Acetylcholine and norepinephrine mediate slow synaptic potentials in normal and epileptic neocortex.
Slow excitatory postsynaptic potentials (EPSPs) were identified in rat neocortical slices. Such potentials, resistant to blockade of glutamate and gamma-aminobutyric acid-A (GABAA) receptors, were partially antagonized by muscarinic or beta-adrenergic antagonists separately, and completely blocked when these agents were added in combination. Slow EPSPs were enhanced by a cholinesterase inhibitor or catecholamine reuptake blockers. Spontaneous epileptic discharges induced by picrotoxin also triggered slow EPSPs. Such potentials were pharmacologically identical to those induced by electrical stimulation under normal conditions. A non-conventional mechanism for synaptic transmission is postulated to account for triggering of slow EPSPs by epileptic discharges.
Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY 10032.
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Benardo
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D004594:Electrophysiology; D004827:Epilepsy / Q000503:physiopathology*; D066298:In Vitro Techniques; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D012016:Reference Values; D013569:Synapses / Q000502:physiology*
D000109:Acetylcholine; D009638:Norepinephrine