Lecture 48 Neuromuscular Control Flashcards
what form of termination of transmitter would NT being returned to axon terminals or transported into glial cells?
- reuptake
Enzymes inactivating neurotransmitters would be?
- breakdown
Neurotransmitters diffusing out of synaptic cleft would be?
- diffusion
Where are small molecule NT made?
- nerve terminal
Where are peptide NTs made?
- in the cell body at ER and golgi packages them
What is lidocaine a derivative of?
- cocaine
- VGNA channel blocker
How does lidocaine block pain?
- it prevents Na from producing AP to tell brain you have pain
Tetrodotoxin
- VGNa channel blocker
Caffeine
- increases cAMP which increases excitability of neuron
How do SSRIs work?
- block reuptake of NTs like seratonin so you are increasing seratonin in blood and altering mood
- reduce anxiety and depression
- seratonin must remodel circuitry in blood bc it takes weeks
What does cocaine do?
- block reuptake in DA and NE
-
What systems to ectasy and amphetamines do?
- effect DA, NE, 5HT neurons
- cause NT to leak out of vessicle and out of reuptake channels (wrong way)
- increases dopamine, norepinerine, seratonin in blood
Where does long term potentiation occur?
- hippocampus
learning and memory
What is long term potentiation?
- strengthening synapse
- increasing sensitivity ( adding more receptors to membrane)
- can also increase the quanta
What are efferent signals?
- motor neurons
- away from CNS
What is a motor unit?
- motor neuron and all the fibers it innervates
What type of receptor does ach bind to in a muscle contraction?
- nicotinic which allows Na+ in the muscle
What happens once Na+ travels into muscle?
- opens voltage gated na channel which makes action potential to spread through muscle
What type of potential does the ach cause?
- it causes an end plate potential that reaches threshold and then an action potential occurs
- unless a diseased state
How does the AP translate into an increase in Ca and ultimately a muscle contraction?
- Na travels down T tubule then interacts which DHPRs
- DHPRS changes conformation to touch RyR1 which will then release Ca for muscle contraction
where does the calcium go from the RYR?
- it goes to the actin and myosin for muscle shortening
- it also goes to other Ryodine receptors to release more calcium for muscle contraction
How does Duchenne muscular dystrophy work?
- mutation in DMD gene encoding dystrophin
- dystrophin provides scaffolding for muscle
- strength of muscle contraction way down bc no scaffolding
What does ache do?
- break down ACh to choline and acetic acid
- essential to make sure we aren’t in tetnus
How do we get rid of calcium to terminate of contraction?
- SERCA pump
- pumping calcium against gradient into SR
- also can pump CA through ATPase out of cell
