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Two divisions of the ANS and alternate names associated with each.

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Two divisions of the ANS and alternate names associated with each.

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Sympathetic Nervous System - Fight, fright, flight.
* Adrenergic
Parasympathetic Nervous System - Rest and digest
* Cholinergic

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Neurotransmitters for Sympathetic Nervous System

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Neurotransmitters for Sympathetic Nervous System

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Acetylcholine (ACH)-cholinergic

*NT released at ganglia from presynaptic nerve endings (both systems)

Norepinephrine (NE)-adrenergic

*NT released at postganglionic nerve endings

*synthesized from dopamine

*released by adrenal medulla and neurons

Epinephrine (EPI)-adrenergic

*acts on adrenergic receptors

*produced by adrenal medulla

Dopamine (DA)

*sympathetic and CNS neurotransmitter

*precursor to NE

*stimulates many receptors (alpha, beta, dopaminergic); different actions based on dose given
*Most of the brain’s dopamine is produced in the midbrain by neurons that connect to the striatum, where the dopamine is released.

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*NT released at ganglia is ACH (cholinergic)

*NT released at postganglionic nerve endings is ACH (cholinergic)

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How dopamine drives brain activity | MIT News | Massachusetts Institute of Technology

&

Part 1 and Part 2 ANS powerpoints in blackboard for this course

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MIT News | Massachusetts Institute of Technology

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Using a specialized magnetic resonance imaging (MRI) sensor, MIT neuroscientists have discovered how dopamine released deep within the brain influences both nearby and distant brain regions.

Dopamine plays many roles in the brain, most notably related to movement, motivation, and reinforcement of behavior. However, until now it has been difficult to study precisely how a flood of dopamine affects neural activity throughout the brain. Using their new technique, the MIT team found that dopamine appears to exert significant effects in two regions of the brain's cortex, including the motor cortex.

"There has been a lot of work on the immediate cellular consequences of dopamine release, but here what we're looking at are the consequences of what dopamine is doing on a more brain-wide level," says Alan Jasanoff, an MIT professor of biological engineering, brain and cognitive sciences, and nuclear science and engineering. Jasanoff is also an associate member of MIT's McGovern Institute for Brain Research and the senior author of the study.

The MIT team found that in addition to the motor cortex, the remote brain area most affected by dopamine is the insular cortex. This region is critical for many cognitive functions related to perception of the body's internal states, including physical and emotional states.

MIT postdoc Nan Li is the lead author of the study, which appears today in Nature.
Tracking dopamine
Like other neurotransmitters, dopamine helps neurons to communicate with each other over short distances. Dopamine holds particular interest for neuroscientists because of its role in motivation, addiction, and several neurodegenerative disorders, including Parkinson's disease. Most of the brain's dopamine is produced in the midbrain by neurons that connect to the striatum, where the dopamine is released.

For many years, Jasanoff's lab has been developing tools to study how molecular phenomena such as neurotransmitter release affect brain-wide functions. At the molecular scale, existing techniques can reveal how dopamine affects individual cells, and at the scale of the entire brain, functional magnetic resonance imaging (fMRI) can reveal how active a particular brain region is. However, it has been difficult for neuroscientists to determine how single-cell activity and brain-wide function are linked.

"There have been very few brain-wide studies of dopaminergic function or really any neurochemical function, in large part because the tools aren't there," Jasanoff says. "We're trying to fill in the gaps."

About 10 years ago, his lab developed MRI sensors that consist of magnetic proteins that can bind to dopamine. When this binding occurs, the sensors' magnetic interactions with surrounding tissue weaken, dimming the tissue's MRI signal. This allows researchers to continuously monitor dopamine levels in a specific part of the brain.

In their new study, Li and Jasanoff set out to analyze how dopamine released in the striatum of rats influences neural function both locally and in other brain regions. First, they injected their dopamine sensors into the striatum, which is located deep within the brain and plays an important role in controlling movement. Then they electrically stimulated a part of the brain called the lateral hypothalamus, which is a common experimental technique for rewarding behavior and inducing the brain to produce dopamine.

