Espana

Question 1

parts of NMJ

Answer 1

Myelin ends so weak blood brain barrier but schwann cells around bulb
cleft
motor endplate manifold
receptors Na channels
primary and secondary clefts
vesicles

Question 2

synaptic transmission

Answer 2

AP goes to presynaptic terminal
voltage gates let Ca in
Vesicles fuse with pre mem
NT release via exo
NT bind to receptors post letting Na in
depolarization open channels to let more Na in 
IPSP or EPSP

Question 3

features of nicotinic receptor

Answer 3

cylindrical
5 subunits: 2 alpha, beta, delta, gamma
only two alphas bind to ACh

Question 4

AP

Answer 4

Action potential when threshold is reached also the Vm change reaching pre side

Question 5

EPSP

Answer 5

Positive influx of ions pushing membrane toward threshold

Question 6

IPSP

Answer 6

negative influx of ions hyperpolarizing

Question 7

EPP

Answer 7

end plate potentials

Question 8

Acetylcholine gating kinetics

Answer 8

Tau is time to rise or decay

either because of time for ACh to go away or for AChr to close (spoiler its to close because ACh goes away faster)

Question 9

Steps of Excitation Contraction coupling

Answer 9

same steps of synaptic transmission cause an action potential in muscle
AP goes through sarcolemma in T tubules
AP opens Ca release from cisternae of SR
Ca binds to troponin changing its shape to remove tropomyosin exposing actin acitve sites
dont need to know rest but myosin bridges and pulling with ATP
until Ca is moved back into SR and tropomyosin blocks it again

Question 10

why is contraction delayed and relaxation slow

Answer 10

delayed as it takes a while for charge to reach SR and release Ca
Ca reuptake is slow?

Question 11

model of probabilities of ligan binding to AChR

Answer 11

R is receptor
A is agonist(ligand)
* is open
each state can move in either direction but
R to AR to A2R to A2R*
then closes faster than release
even more complicated because desensitization

Question 12

myesthinia gravis

Answer 12

autoimmune kills AChR so weak contractions like droopy eye

Question 13

choline acetyltransferase deficiency

Answer 13

make less ACh

treated with agonsits

Question 14

acetylcholinesterase deficiency

Answer 14

cant break it up so cant relax, end plate destruction

Question 15

Slow channel syndrome

Answer 15

Mutation of AChR
Longer EPP
Longer recep opening
increased open probablitiy
slow decay/slower Tau because channels stay open longer
longer decay means more likely to summate
happens because mutated receptors can respond to choline not just ACh
patients have some mutated some normal recept