Neuronal excitability - excitatory vs inhibitory ion channel/receptor mechanisms
Core concept
- Excitability = balance of depolarising cation influx against hyperpolarising Cl- influx / K+ efflux
- Glutamate = principal excitatory; GABA (brain) and glycine (cord, brainstem) = principal inhibitory
Excitatory
| Receptor | Type | Ion | Note |
|---|---|---|---|
| AMPA | ionotropic | Na+ (K+) | fast EPSP; GluA2-lacking forms are Ca-permeable |
| NMDA | ionotropic | Ca2+ + Na+ | slow, coincidence detector |
| Kainate | ionotropic | Na+ | pre- and postsynaptic modulation |
| mGluR1-8 | GPCR | - | slow modulation |
| nAChR | ionotropic | Na+/Ca2+ | NMJ and CNS |
Inhibitory
| Receptor | Type | Ion | Note |
|---|---|---|---|
| GABA-A | ionotropic | Cl- in | benzodiazepines, barbiturates, propofol, ethanol, neurosteroids |
| GABA-B | GPCR (Gi) | K+ out, dec Ca2+ | baclofen; slow IPSP |
| Glycine | ionotropic | Cl- in | brainstem/cord; strychnine antagonist; blocked by tetanus toxin |
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