Effects of raphe stimulation on hippocampal and neocortical activity and behaviour

In chronically prepared rats, electrical stimulation (100 Hz, 0.1 ms pulses) of the dorsal raphe nucleus, some sites in the median raphe nucleus, and adjoining regions of the midbrain produced locomotion accompanied by hippocampal rhythmical slow activity (RSA) and neocortical low voltage fast activ...

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Veröffentlicht in:Brain research 1991-12, Vol.568 (1), p.244-252
Hauptverfasser: Peck, Barbara Kay, Vanderwolf, C.H.
Format: Artikel
Sprache:eng
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Zusammenfassung:In chronically prepared rats, electrical stimulation (100 Hz, 0.1 ms pulses) of the dorsal raphe nucleus, some sites in the median raphe nucleus, and adjoining regions of the midbrain produced locomotion accompanied by hippocampal rhythmical slow activity (RSA) and neocortical low voltage fast activity (LVFA). Both the behaviour and the cerebral waveforms persisted after injection of scopolamine HBr (5 mg/kg, s.c.). Median raphe stimulation usually produced behavioural freezing or an unnatural forced movement accompanied by RSA and LVFA. The behavioural response and the LVFA were not affected by scopolamine but scopolamine eliminated the RSA, replacing it with a low amplitude irregular (suppressed) pattern.p-Chlorophenylalanine (PCPA, 500mg/kg/day× 3, i.p.) reduced the RSA and LVFA normally present during walking after scopolamine but did not reduce the hippocampal suppression produced by median raphe stimulation in scopolamine-treated rats. Hippocampal suppression and LVFA in response to median raphe stimulation were also present in urethane (1.0–1.5 g/kg, i.p.) anesthetized rats, whether pretreated with PCPA or not. Stimulation at most other midbrain sites produced RSA and LVFA in the urethane condition. RSA was abolished in the urethane plus scopolamine condition. The data support the view that scopolamine-resistant RSA and LVFA are dependent on serotonergic projections. The hippocampal suppression produced by median raphe stimulation may be dependent on non-serotonergic neurotransmission.
ISSN:0006-8993
1872-6240
DOI:10.1016/0006-8993(91)91404-O