Pharmacology of neuromuscular junction

Question 1

what are the three levels of motor input

Answer 1

1) cortical level = highest level of neuronal activity
2) Subcortical= primitive = food , water , reproduction
3) Spinal cord levels = homeostasis , reflex etc

Question 2

outline the release of ACH in NMJ
(4)
muscle cell
(4)

Answer 2

1-Impulse arrives , causing ca2+ channels to open
2-This causes Exocytosis of ACH vesicles
3-Ach binds to receptor and this causes ligand gated na+ channels to open = depolarisation =AP
4-eventually V-G channels open too

ON THE MUSCLES CELLS :

• AP deep into sarcolema
• T-tubules
• V-G ca2+ channels on T-tubules, coupled to Ryanodine Receptors on Sarcoplasmic reticulum cause INTRACELLULAR CA2+ release
• Contraction occurs
• HOWEVER = ca2+ pump limits contraction ( by pumping ca2+ back into the SR)

Question 3

what is a twitch potential ?

Answer 3

1 AP = 1 TWITCH ( building block of contraction )

Question 4

what is myasthenia graves?

m

Answer 4

Myaesthenia Gravis :autoimmune
1- antibodies against nicotinic ACH recptors
2-Causes muscle weakness
3-Too few receptors + unchanged ACHE = end plate potential is too low FOR AP

Question 5

How is ACHe cleared ? (1)

Answer 5

1-enzyme acetylcholinesterase –>converts ACHE –>Choline + Acetate

Question 6

what is eaton Lambert sydrome ?(3)

Answer 6

1-Antibodies against Nerve terminal ca2+ channel (autoimmune )
2-ONLY SMALL AMOUNT OF ACHE in cleft
3-Poor ACHE release
4- no good contraction

Question 7

what are some pharmacological manipulations of NMJ?
(3)
examples ?
(3)

Answer 7

1-DECREASING ACHE release = Botox ( Botulinus Toxin = flaccid paralysis )

2-Alter ACHE binding = muscle relaxant in surgery and also lethal injection for death
-CURARE = competitive antagonist of nicotinic ACH receptor

3-Change ACHESTERASE activity = Good effects on Treating myasthenia Gravis and paralysis