Then, the researchers used their dopamine sensor to measure dopamine levels throughout the striatum. They also performed traditional fMRI to measure neural activity in each part of the striatum. To their surprise, they found that high dopamine concentrations did not make neurons more active. However, higher dopamine levels did make the neurons remain active for a longer period of time.

"When dopamine was released, there was a longer duration of activity, suggesting a longer response to the reward," Jasanoff says. "That may have something to do with how dopamine promotes learning, which is one of its key functions."
Long-range effects
After analyzing dopamine release in the striatum, the researchers set out to determine this dopamine might affect more distant locations in the brain. To do that, they performed traditional fMRI imaging on the brain while also mapping dopamine release in the striatum. "By combining these techniques we could probe these phenomena in a way that hasn't been done before," Jasanoff says.

The regions that showed the biggest surges in activity in response to dopamine were the motor cortex and the insular cortex. If confirmed in additional studies, the findings could help researchers understand the effects of dopamine in the human brain, including its roles in addiction and learning.

"Our results could lead to biomarkers that could be seen in fMRI data, and these correlates of dopaminergic function could be useful for analyzing animal and human fMRI," Jasanoff says.

The research was funded by the National Institutes of Health and a Stanley Fahn Research Fellowship from the Parkinson's Disease Foundation.

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Using a specialized magnetic resonance imaging (MRI) sensor that can track dopamine levels, MIT neuroscientists have discovered how dopamine released deep within the brain influences distant brain regions.

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The receptors of Sympathetic nervous system with the main locations of each receptor

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The receptors of Sympathetic nervous system with the main locations of each receptor

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Alpha 1: Found on glands, smooth muscles, eyes, most arteries and veins.
*Smooth muscle contraction and vasoconstriction -> Increased BP
*Dilation of pupils - mydriasis
*Stimulated by NE & EPI (catecholamines)

Alpha 2: Relaxation/inhibition; PARASYMPATHETIC RESPONSE. Found on adrenergic nerve ending.
*Decreases contraction of smooth muscle -> Vasodilation, lowers BP
*Decreases releases of NE/regulates the release
*negative feedback system

Beta 1: Location on the heart - STIMULATION
* INCREASES force of contraction (+inotropic)
* INCREASES heart rate (+chronotropic)
* INCREASES conduction (+dromotropic)
* Stimulated by NE & EPI (stronger effect by EPI)

Beta 2: Located on smooth muscle, lungs, uterus, skeletal muscle arteries, coronary arteries - RELAXATION
* Smooth muscle relaxation
* Bronchodilation
* Uterine relaxation
* Relaxation of coronary arteries and skeletal muscle blood vessels - vasodilation
* Stimulated by EPI only

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The receptors of Parasympathetic nervous system with the main locations of each receptor

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The receptors of Parasympathetic nervous system with the main locations of each receptor

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Muscarinic:

* located on cardiac, smooth muscle, and glands

* at parasympathetic postganglionic nerve endings

* decrease HR, bronchoconstriction, digestion, GI secretions, and urination, pupillary constriction

Nicotinic 1 (Nn):

* at ganglia of parasympathetic nerves and sympathetic nerves (synapse area)

Nicotinic 2 (Nm):

*somatic, neuromuscular junction of skeletal muscle

•If stimulated, muscle contracts. (Somatic Nervous system-voluntary control; division of Peripheral Nervous System)

(ALL are stimulated by ACH)

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The end organ responses that occur when each transmitter is stimulated in the Parasympathetic nervous system.

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The end organ responses that occur when each transmitter is stimulated in the Parasympathetic nervous system.

