Cholinergic modulation of synaptic transmission in the rat visual cortex in vitro.
Cholinergic synaptic modulation in the rat visual cortex was studied using intracellular recordings from slice preparations. A cholinergic agonist, carbachol (CCh), reduced fast excitatory as well as fast and slow inhibitory postsynaptic potentials evoked by white matter stimulation. This effect was antagonized by atropine. CCh perfusion did not reduce glutamate- or gamma-aminobutyric acid-induced depolarizations, suggesting the presynaptic mechanism of the suppression. CCh augmented firing over a long period after transsynaptic stimulation combined with a long depolarizing current pulse, not only due to a decrease in firing accommodation but also due to disinhibition. CCh also induced a large sustained depolarization and bursting of action potentials triggered by tetanic stimulation. These results suggest that cholinergic modulation results in a prolonged increase in neuronal excitability during the late phase of synaptic transmissions at least partly by the mechanism of decreasing inhibitory transmissions, particularly when the synaptic inputs are strongly activated.
Laboratory of Neurobiology, Rockefeller University, New York, NY 10021.
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Murakoshi
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002217:Carbachol / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D005071:Evoked Potentials / Q000187:drug effects; D005971:Glutamates / Q000494:pharmacology; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009433:Neural Inhibition; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission / Q000187:drug effects*; D014793:Visual Cortex / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005971:Glutamates; D005680:gamma-Aminobutyric Acid; D001285:Atropine; D002217:Carbachol