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Effects of phencyclidine on the spontaneous activity of monoaminergic neurons

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Abstract

Intravenous phencyclidine (PCP) increased the firing rate of a population of slow firing dopaminergic neurons recorded in the substantia nigra of chloral hydrate anesthetized rats. PCP also significantly reduced the potency of i.v. d-amphetamine to inhibit the firing of dopaminergic neurons. The drug produced little changes in the activity of serotonergic neurons of the dorsal raphe and consistently inhibited the firing of noradrenergic neurons in the locus coeruleus.

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    Citation Excerpt :

    Major behavioral effects of low, but not high, doses of PCP and MK-801 can be antagonized by catecholamine depletion or by administration of dopamine receptor antagonists (Fessler et al., 1980; Clineschmidt et al., 1982; Criswell et al., 1993; Willins et al., 1993), indicating that these effects of PCP and MK-801 are largely dopamine-dependent. Moreover, systemic administration of PCP or MK-801 even at very low doses potently activates dopamine neurons in the ventral tegmental area (VTA) (Raja and Guyenet, 1980; Freeman and Bunney, 1984; Pawlowski et al., 1990; Murase et al., 1993). Recent studies demonstrate that MK-801, like PCP, increases dopamine output to the greatest extent in a limbic cortical area, the medial prefrontal cortex, and also significantly in the nucleus accumbens (NAC), but not e.g. the dorsolateral striatum, as assessed by microdialysis techniques in freely moving rats (Wedzony et al., 1993; Wolf et al., 1993; Hertel et al., 1995; Mathe et al. 1996, 1998; Miller and Abercrombie, 1996).

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