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Heart - Decreases heart rate and AV conduction
Intestines, GI motility, and secretions - increased
Postganglionic neurotransmitter - AcH released
Pupil of the eye - Constriction (miosis)
Respiratory passages, lower - bronchoconstriction
Urinary bladder - Contraction
Urinary sphincter - Relaxation

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The end organ responses that occur when each transmitter is stimulated in the sympathetic nervous system

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The end organ responses that occur when each transmitter is stimulated in the sympathetic nervous system

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Adrenal medulla - release of epinephrine
Arteries - vasoconstriction
Heart - Increases heart rate and AV conduction & Increases contractility
Intestines, GI motility, and secretions - Decreased
Postganglionic neurotransmitter - norepinephrine released
Pupil of the eye - Dilation (mydriasis)
Respiratory passages, lower - Bronchodilation
Urinary bladder - relaxation
Urinary sphincter - contraction

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Effects of Sympathetic and Parasympathetic Stimulation

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Effects of Sympathetic and Parasympathetic Stimulation

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Pg. 60 - Pharmacology: An Introduction with Additional Material

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Drug classifications for sympathetic nervous system

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Drug classifications for sympathetic nervous system

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•Sympathomimetics: drugs that mimic the sympathetic system (adrenergics, agonists)

•Sympatholytics: drugs that work against the sympathetic system (adrenergic blocking, blockers, inhibitors, antagonists)

Alpha 1: Adrenergic Agonists Drugs
1. ephedrine (Adrenalin®)-increases BP

2. phenylephrine (Neo-Synephrine®)- increases BP, nasal decongestant
Uses: severe allergic reactions/anaphylaxis, shock, cardiac arrhythmias

Alpha 1: Adrenergic Blocking Drugs
1. prazosin (Minipress®)-HTN

2. terazosin (Hytrin®) -HTN, BPH

3. doxazosin (Cardura®)-HTN, BPH
Uses: Hypertension, Benign Prostatic Hyperplasia

Beta 1 Adrenergic Agonists Drugs
1. dobutamine

Uses: treatment of shock, increases blood pressure, and increases heart function
Beta 2 Adrenergic Agonists Drugs
1. albuterol (Proventil®, Ventolin®)-bronchodilator

2. terbutaline (Brethine®)-bronchodilator, uterine relaxant

3. formoterol (Foradil®)-bronchodilator

4. salmeterol (Serevent®)-bronchodilator

Uses: asthma, respiratory illness/disease, preterm labor

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Drug classifications for parasympathetic nervous system

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Drug classifications for parasympathetic nervous system

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Parasympathomimetics: drugs that mimic the parasympathetic system (agonists, cholinergics)

Parasympatholytics: drugs that work against parasympathetic system (antagonists, anticholingerics)

Colinergics/Parasympathomimetics: DIRECT
1. acetylcholine-used for miosis, cataract and other eye surgeries

MOA: pupil constriction

2. pilocarpine (Pilocar® )-used for glaucoma

MOA: pupil constriction; decreases amount of fluid in eye; decreases  intraocular pressure

3. bethanechol (Urecholine®)-used for urinary retention and ileus/intestinal stasis

MOA: stimulates muscarinic receptors of bladder and GI tract to prevent constipation and urinary retention post-op and in the elderly

Colinergics/Parasympathomimetics: INDIRECT
MOA:
* inhibit acetylcholinesterase, the enzyme that destroys ACH in the synapse

*increases ACH

Drugs:

*neostigmine (Prostigmin®)

Uses: urinary retention and intestinal stasis/ileus, reversal of anticholinergic- rocuronium bromide (Zemuron®) with respiratory paralysis from anesthesia by increasing ACH at the nicotinic 2 (Nm) receptors on skeletal muscle, treatment for myasthenia gravis
Anticholinergics/Parasympatholytics

1. atropine -antidote for cholinergic poisoning

*increase HR, decreases vagus nerve activity (parasympathetic), pre-op med-slows digestion and urination, mydriasis

