ANS Flashcards
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
Effector Limb
Comprised of the sympathetic autonomic nervous system (SANS) and parasympathetic autonomic nervous system (PANS)
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
In PANS
*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)
ACh
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)
