Synapses

Question 1

what are the two major categories of neurotransmitters

Answer 1

small- biogenic amines, glutamate, GABA, AcH

large/neurohormones- opioids, cannabinoids, vasopressin, oxytocin, GnRH

Question 2

two major receptor classes

Answer 2

ionotropic- ligand gated channels w/ ion channel at core.. amino acids line the pore that confers ion selectivity. operate in milliseconds. ligand binding causes a confirmational change. do not requre ATP

metabotropic- g-coupled receptors w/o ion channel. ligand gating activates second messengers that affect neighboring ion channels. produce slower effects than ionotropic

Question 3

major excitatory receptors

Answer 3

nicotinic AcH (skeletal and neuronal)
glutatamate- (NMDA, AMPA, Kainate)
purinergic- (adenosine and ATP)

Question 4

major inhibitory receptors

Answer 4

GABA type A (major fast inhibitor in the brain)

glycine- (major fast inhibitor in spinal cord)

Question 5

define NT excitation

Answer 5

drive membrane potential towards a value that is more depolarized than the threshold potential for an AP

Question 6

what is the NT/receptor combination at neuro muscular junctions

Answer 6

AcH/ nicotinic AcH receptors

Question 7

safety factor

Answer 7

each AP in the presynaptic cell gives rise to an AP in the post synpatic cells

Question 8

how are the safety factors in the musculature different than those in the CNS?

Answer 8

in the musculature, a presynaptic AP = postsynaptic AP

in CNS, presynaptic APs release very little NT

Question 9

active zones

Answer 9

found in the presynaptic terminal of the nmj, it is the combination of vesicles docked to the cytoskeleton adjacent to voltage dependent Ca channels. when Ca enters, it will trigger fusion and exocytosis of AcH from within the vesicles

Question 10

describe the Ca influx in the presynaptic vesicle

Answer 10

huge driving potential, nernst potential is +100. rapidly increases free {Ca}, but only near the membrane. this allows it to be quickly buffered back down.

Question 11

synaptic delay

Answer 11

time it takes for arrival of AP in presynpatic terminal until influx of postsynpatic current

Question 12

SNARE

Answer 12

proteins on the vesicle and membrane that are responsible for the proper fusion and exocytosis of NTs. when in contact, they undergo a confirmational change in the a-helicies and zipper together, releasing energy that feeds fusion of the vesicles

Question 13

synaptotagmin

Answer 13

calcium sensor in the SNARE complex. Ca binding releases binding proteins from the complex and allows the conformational changes that promote membrane/vesicle fusino to occur

Question 14

quantum

Answer 14

release of NT occurs in discrete packets because of their vesicle-mediated release mechanism

Question 15

botulinum and tetanus toxins

Answer 15

target SNARE proteins involved in vesicle release

botox is targeted to acidic vesicles, where the pH releases the light chain into the cytoplasm. it can then cleave SNAREs

tetanus si retrogradely transmitted through a-motorneurons to secondary inhibitor interneurons

Question 16

nicotinic AcH R

Answer 16

found at nmjs, ionotropic

permeable to both Na and K. Na flows in, K flows out. drives potential to 0 mV. selectivity slightly favors Na

Question 17

reversal potential

Answer 17

“equilibrium potential” in ionotropic pores w/ 2 ions. movement across the reversal potential causes flux to reverse direction

Question 18

what is the action of any NT at an ionotropic receptor

Answer 18

drive the membrane potential towards the reversal potential

Question 19

what are the 2 ways neurons can alter their efficacy?

Answer 19

efficacy= strength

1 altering # of vesicles released
2 altering probability that any vesicle will be released

given by equation

mean quantal content = number of vesicles x probability of vesicle being released

Question 20

why are nmj synapses so effective

Answer 20

each AP releases lots of AcH

and the postsynaptic fibers are specialized (lots of receptors found at the top of postsynpatic folds) to optimize the ACh

Question 21

lambert eaton syndrome

Answer 21

autoimmune disorder where Abs directed at presynaptic VDCC in presynaptic motorneurons and cholinergic neurons in the ANS. results in defectuve synaptic transmission

manifested by muscle weakness, fatigue, difficulty walking, speech and swallowing difficulties

treated w/ voltage dependent K blocking drugs

Question 22

post synaptic nmj specialization

Answer 22

clusters of AChRs at the tops of membrane folds

high density voltage dependent Na channels in the troughs which trigger excitation/contraction

folds form a funnel that directs free ACh. this funnel has a basal lamina w/ AChE embedded, which breaks down free ACh

Question 23

AChE

Answer 23

breaks down ACh. binds at 2 sites and releases free choline

Question 24

ligand gated desensitization

Answer 24

if ligand remains bound for an extended period of time, then the receptor will undergo a conformational change that results in a non-conducting state

Question 25

organophosphates

Answer 25

pesticides, weapons

inactivate AChE and cause desensitization

Question 26

myasthenia gravis

Answer 26

autoimmune disease where Abs generated against the AChRs but do not cause excitation

results in compromised synaptic transmission

msucle weakness, ptosis, slurred speech, difficult swallowing, facial weakness