GABA-activated chloride channels in secretory nerve endings.
Neurotransmitters acting on presynaptic terminals regulate synaptic transmission and plasticity. Because of the difficulty of direct electrophysiological recording from small presynaptic terminals, little is known about the ion channels that mediate these actions or about the mechanisms by which transmitter secretion is altered. The patch-clamp technique is used to show that the predominant inhibitory presynaptic neurotransmitter, gamma-aminobutyric acid (GABA), activates a GABAA receptor and gates a chloride channel in the membranes of peptidergic nerve terminals of the posterior pituitary. The opening of a chloride channel by GABA weakly depolarizes the nerve terminal membrane and blocks action potentials. In this way, GABA limits secretion by retarding the spread of excitation into the terminal arborization.
Zhang
S J
SJ
Department of Physiology, University of Wisconsin Medical School, Madison 53706.
Jackson
M B
MB
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002707:Chlordiazepoxide / Q000494:pharmacology; D018118:Chloride Channels; D002712:Chlorides / Q000378:metabolism*; D058787:GABA-A Receptor Antagonists; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008565:Membrane Proteins / Q000187:drug effects / Q000502:physiology*; D009118:Muscimol / Q000494:pharmacology; D009411:Nerve Endings / Q000187:drug effects / Q000502:physiology*; D010852:Picrotoxin / Q000494:pharmacology; D010904:Pituitary Gland, Posterior / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011963:Receptors, GABA-A / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
D001640:Bicuculline; D002707:Chlordiazepoxide; D018118:Chloride Channels; D002712:Chlorides; D058787:GABA-A Receptor Antagonists; D008565:Membrane Proteins; D009118:Muscimol; D010852:Picrotoxin; D011963:Receptors, GABA-A; D005680:gamma-Aminobutyric Acid