The stimulation of cholecystokinin receptors in the rostral nucleus accumbens significantly antagonizes the EEG and behavioural effects induced by phencyclidine in rats.
P Popoli, R Reggio, A Pezzola, A Scotti de Carolis
Psychopharmacology July 1995 DOI: 10.1007/bf02246188 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal experiment Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | Cholecystokinin (CCK) phencyclidine (PCP) PD 135-158 lorglumide |
| Dose | CCK 10 ng; PD 135-158 1 ng; lorglumide 1 microgram |
| Key findings | CCK (10 ng) injected into the rostral nucleus accumbens inhibited PCP-induced EEG and behavioral effects in rats; this inhibition was blocked by a CCKB receptor antagonist but not by a CCKA receptor antagonist. The authors propose that CCK may act as a neuroleptic and that accumbens CCKB receptors may be involved. |
Abstract
The influence of cholecystokinin (CCK), bilaterally injected into the rostral nucleus accumbens, on the EEG and behavioural effects induced by phencyclidine (PCP) has been studied in rats. CCK (10 ng) significantly inhibited PCP-induced EEG effects (increase of spectral power with respect to pre-drug tracing; increase of relative power distribution in the slowest frequency bands), and behavioural effects (circling and ataxia). The inhibitory effects of CCK were completely antagonized by 1 ng PD 135-158, a selective CCKB receptor antagonist, but not by lorglumide (1 microgram), a selective CCKA receptor antagonist. Since the effects induced by PCP in rodents have been proposed to be an experimental correlate of the psychotic symptoms it induces in humans, these results indicate that CCK may act as a neuroleptic. They also suggest that CCKB receptors located in the rostral nucleus accumbens may be involved in the neuroleptic-like activity of CCK.