Drugs Relating to Electrophysiology Flashcards
GLU
Aka Glutamate
(excitatory neurotransmitter)
Binds to NMDA receptor (mixed Na+/Ca++ channel) to depolarize (easier for AP to occur)
GABA
Inhibitory neurotransmitter
Binds to GABAa receptor (Cl- channel) to hyperpolarize/resist depolarization (harder for AP to occur)
Phenobarbital
Increases activation of GABAa RECEPTOR (inhibits neuron firing bc there is an increase in inhibitory neurotransmitters)
Diazepam
Increases activation of GABAa RECEPTOR (inhibits neuron firing bc there is an increase in inhibitory neurotransmitters)
Tiagabine
Inhibits GAT-1 –> inhibits GABA uptake (TRANSPORTER) which increases [GABA] in cleft
Vigabatrin
Inhibits GABA-T –> decreases GABA breakdown (ENZYME) which increases [GABA] available to be released into cleft
Felbamate
Inhibits NMDA RECEPTOR (decreases excitatory due to less uptake of GLU)
Gabapentin
Increases GABA release + Decreases GLU release (NEUROTRANSMITTERS)
Phenytoin
Prolongs Na+ channel inactivation –> increases refractory period –> resists depolarization (ION CHANNEL)
Carbamazepine
Prolongs Na+ channel inactivation –> increases refractory period –> resists depolarization (ION CHANNEL)
Ethosuximide
Inhibits Ca++ channels (ION CHANNEL)
Permethrin
General: holds Na+ channels open (causing depolarization)
Low Dose: some Na+ channels open (like leak channels) –> Vm slowly depolarizes towards thresholds (causing uncontrolled APs)
High Dose: Depolarization Blockage = Na+ channels open and cause large depolarization + can’t repolarize
Lidocaine
General: Na+ channel blocker
Low Dose: prolongs inactivation of Na+ channels (decreases firing AP)
High Dose: blocks opened Na+ channels (prevents APs)