Abstract: Both the naturally occurring (—)‐isomer and the synthetic (+)‐isomer of nicotine caused release of 3H from a crude synaptosomal fraction of rat brain prein‐cubated with [3H]dopamine. The isomers were equipotent in producing this response, which was concentration‐dependent, a significant effect on the fractional release of dopamine being observed at 10−4M nicotine. The effect did not appear to be the result of synaptosomal damage, as levels of the intrasynaptosomal marker lactate dehy‐drogenase did not increase in the supernatant. Nicotine‐induced release was inhibited by removal of external Ca2+ and by the presence in vitro of pempidine (230 μ.M). Neither hexamethonium (500 μ.M) in vitro nor the chronic administration of (‐)‐nicotine in vivo had any effect on the nicotine‐induced release of [3H]dopamine. It is concluded that nicotine exerts this effect via a presynaptic nicotinic receptor of the “ganglionic” type, but that this receptor differs from that in the periphery by showing a relative lack of stereospecificity. There is no evidence of a functional “down regulation” in this receptor on chronic exposure to nicotine in vivo.
|Number of pages||6|
|Journal||Journal of Neurochemistry|
|State||Published - May 1983|
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience