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tricyclic antidepressants (TCAs) and SSRIs can bind to TrkB receptors --> enhances behavior actions, including increase in neuroplasticity

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GPCR-RTK heteroreceptor complexes lead to transactivation of RTK promoter --> develop via activation of intracellular pathways of GPCRs involving increase CA ions

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all heteroreceptors are relevant to learning and memory by forming post synaptic membranes for short term memory that tern into long term

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inhibit this Gal connection will help w antidepressive effects of SSRIs

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Gal has affinity for and activates Gal R1 & R2 heterodimer --> produces anxiety and depression behaviors

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this response to SSRIs is also relevant in astroglia
> specifically in heteroreceptor complexee that respond to integration of DA and 5-HT signals

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could be helpful for psychosis and schizophrenia

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hallucinogenic drugs are post synaptic 5-HTR agonist
> increases Bmax values of D2R antagonist binding sites --> increased affinity of D2R promoter agonist binding --> induced some psychotic like rxns

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selective serotonin reuptake inhibitors (SSRIs)

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selective serotonin reuptake inhibitors (SSRIs)

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increased extracellular serotonin lvls induced by SSRIs activates all 5-HTR subtypes
! some 5-HTR reduce depression, others enhance depression!

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heteroreceptor complexes --> signal integration

allosteric receptor-receptor iteraxn --> CNS disease

> serotonin (5-HT) heteroreceptor complexes --> MDD

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CNS disease

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G protein-couples receptors (GPCR) homo and heteroreceptor complexes interaction w e/o and other adaptor proteins --> integration in the CNS

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can be a problem to get medication into the brain

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low energy requirement --> can operate in anaerobic conditions
neurons can't!

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the more the sleep, the shorter your dendritic spines! get good sleep to learn better!

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dendritic spine length aren't set in stone, they change based on experience, learning, memory --> neuroplasticity

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dendritic spines is where synaptic connections occur

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key: neurotransmitters or neuropeptides from pre-synapse
lock: receptors at post-synapse that only accept certain NTs or NPs

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shape is optimized for what that type of neuron has to do the most, form --> fxn
for ex. more synapses if it's connected to lots of neurons

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cell numbers:
neurons 10-30% of cell number
glia 50-90%
microglia and support cells <10%

cell volume:
neurons and glia are abt the same

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purple = specifically highlighted during lecture

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there is a *space* btwn the cells, they're not actually touching

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synaptically connected neurons that experience cell death destroy entire pathways

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prion disease is common to all neurodegenerative disease

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prion disease is common to all neurodegenerative disease

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- prion disease: proteinacious infaction agents (easier to say than proin)
- prions: proteins with same amino acid sequence as cellular non-pathogenic proteins
- PrPSc (prion proteins scrapie) has diff 3d conformation than PrPC (prion proteins cellular) even tho they have the same sequence
- after being exposed to pathological PrPSc, they infect by making PrPC change their protein folding
> forms insoluble fibrils that accumulate

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neurons live for decades, but when cell death begins, it starts a domino effect for other vulnerable cells

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paraneoplastic and autoimmune brain diseases

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paraneoplastic and autoimmune brain diseases

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paraneoplastic disease: tumor located outside the NS that releases substances negatively affecting neural fxn

autoimmune paraneoplastic diseas: antibodies formed in response to antigens produced by tumor, impacts synaptic transmission

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primary intracranial tumors are not neuronal

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primary intracranial tumors are not neuronal

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1. mature neurons don't divide (terminally differentiated)
2. paucity of progenitor cells in the NS in adults
--> not true in children

tumors from progenitor cells are making glia
for ex.
astrocytomas (neoplasms of astrocytes) --> usually malignant and spread along white matter tracts --> so surgery isn't an option and chemo is hard to target on non dividing cells

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most brain tumors metastises are from a metastasizing cancer in the "the big three neoplasms", lung, breast, melanoma

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adult cells are de-differentiated through directed expression of a suite of transcription factors and then differentiated into neurons w/ different factors

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symmetric division gives 2 more progenitor cells
asymmetric division gives 1 progenitor and 1 differentiated cell
> in NS, asymmetric gives 1 progenitor cell and 1 neuron, oligodendrocyte, or astrocyte

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stem cells are progenitor cells in the NS

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stem cells are progenitor cells in the NS

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neuronal progenitor cells: type of stem cell
embryonic stem cells are pluripotent --> become any kind of tissue
NS stem cells are multipotent --> select routs of differentiation into neurons or glia

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react to damage: injury (even slight) and disease
become reactive when they sense substances indicative of damage or disease: viruses, bacteria
when reactive, promote inflammation and phagocytose damaged tissues / foreign matter --> only benefitial during early stage of disease

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ionic homeostasis in extracellular fluid surrounding neurons, especially K+ ion

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support PNS neurons in sensory and autonomic ganglia

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gray matter: nuclei and cortices dominated by cells and and dendrites (appear gray in unstained brains)

white matter: regions of cells and areas containing axonal tracts

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-multi neuronal, multisynaptic chains of connexn
- axons form bundles
> tracts in CNS
> nerves in PNS

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Central vs Peripheral differentiated by location of soma

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- made of actin (neuron-specific neurofilament) and microtubules
- microtubules de/stabilized by protein: tau
- dyenin and kinesin: molecular motors that shuttle cargo up and down axon

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anterograde axonal transport: substances made in soma to synaptic terminals to be used

retrograde axonal transport: substances from synaptic terminals back to soma

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- head only, around the anterior neural crest & tubes
- thicken w/in the ectodermal layer
- origin of most peripheral sensory ganglia
- non-neural structures: lens, sclera, anterior pituitary, hair cells of ear

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- edges of neural plate form neural crest
- migrate throughout embryo body
- neural crest derived cells make up most of PNS (neurons & glia)
- many non-neuronal tissues (dermal bone, melanocytes, arachnoid, pia)

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- neural tubes derives from neuroectoderms, neural plates that run length of embryo
- neurons & glia of CNS are from neural tube progenitor cells
- choroid epithelium lining of brain's ventricles and pineal gland derive from neural tube (non-neuronal tissue)

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BBB contains lease permeable capillaries of the body
excludes harmful substance

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forms endfeet on the blood brain barrier (BBB) --> allows astro to release substance into blood stream (detoxfiying the brain)

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- bipolar-shaped cells the width of the cortex in the CNS
- primary progenitor cell capable of generating neurons, astrocytes, and oligodendrocytes
- newborn neurons use radial glia as scaffolds to travel along to final desination

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myelin sheath of PNS

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make up myelin sheath in CNS

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glia background: glia are the glue of the brain

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glia background: glia are the glue of the brain

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- communicate through gap junctions, not synapses
- not electrical
- maintain ion balance
- maintain action potential rate
- proliferate postnatally --> primary brain tumor

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transmits info from photoreceptor (rod/cone cells) --> ganglion cells

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- short axons, branch locally to innervate neighboring neurons
- usually btwn primary sensory and primary effector neurons
- aka local circuit neurons

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- mechanoreceptors: provide info abt sensations
- proprioceptors: type of mechano; spacial abt lmbs and other body parts
- nociceptors: pain and temp changes
- vision: retinal cells, not retinal ganglion cells
- auditory: convert pressure waves via hair cells

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transmit sensory info to brain or SC
somatic sensory system: touch, pressure, vibration, limb position, heat, cold, pain
cell bodies are in ganglia throughout the spine

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- invertebrates: response to neurotransmitter release can be excitatory or inhibitory
- vertebrates: only excitatory (contractile)
- muscle relaxation & inhibition occurs by inhibition of the motor neuron itself

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cell body in SC, axon projects to directly/indirectly control effector organs, mostly muscles and glands

upper motor neurons are cortico-spinal interneurons from motor cortex descending to SC, activate lower motor neurons through synapse

neuromuscular junction (NMJ): synapse btwn motor neuron and muscle fiber

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long axon that extends into the brain
--> forms optic nerve, optic chiasm, optic tract

some RGCs axon form retinohypothalamic tract --> circadian rhythms, pupillary light reflex

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- receives visual info from photoreceptors via bipolar cells and retina amacrine cells
- info transmitted to thalamus, hypothalamus, mesencephalon, or midbrain

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hippocampus, amygdala, cortex
CNS fxns: learning, memory cognition, motor control

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dendrite spines:
short & stubby is best

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synapse: location where pre-synaptic (send) element communicates w post-synaptic (receiving) element

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all types of neurons have 4 fxn-al regions

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embryo has 3 layers of cells: germ layers
outer, middle, inner
ecto, meso, endo-derm

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notch signaling leads to diff neuronal differentiation

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principle of dynamic polarization:
electrical signals in neurons flow in one direction
receiving (dendrites) --> axon hillock
neurons make connections only to certain post-synaptic target cells

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Santiago Ramón y Cajal 1852 - 1934
- used Golgi's silver nitrate staining technique to study NS
- Neuron theory: nerve cells are separate

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- GABAergic neurons (inhibitory)
- cerebellum
- stacked like dominos
- large of dendritic spines
- send inhibitory projections to deepcerebllar nuclei and are sole output of all motor coordination in the cerebrallar cortex

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clear neurotransmitters from synapse so signal isn't continuous
--> presynaptic neurons doesn't need/want to be firing onto post synaptic neuron constantly

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- protect brain by ingesting bacteria, dead cells, foreign particles --> fight infection
- 20% of glial cells
- main immune defense for NS

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yellow = article

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green = textbook

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blue = lecture slides