Wk 4 Neural Communication Flashcards
Hyperkalemia results
increased extracellular [K+] causes depolarization–>VG Na+ channels cannot be inactivated–> no AP
Tetrodotoxin function
blocks VG Na+ channels, found in pufferfish
Hyperkalemic periodic paralysis
mutation in VG Na+ channel, stay open during hyperkalemia causing transient paralysis
Absolute refractory period
stimulus produces no AP
Relative refractory period
stimulus produces but AP is not same amplitude
Why do APs not travel backward “up” axon?
A ==> B ==> C
A depol and brings Na+ into axon, diffusing in all directions and depolarizing B. B then repeats this for C, but cannot travel backwards because the ion channel upstream is still in its absolute refractory period
Spacing of Na+ channels in unmyelinated and myelinated fibers
close in unmyelinated, only at nodes of myelinated
Pathology of MS
demyelination of myelinated axons in CNS
Lidocaine–mechanism of action
blocks VG Na+ channels, affects C fibers (pain) most because only affects small area, most likely to disrupt C fibers because A and B fibers have VG Na+ channels only at nodes. reason we can move a muscle before we can feel it after being injected with lidocaine
How does diameter of an axon affect its ability to conduct a signal?
larger diameter ==> faster conduction
2 types of synapses
electrical
chemical
How often do synapses fail?
> 50% of the time
3 stages of chemical synapse signal transmission
- NT release
- NT binding
- Active termination (diffusion, degradation, reuptake)
Most secure synapse
auditory (then neuromuscular junction)
Describe the steps in depolarization of axon terminal/NT release
- AP travels down to axon terminal
- VG Ca2+ channels open
- Ca2+ enters nerve terminal
- NT vesicles fuse to membrane (exocytosis)
Botulinum toxin
destroys NT docking proteins on nerve terminal, no ACh released ==> flaccid paralysis
Tetanus toxin
travels up to inhibitory neuron, block inhibitory glycine release ==> tetanic paralysis
Dale’s Principle
neuromodulators affect primary NT release, each axon terminal releases same set of NT
3 primary NT types
- “classic” like ACh, NE, Epi
- peptides like insulin
- gases like NO
3 types of receptor activation
- autocrine
- paracrine
- hormonal
Two types of NT receptors
ionotropic–fast
metatropic–slow
ionotropic NT receptors
use ion channels, ligand and ion flow are coupled in same protein
metatropic NT receptors
uses second messenger systems
agonist
elicits same action as NT
