Nicotinic depolarization of optic nerve terminals augments synaptic transmission.
The role of acetylcholine (ACh) as the neurotransmitter at the vertebrate neuromuscular junction has served as a model in the study of synaptic physiology throughout the nervous system, but its function in the brain has remained obscure. Nicotinic ACh receptors are found on afferent nerve terminals in several regions of vertebrate brain, and nicotinic agonists can cause transmitter release (as measured biochemically). Yet there is no direct evidence that activation of these receptors modulates synaptic function. Here I report that nicotinic agonists directly depolarize optic nerve terminals in goldfish tectum recorded via sucrose gap and simultaneously enhance synaptic transmission recorded via tectal field potentials. I also show that a recurrent cholinergic circuit in tectum, acting on these terminals, initiates antidromic impulses that cause repeated transmission at the retinotectal synapses.
King
W M
WM
Department of Biological Sciences, State University of New York, Albany 12222.
D000818:Animals; D006054:Goldfish; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D018733:Nicotinic Antagonists; D009900:Optic Nerve / Q000187:drug effects*; D011978:Receptors, Nicotinic / Q000187:drug effects*; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic