Abstract
Three groups of meso-accumbens (Acc) neurons in the ventral tegmental area were differentiated by their antidromic discharge property; dopaminergic type 1 (n = 10), non-dopaminergic type 2 (n = 2) and unclassified (n = 2) neurons. During repetitive activation at 10 Hz, the latency of the initial segment (IS) spike, which was often not followed by the somadendritic (SD) spike, was gradually prolonged in type 1, but not in type 2 and unclassified neurons. The latency prolongation of type 1 neurons was reduced to about a half of the normal in rats treated with kainic acid plus haloperidol, but only slightly when treated with kainic acid or picrotoxin. The rate of SD invasion tended to increase after all kinds of chemical treatment. Stimulation of the medial forebrain bundle in type 1 neurons gave responses comparable to Acc stimulation. It is suggested that the latency prolongation of IS spike is produced mainly by axonal mechanism. But additional somatic mechanisms such as dopaminergic self-inhibition and GABAergic and non-GABAergic inputs from the Acc would make some contribution, and at the same time produce frequent suppression of the antidromic SD spike.
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