L/D 3: Synaptic Potentials

Question 1

how does the time constant of the cell membrane allow temporal summation of synaptic potentials?

Answer 1

EPSP shoots up quick, declines slowly, optimal for another EPSP to come along and summate
explanation:
τ = RmCm = time to 63% charge or discharge
τ is low (fast) on EPSP depolarization because R is lower (receptor opens Na/K channels)
τ is high (slow) on EPSP repolarization because R is higher (Na/K channels closing)

Question 2

what dendrite geometric factors influence the efficacy of a given excitatory synaptic input in activating a cell AP?

Answer 2

• radius of dendrite (greater λ)

- proximity of dendrite to axon hillock

Question 3

what synaptic ion channel characteristics influence the efficacy of a given excitatory input?

Answer 3

• ionotropic vs metabotropic receptor (quick action low amplitude vs slower action larger amplitude)
• Na/K permeability of opened ion channels

Question 4

how does decreasing membrane resistance affect temporal and spatial EPSP summation?

Answer 4

makes it harder to summate (higher stimulation strength/frequency needed)
explanation:
Rm down, then τ down and λ down
so EPSP moves quicker and disperses quickly, harder to summate

Question 5

how does increasing membrane resistance affect temporal and spatial EPSP summation?

Answer 5

easier to summate (lesser stimulation strength/frequency needed)
explanation:
Rm up, then τ up and λ up
so EPSP travels slower and lasts longer, easier to summate

Question 6

does changing Rm change Cm?

Answer 6

no
C = ε ε0 A/x
channels are such small proportion of membrane that dielectric constant remains unchanged

Question 7

what are the mechanism by which IPSPs reduce the effectiveness of EPSPs?

Answer 7

2 ways
hyperpolarize - open K+ channels (Ek < Vm)
stabilize - open Cl- channels (Ek ~ Vm)

Question 8

what is a reversal potential

Answer 8

it is the equilibrium potential for a given ion channel

• if that channel is permeable only to K+, then Vrev = Ek
• if that channel is equally permeable to both K+ and Na+, then Vrev = (Ek+Ena)/2
• if that channel is unequally selective for multiple ions, then Vrev = ΣgiEi / Σgi

Question 9

what is reversal potential of a post-synaptic potential originated by the opening of K+ selective channels

Answer 9

Vrev = Ek

Question 10

what is reversal potential of a post-synaptic potential originated by the opening of Na+ selective channels

Answer 10

Vrev = Ena

Question 11

what is reversal potential of a post-synaptic potential originated by the opening of channels equally selective for Na+ and K+

Answer 11

Vrev = (Ena+Ek)/2

Question 12

what is reversal potential of a post-synaptic potential originated by the opening of channels unequally selective for multiple ions

Answer 12

Vrev = ΣgiEi / Σgi

from Inet = 0 = ΣIi = Σgi(Vm-Ei

Question 13

how would you determine whether decreased motor output stems from a problem with the motor nerve (axon), the muscle itself, or the synapse?

Answer 13

• stimulate motor nerve, if AP, no prob
• stimulate muscle endplate, if contract, no prob
• stimulate nerve, if no contract, synapse prob

Question 14

if both motor nerve and effector muscle are electrically functional but there is a synaptic problem, ho to ascertain whether problem is pre or post synaptic?

Answer 14

pipette NT into synapse, see if responds

Question 15

if you stimulate a motor nerve repetitively and the muscle response progressively lessens, what does this indicate?

Answer 15

NT production/recycling is not keeping up with stimuli

Question 16

if you stimulate a motor nerve repetitively and the muscle response is constant but weaker than normal, what does this indicate?

Answer 16

either

• fewer vesicle released (but MEPP is normal)
• less NT per vesicle (MEPP is abnormally low)

Question 17

what does a low MEPP indicate

Answer 17

-low quantal content

low NT concentration in vesicles

Question 18

what do normal MEPPs but low EPPs indicate

Answer 18

problem with vesicle release

but vesicles have normal quantal content

Question 19

if you suspect a problem with vesicle release in the neuromuscular junction, what factor do you suspect and how do you test it?

Answer 19

Ca++

increase Ca++ gradient to see if mechanism is working

Question 20

Lambert-Eaton myasthenic syndrome (LEMS)

Answer 20

probably autoimmune disorder probably due to shared antigenic sites between neuroectodermal tumor and NT vesicle release machinery
-results in muscle weakness, fatigue, ANS sysfunction

Question 21

myasthenia gravis

Answer 21

auto-immune disease in which circulating antibodies target N2 nicotinic ACh receptors causing cross-linking and promoting degradation. muscle fatigue and weakness

Question 22

how does myasthenia gravis affect the autonomic nervous system?

Answer 22

it doesn’t
-targets N2 receptors only (motor endplates)
does NOT target N1 receptors (autonomic ganglia)

Question 23

suggest 3 pharmacological strategies to alleviate symptoms of myasthenia gravis

Answer 23

• inhibit ACh-E
• inhibit ACh-Na symports and reuptake (not as good because may run low on ACh-E)
• immunosuppresants