Autonomics I

Question 1

Signaling via ANS vs Somatic (how many steps?)

Answer 1

ANS = 2 step
Somatic = 1 step

Question 2

What are the 2 parts of the ANS and how are they divided?

Answer 2

Sympathetic (thoracolumbar) and parasympathetic (craniosacral); designation is ANATOMICAL

Question 3

Compare length of preganglionic and postganglionic fibers in sympathetic vs parasympathetic

Answer 3

Sympathetic: preganglionic fibers = short; postganglionic = long

Parasympathetic: preganglionic fibers = long and postganglionic = short

Question 4

Parasympathetic/sympathetic inputs often in opposition to an organ; name an exception

Answer 4

Salivary glands–>both arms stimulate the gland and cooperate instead of oppose action

Question 5

Neurotransmitters/Receptors for somatic neuron

Answer 5

NT is Ach–>binds to Nm-type nicotinic receptors

Question 6

Neurotransmitters/Receptors for parasympathetic

Answer 6

Pregang release Ach at Nn-type nicotinic receptor; Postgang release Ach to muscarinic receptor (metabotropic M1-M5)

Question 7

Neurotransmitters/Receptors for sympathetic

Answer 7

Pregang release Ach at Nn-type nicotinic receptor; Postgang USUALLY release norepi to adrenergic receptor (metabotropic a&b)

Question 8

Branching patterns/output

Answer 8

sympathetic = diffuse output with extensive branching (1:20 ratio of pre to postgang fibers); parasymp = discrete (1:1 ratio)

*also note that release of NE and eli from adrenal medulla add to total body sympathetic activation

Question 9

Exceptions to postganglionic sympathetic neuron rule (not all release NE)

Answer 9

1) Sweat glands utilize Ach

2) Renal vessels utilize dopamine

Question 10

Cholinergic transmission path

Answer 10

1) acetyl-CoA + choline (by choline acetyltransferase)–>acetylcholine
2) Ach release triggered by AP causing Ca+2 influx through channels and fusion of vesicular/plasma membranes
3) Ach interacts w/targets and is removed by achetylcholinesterase (cleaves Ach to choline and acetate)

Question 11

Adrenergic transmission path

Answer 11

1) tyrosine hydroxylated to DOPA
2) DOPA decarboxylated to dopamine
3) dopamine hydroxylated to NE (inside vesicles)
4) NE release by vesicle, then metabolized and excreted

Question 12

M2/M4 receptors do what?

Answer 12

couple to Gi and inhibit adenylate cyclase (reducing cAMP levels) and/or activate K+ channels (causing hyperpolarization)

M2 affect slowing of heartbeat and inhibition of NT release by M2

Question 13

M1/M3/M5 receptors do what?

Answer 13

couple to Gq and activate phospholipase C–> increase DAG and IP3 (and thus Ca+2) levels

M1 affect neuroregulation, M3 affect smooth muscle contraction

Question 14

alpha1 receptors do what?

Answer 14

couple to Gq and activate phospholipase C–> increase DAG and IP3 (and thus Ca+2) levels

alpha1 affect smooth muscle contraction

Question 15

alpha2 receptors do what?

Answer 15

couple to Gi and inhibit adenylate cyclase (reducing cAMP levels) and/or activate K+ channels (causing hyperpolarization)

alpha2 inhibit NT release

Question 16

beta1/beta2/beta3 receptors all do what?

Answer 16

couple to Gs–>increase adenylate cyclase –> increase cAMP

beta1 increase force/rate of contraction of heart
beta2 cause smooth muscle relaxation
beta3 cause lipolysis

Question 17

Presynaptic regulation – what are some examples?

Answer 17

1) autoreceptors = presynaptic receptors that respond to the transmitter substances released (release of NE from terminal activates alpha2 receptors and diminishes further release of NE)
2) heterorecepors = respond to transmitter other than those released from the terminal

Question 18

mechanism for M3 receptor action on pupillary constriction

Answer 18

Ach release from postgang parasymp–>couple to Gq and activate phospholipase C–> increase DAG and IP3 (and thus Ca+2) levels–>activation of myosin light chain kinase–>phosphorylates myosin–>contraction of pupillary muscle

Question 19

Response of pilocarpine injection

Answer 19

stimulates M3 receptor to increase salivation