2. dicyclomine (Bentyl®)- used for GI disorders (ulcers, colitis, IBS)

decreases GI secretions and motility

3. ipratropium bromide (Atrovent®)-bronchodilation

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Autonomic Nervous System

I.          Alpha-1 Adrenergic Agonists

ephedrine

phenylephrine (Neo-Synephrine®)

II.        Adrenergic Agonists

epinephrine (Adrenalin®)

III.      Alpha-1 Adrenergic Blockers

prazosin (Minipress®)

terazosin (Hytrin®)

doxazosin (Cardura®)

IV.      Beta-1 Adrenergic Agonists

dobutamine

V.       Beta-2 Adrenergic Agonists

formoterol (Foradil®)

albuterol (Proventil®, Ventolin®)

terbutaline (Brethine®)

VI.     Beta Blockers

1. Nonselective

nadolol (Corgard®)

propranolol (Inderal®)

timolol (Blocadren®)

1. Selective

atenolol (Tenormin®)

metoprolol (Lopressor®)

VII.    Direct Acting Cholinergic Agonist

acetylcholine

pilocarpine (Pilocar®)

bethanechol (Urecholine®)

VIII.    Indirect Acting Cholinergic Agents

neostigmine (Prostigmin®)

IX.  Anticholinergics

atropine

dicyclomine (Bentyl®)

Somatic System

I.       Skeletal Muscle Relaxants

1. Peripherally Acting

Depolarizing Agent

succinylcholine

Non-depolarizing Agent

rocuronium bromide (Zemuron®)

Direct Acting

dantrolene (Dantrium®)

1. Centrally Acting

cyclobenzaprine (Flexeril®)

carisoprodol (Soma®)

methocarbamol (Robaxin®)

orphenadrine citrate (Norflex®)

chlorzoxazone  (Parafon Forte DSC®)

metaxalone (Skelaxin®)

Respiratory System and Allergy Drug Therapy

I. Mast Cell Stabilizers

cromolyn Sodium (Intal®, Nasalcrom®)

II. Bronchodilators

1. Sympathomimetics/beta-2 agonists  (Short and long acting)

albuterol (Proventil®, Ventolin®)

formoterol (Foradil®)

terbutaline (Brethine®)

salmeterol (Serevent®)

1. Xanthine Derivatives

theophylline (Theo-Dur®)

aminophylline (Paladron®)

III. Cysteinyl Leukotriene Receptor Antagonists/Inhibitors

montelukast (Singulair®)

IV. Anticholinergics

ipratropium bromide (Atrovent®)

V. Combination Bronchodilators

ipratropium bromide + albuterol sulfate (Combivent®)

VI. Antihistamines

1. Generation I (sedating)

brompheniramine (Dimetapp®)

chlorpheniramine (Chlor-Trimeton®)

clemastine (Tavist®)

diphenhydramine (Benadryl®)

hydroxyzine (Atarax®)

promethazine (Phenergan®)

azelastine (Astelin®, Astepro®)

1. Generation II (non-sedating)

loratadine (Claritin®)

fexofenadine (Allegra®)

cetirizine (Zyrtec®)

VII. Corticosteroids (asthma or allergic rhinitis, inhaled or nasal)

budesonide (Rhinocort®, Pulmicort®)

mometasone (Nasonex®, Asmanex®)

fluticasone (Flonase®, Flovent®)

flunisolide (Nasalide®)

triamcinolone (Nasacort®, Azmacort®)

VIII. Antitussives

a. Narcotic

hydrocodone (Hycodan®)

codeine/guaifenesin (Robitussin AC®)

b. Non-narcotic

dextromethorphan/guaifenesin (Robitussin DM®)

benzonatate  (Tessalon Perles®)

IX. Decongestants

oxymetazoline (Afrin®)

pheniramine (Dristan®)

phenylephrine (Neo-Synephrine®)

pseudoephedrine (Sudafed®)

X. Expectorants

guaifenesin (Robitussin®, Mucinex®, Organidin®)