Pre- and post-synaptic inhibition.
We now know a great deal about central inhibitory mechanisms: how they are organized in various neuronal circuits ("feed-forward" and "feed-back" inhibitions, inhibition of inhibitory cells giving "disinhibition" which releases neuronal activity in a finely graded and particularly safe manner); how they exercise a preponderant control over much of central neurl activity (9, 13, 14, 57); and of course, how inhibition operates at the cell membrane, by increasing Cl- permeability; this has a stabilizing action post-synaptically, but presynaptically, in afferent fibers, it depresses transmitter release from afferent terminals. In addition, there is some evidence that GABA transport may be electrogenic and therefore may significantly modulate membrane excitability, and that GABA may selectively depress Ca2+ influx in afferent terminals and thus inhibit transmitter release particularly effectively. However, it is by no means certain that we are fully aware of all the possible ways in which GABA affects neuronal excitability and synaptic transmission, and there may well be further exciting surprises in store.
D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D004553:Electric Conductivity; D005727:Ganglia, Spinal / Q000187:drug effects / Q000502:physiology; D005971:Glutamates / Q000494:pharmacology; D005998:Glycine / Q000494:pharmacology; D006321:Heart / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D013569:Synapses / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D005971:Glutamates; D005680:gamma-Aminobutyric Acid; D005998:Glycine