Overview of ANS Lectures

Question 1

Sympathetics ANS (SANS) has what distribution? what length of pre-gang and post-gang fibers? What neurotransmitters are released?

Answer 1

-SANS has thoraco-lumbar distribution with short pre gang that release Ach and long post gang that release mainly NE (only exception being Ach release from SANS fibers causing constriction of sweat glands)

Question 2

Describe how a signal occurs in the adrenal medulla

Answer 2

pregang fibers activate chromaffin cells to release Epi from medulla which goes to affect other sites

Question 3

What is the job of the superior cervical ganglion? What structures does it innervate and overall function

Answer 3

• only SANS that innervates head and neck.
• post gang axons innervate the pineal gland and involved in Circadian rhythm (control of production of melatonin)
• post gang axons of superior cervical ganglion innervate internal carotid artery and form internal carotid plexus. carries post gang axon to the eye, lacrimal gland, mucous membranes of mouth, nose, pharynx, and blood vessels of head
• vasoconstriction of the iris and sclera, pupillary dilation, widening of the palpebral fissure, and reduction of tear production

Question 4

Parasympathetics has what distribution? What nerves make it up? Neurotransmitters and length of axons?

Answer 4

-PANS has a cranio-sacral distribution involving 4 cranial nerves (3,5,9,10) and sacral efferents 2,3,4. Distribution through long pre gang and release Ach and short post gang that release Ach

Question 5

Draw the flow chart of how receptors (cholinergic, adrenernic are catogerized)

Answer 5

See notes

Question 6

Draw the brain and spinal cord with pre and post gang fibers for the following: parasym, sym (muscles, sweat glands, kidney smooth muscle), skeletal muscle and adrenal glands w/ type of receptor

Answer 6

See notes

Question 7

Provide g-protein class, major fnction, and categories for the following: alpha 1,2 beta 1,2, m1-m3, d1-d2, h1-h2, v1-v2

Answer 7

first aid pg. 244

Question 8

Draw the following g-coupled pathways: Gq, Gi, Gs

Answer 8

first aid pg. 244

Question 9

Describe clinical signs of Horner’s syndrome and what causes dysfunction?

Answer 9

-damage to T1-T3 region of spinal cord (superior cervical ganglion) causing drooping eyelid (ptosis), constriction of pupil (miosis), and sinking of eyeball (Down and out)

Question 10

1. Parasympathetic cranial nerve input is physiotopically organized where? 2. Area known for ANS responses to fear. 3. Primary seat of visceral sensation w/ laterlization? Which side does what?

Answer 10

1. nucleus solitary tract w/ further projections to the parabrachial complex
2. prefrontal cortex and amygdala
3. right insular cortex: parasym input from viscera, left insular cortex: symp from viscera

Question 11

What is the cause of dysautonomia in diabetes and Guillain Barre Syndrome? Shy-Drager syndrome/

Answer 11

• diabetes and Guillian Barre: due to demyelination of peripheral effector limbs
• Shy-Drager: due to degeneration w/n control centers of brain

Question 12

In diabetes, what fibers are most likely to be demyelinated?

Answer 12

-pre gang fibers, and the reason why this and gullian barre syndrome are known more for parasym loss.

Question 13

Classic symptoms of dysautonomia? and other causes

Answer 13

• excessive fatigue, excessive thrist, panic attacks, fast heart rate, slow heart rate, syncope, mydriasis, constipation, diarrhea, acid reflux, visual distances, seizures
• autoimmune disease, lyme disease, neurodegeneration, genetic, spinal cord injury, trauma

Question 14

State the site of release, mol. weight, biotransformation process, removal process of the following: small, large, and gas neurotransmitters

Answer 14

• small: syn at the site of action, have small mol weight ( 1,000, biotransformed by non-specific esterases, not taken back up, and act thru specific transmembrane receptors
• gas: (NO, CO): syn at site of action, simply diffuse away for termination of action, act thru intracellular receptors (guanylate cyclase), can retrogradely diffuse back across the synapse to the presynaptic side and icnrease future release of neurotransmitter as occurs in long term potentiation

Question 15

Discuss how Ach is made, inhibitors, transport channels. Walk thru the entire formation up until it is removed

Answer 15

• Choline enters the axon with Na in a CHT channel. AcCoA (inhibited by methyl mercury) combined w/ choline via choline acetyl transferase to yield Ach
• Ach enters a vesicle via a H+ counter-transporter vesicular Ach transporter (VAT) which is inhibited by vesamicol
• Ca enters the cell and SNAP and SNAREs allow the vesicle to dock (inhibited by botulinum toxin)
• Acts thru nicotinic and muscarinic receptors
• degraded by acetyl choline esterase or by non-specific esterase in plasma (butyrylcholinesterase)
• Choline is taken back up by choline transporter (CHT) which is inhibited by hemicholinium

Question 16

Discuss how NE is made, inhibitors, transport channels. Walk thru the entire formation up until its removed

Answer 16

course notes w/ ne pic