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Journal of Neuroscience, Vol 15, 1144-1149, Copyright © 1995 by Society for Neuroscience
Depolarization inactivation of dopamine neurons: an artifact?
G Mereu, V Lilliu, P Vargiu, AL Muntoni, M Diana and GL Gessa
Department of Experimental Biology, University of Cagliari, Italy.
A widely accepted theory postulates that, in rats, chronic treatment with
neuroleptics causes the depolarization inactivation of the majority of
midbrain dopamine (DA) neurons. The present study was aimed to verify
whether general anesthesia and/or other factors might contribute to the
depolarization inactivation of A9 and A10 DA neurons. To investigate on the
possible role played by DA receptor subtypes, three representatives DA
antagonists were used: haloperidol (a mixed D1/D2), (-)-sulpiride (a
selective D2) and SCH 23390 (a selective D1). In agreement with previous
studies, where neuronal sampling was carried out in animals under chloral
hydrate anesthesia, chronic treatment with haloperidol (0.5 mg/kg daily for
21-28 d) produced a profound reduction (about 80%) in the number of
spontaneously active A9 DA neurons. However, when neuronal sampling was
performed in unanesthetized rats, the single administration of haloperidol,
(-)-sulpiride, or SCH 23390 (0.5, 25, and 0.3 mg/kg respectively 2-3 hr
beforehand) increased the number of spontaneously active A9 and A10 DA
neurons and their firing rate, whereas the chronic administration of these
drugs (daily for 21- 28 d) failed to reduce the number of spontaneously
active A9 and A10 DA neurons. The inhibitory effect of apomorphine on the
firing rate of A9 and A10 DA neurons was prevented 3-4 hr after the acute
or last injection of chronic haloperidol or (-)-sulpiride. However, the
inhibitory effect was potentiated 24 hr after the last administration of
the chronic regimen with these neuroleptics, but it was not influenced by
either acute or chronic treatment with SCH 23390.(ABSTRACT TRUNCATED AT 250
WORDS)
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