting discovery of how our vivid everyday memories relate to molecular and cellular brain processes.

Adult Neurogenesis in the Dentate Gyrus and Memory

Importantly, the hippocampus, specifically the subgranular zone of the DG, is one of two sites of neurogenesis in the adult brain ( Altman, 1963; Altman and Das, 1965). Some of the dividing neural progenitor cells survive, differentiate into neurons and incorporate into the hippocampal network. The physiological, especially the behavioral role of adult neurogenesis is a subject of controversies until today. Newly born neurons in the DG are proposed to facilitate learning in the hippocampus by separating overlapping patterns in hippocampal inputs, thus ensuring formation of distinct representations.

Enhancing adult neurogenesis in the DG was found to suffice for improvement of pattern separation ( Sahay et al., 2011) and another recent study ( Nakashiba et al., 2012) suggested that newly-born hyper-excitable neurons may participate preferentially in pattern separation, while older adult granule neurons provide mainly pattern completion (a complementary process which allows adding missing features into incomplete hippocampal representations). This study did not focus directly on the autoassociative network in CA3, but in light of paper by Rolls (2013), I propose that strong, "consolidated" synapses between older granule neurons via mossy fibers to CA3 may provide a significant contribution to pattern completion. It should be noted that a precise balance between pattern completion and pattern separation is probably one if the functions of CA3 upstream region innervated by mossy fibers from dentate granule cells, which mediates a proper hippocampus function and such interplay may be disrupted in memory disorders ( Hanson and Madison, 2010).

Studies also showed that hippocampal neurogenesis promotes behavioral flexibility in mice. A study by Garthe et al. (2009) demonstrated the subtle but significant effects of neurogenesis ablation. Using chronic treatment with a cytostatic temozolomide and efficient recovery protocol, the memory differences between mice with and without adult neuronal proliferation were revealed in the MWM not by traditional measures such as distance to reach the platform, but by evaluating spatial/non-spatial strategies possessed in the maze. Robust evidence on behavioral flexibility account of neurogenesis has been provided by Burghardt et al. (2012), who showed that neurogenesis ablation in mice led to impairments of reversal learning in active place avoidance task (reviewed by Stuchlik et al., 2013). It also disrupted flexible incorporation of second reference frame (second to-be-avoided place, i.e., two-frame place avoidance; reviewed in Stuchlik et al., 2013). The deficit could not be explained by alteration of memory extinction, or with inability to acquire new memory in a novel environment; these functions were spared in both groups. Interestingly, the flexibility impairment was accompanied by immediate-early gene Arc up-regulation, suggesting effects on excitability and plasticity of the hippocampal network ( Pevzner et al., 2012).

Recently, time-limited role of new, hyper-excitable granule neurons in the DG in hippocampus-dependent memory has been shown by optogenetic approach ( Gu et al., 2012). This study showed that newly born cells form functional synapses on pyramidal neurons of CA3 region from 2 weeks after their birth reaching a stable state at 4 weeks. Newborn neurons at this age were more plastic than neurons at other stages. The study also showed that switching off this cell type of 4-week-old cells after encoding disrupted retrieval of hippocampal memory. This suggests that these 4 weeks represent a functional time window for adult-born neurons in hippocampus-dependent memory retrieval ( Gu et al., 2012). Using multiple high-resolution methods, a study of Ikrar et al. (2013) clearly documented that blocking adult neurogenesis increased excitability in the DG networks while its enhancement has reduced it, and also pointed to an important role of inhibitory GABAergic interneurons ( Ikrar et al., 2013).

Short Notes on Some Other Factors Affecting LTP, Neurogenesis and Memory

There are additional factors affecting memory, LTP, and neurogenesis. For instance, a recent study on human glial cells implanted into mouse hippocampus documented enhanced LTP, suggesting strong functional role of this cell type in the brain ( Zhang and Barres, 2013). Neurogenesis is also significantly affected by ageing, stress and disease but contrarily enhanced e.g., by enriched environment ( Kempermann et al., 1997) and physical exercise ( van Praag et al., 1999). Generally, all these phenomena in parallel affect memory as well ( Nilsson et al., 1999; Lithfous et al., 2013). An intriguing study by Van der Borght et al. (2007) showed beneficial effects of physical exercise and dietary restriction on spatial T-maze performance and surprisingly, T-maze learning and reversal training actually led to reduced neurogenesis, suggesting optimal balance of these processes for proper memory maintenance.

Of high importance is the role of sleep in memory ( McCoy et al., 2013). It has been shown that during both non-REM and REM sleep cellular processes may take part, subserving memory ( Benington and Frank, 2003). A factual necessity of sleep for forming and consolidation of memories has emerged recently ( Prince et al., 2014). Sleep is also related to neurogenesis ( Mueller et al., 2013) as well as to LTP ( Kim et al., 2005). From a pharmacological point of view, a recent study have shown that anti-diabetes drug metformin might offer a promising way of increasing adult neurogenesis and memory function ( Wang et al., 2012) that is impaired in several neuropsychiatric disorders.

Conclusions

Much evidence converges on the view that learning and memory, synaptic plasticity and neurogenesis are inter-related phenomena. Specifically, the latter two are considered to provide substrate for specific aspects of learning and memory function. LTP maintenance probably underlies memory retention and its inhibition erases memory. Encoding of a memory trace induces LTP in subset of hippocampal synapses. Neurogenesis underlies specific dynamic and flexible features of learning and memory phenomena in the precisely regulated and time-restricted manner. Nowadays and in the future, collaborative and multi-disciplinary efforts involving optogenetics, transgenes, in vivo patch-clamp etc. will bring significant insight into mechanisms of memory.

Conflict of Interest Statement

The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Acknowledgments

This work was supported by GACR grant 14-03627S, Academic project M200111204, and institutional support RVO67985823. We thank all colleagues from the laboratory for their support, to Prof. P. Mares for critical reading and comments on the manuscript and to T. Hua and P. Luketic for proofreading.

References

Hebb, D. (1949). The Organization of Behavior. New York: Wiley.

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Mueller, A. D., Meerlo, P., McGinty, D., and Mistlberger, R. E. (2013). Sleep and adult neurogenesis: implications for cognition and mood. Curr. Top. Behav. Neurosci. doi: 10.1007/7854_2013_251. [Epub ahead of Print].
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Dynamic learning and memory, synaptic plasticity and neurogenesis: an update

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Mammalian memory is the result of the interaction of millions of neurons in the brain and their coordinated activity. Candidate mechanisms for memory are synaptic plasticity changes, such as long-term potentiation (LTP). LTP is essentially an electrophysiological phenomenon manifested in hours-lasting increase on postsynaptic potentials after synapse tetanization.