BIOL 3051 Chapter Notes - Chapter 9.3: Carbamazepine, Lidocaine, Signal Transduction
24 Apr 2020
School
Department
Course
Professor
Document Summary
Stimulus ap propagation synaptic transmission to cns processing & plasticity in spinal dorsal horn brain. Nociceptor transduction: nociceptive sensory neurons are activated by noxious (harmful) stimuli, ap propagates to dorsal horn of spinal cord, blockade of ap (by gaba activating interneurons) prevents signal transduction. Activation & inactivation of na+ channel: opening of activation gate during depolarization, delayed closing of inactivation gate during depolarization, recovery from inactive state (to closed) requires hyperpolarization. Two gates involved: activation & inactivation gate. Inactivation gate closed shortly after activation gate opening during depolarization. Hyperpolarization opens the inactivating gate, closes the activation gated closed conformation. Its stabilize neural membrane to limit seizure active: carbamazepine stabilizes inactive state (w/loop) prevents depolarization, prevents depolarization by decreasing na+ influx, carbamazepine is na+ channel blocker in inactive state. Action potential inhibition- lidocaine: lidocaine binds to inactive state of na+ channel, higher the concentration of lidocaine, lower conductance of current more depolarizing.
