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Flashcards in ANS Deck (34):

Effector Limb

Comprised of the sympathetic autonomic nervous system (SANS) and parasympathetic autonomic nervous system (PANS)


SANS (Sympathetic Autonomic Nervous System)

Think scared. "Fight or Flight" response.
*thoraco-lumbar distribution
*Pre-ganglion = ACh release
*Post-ganglion = NE release (except where ACh is released to constrict sweat glands).
= patterned Response that prepares the body to fight or run away.
*Enhances cardiovascular function to increase muscle activity, energy expenditure, enhances far vision


Thoraco-lumbar distribution

Short pre-ganglionic fibers that release acetylcholine (ACh)
Long post-ganglionic fibers that release norepinephrine (except in the exception of sweat gland constriction where ACh is released)


PANS (parasympathetic Autonomic Nervous System)

"Rest and Relax" responses
*Cranio-sacral distribution
*Pre-ganglionic = ACh
*Post-ganglionic = ACh
*Enhances blood flow to the digestive organs, slows HR, a facilitates near vision.


Cranio-Sacral distribution

*Long pre-ganglionic fibers release ACh
*Short Post-Ganglionic Fibers release ACh
Ganglia near target structures allow for signal amplification


Adrenal Medulla

Part of the SANS system,
simulated by ACh, releases epinephrine (Epi)
*Viewed as post-ganglionic effector
*Pre-ganglionic fibers activate chromaffin cells (ACh) which releases Epi to circulate hormonally to target sites.


Sensory Limb

Utilizes same pathways as the effector limbs, except the fibers are from targets are afferent to the CNS
*Project primarily to the insular cortex


Insular Cortex

Primary receptor for visceral sensation with lateralization. PANS visceral sensation is afferent to the right insular cortex, while SANS visceral sensations are afferent to the left insular cortex.
*Fibers project to other areas to produce coordinated ANS responsiveness


Vaso-vagal Syndrome

Result of increased PANS outflow (primarily Vagus) and reduced SANS activity initiated from CNS "triggers" that produce lightheadedness, feelings of malaise, being hot or cold, sweating, cognitive "fuzziness", changes in vision, difficulty initiating speech (Stuttering).
*Can proceed to fainting (Vaso-Vagal Syncope) due to orthostatic hypotension


Orthostatic Hypotension

Significant decrease in blood pressure caused by reduced SANS outflow leading to hypoxia in the brain, and fainting.
Ex: seeing blood, severe pain, significant arousal, lack of sleep, or severe coughing.


Dysautonomia or Autonomic Dysfunction

Catch-all term for variety of syndromes and symptoms associated with a dysfunction of the ANS
Ex: postural orthostatic tachycardia syndrome (POTS), inappropriate sinus tachycardia (IST), vasovagal syncope,etc.


Small Molecular Neurotransmitters

Synthesized at the site of release, small molecular weight, biotransformed by specific enzymes, taken back up to aid in termination, act through specific transmembrane receptors
Ex: NE and ACh (most common in ANS)


Large Molecule Neurotransmitters

Released by higher levels of excitation, augments small molecule function or can even reverse it.
*Synthesized in the nucleus and anterogradely transported to the terminal, large molecular weight proteins, biotransformed by non-specific esterases, not taken back up, act through specific transmembrane receptors


Gas Neurotransmitters

Diffuse as a gas
*synthesized at site of action, diffuse away for termination of action, act through intracellular receptors after diffusing into target sites, NO can retrogradely diffuse back across synapse to the presynaptic side and increase future release of neurotransmitters (long term potentiation, LTP)



Synthesized by choline acetyl transferases (ChAT) from choline and acetyl co-A
Concentrated in vesicles by Vesicular ACh Transporter (VAT)
Traditional Ca dependent-release mediated through SNAPs and SNAREs
Acts through nicotinic and muscarinic receptors
Degraded by acetylcholine esterase (AChE) to choline and acetyl co-A and by non-specific esterases in plasma (butyrylcholinesterases)
Choline is taken back up by choline transporter (CHT)


Norepinephrine (NE)

Synthesized via the catecholamine pathway involving tyrosine hydroxylase (TH). Levadopa is the end product of TH, is converted to dopamine (DA) by aromatic amino acid decarboxylase (AAAD). DA is then converted the NE by DA beta hydroxylase, further converted to Epi by phenyl-ethanolamine-N-methyl transferase in the adrenal medulla
*Concentrated in vesicle by vesicular monoamine transferase (VMAT)
*Biotransformed by catechol-O-methyl transferase (COMT) and monoamine oxidase (MAO-A and MAO-B), primary breakdown product is Vanilla-mandelic acid (VMA) [use of MAOIs prevent the breakdown of NE by MAOs]
*85% of NE released is taken back up into the terminal by NE transporter (NET)
*Guanathidine is also taken by NETs as well as VMAT where it replaces NE in vesicles depleting them of NE and reducing release and tone


Epinephrine (Epi)

Synthesized by phenyl-ethanolamine-N-methyl transferase (PENMT) in response to ACh acting on Nn receptors
Circulates in the adrenal medulla
Considered a post-synaptic effector
Does not cross the BBB readily
Release increased in chromaffin tumors (pheochromocytoma) along with increased NE release


Dopamine (DA)

Plays a minor role in ANS function where it induces renal vasodilation while enhancing inotropy.
Frequently used in cases with severe blood loss and treatment of some types of shock.
Share common catabolizing enzyme MAO and COMT with NE and Epi
Share common anabolic pathway VMA and HVA


Nicotinic Receptors

Activated by NE and ACh
Subtypes: Nm and Nn


Muscarinic Receptors

Activated by ACh and NE
Subtypes: M1-5


Nn receptor

Nicotinic neuronal receptor
Found on chain ganglia, and in the CNS.
They are ionotropic receptors that enhance Na channel conductance


Nm receptor

Nicotinic muscular receptor
Found on muscular effector sites, and are traditional receptor at neuromuscular junction.
Also a Na ionotropic receptor


M1, M3, and M5

Enhance intracellular Ca and regulate IP3 and diacyl-glycerol (DAG). Found in various locations
*M1 mainly involves cardiac effects
* M3 is Exocrine glands, vessels (smooth muscle/endothelium) CNS


M2 and M4

Open K channels and inhibit adenylyl cyclase. Found mainly in myocardium and CNS.
M2 is an autoreceptor


NE receptors

Alpha and Beta (adrenergic)


Alpha 1 receptor

Post-synaptic receptor, induces smooth muscle contraction and has several functions in the CNS
Second messenger transducer is similar to M1 functional family (increases intracellular Ca and regulates IP3 and DAG).
*Vasoconstriction and increased BP


Alpha 2

Autoreceptor - Reduces further release of NE.
*Also located on post-synaptic membranes in the CNS.
*Inhibit adenylyl cylase.


Beta 1 receptor

Enhances adenylyl cyclase activity and exists on many target sites.
*mainly the heart
Also pre-synaptic ACh terminals


Beta 2 receptor

Enhances adenylyl cyclase activity
Predominantly lung/other body organs. Smooth muscle but with some cardiac effect.


Beta 3 receptor

Enhances adenylyl cyclase activity - mainly in fat cells


Direct Acting Agonists

Affinity for the receptor as well as efficacy, can posses other receptor subtype specificity


Direct acting antagonist

Possess affinity for a receptor but no efficacy, can possess receptor subtype specificy


Indirect Acting agonist

No affinity for the receptor, but possesses efficacy, DO NOT possess receptor subtype specificy


Indirect Acting antagonist

neither possess affinity for the receptor nor efficacy, and DO NOT have receptor subtype specificy