Effect of minor tranquillisers on hippocampal θ rhythm mimicked by depletion of forebrain noradrenaline

THERE are similarities between the behavioural effects of minor tranquillising drugs and those of lesions to the septal area and hippocampus1. Since the septal area contains the pacemaker

cells for the hippocampal theta rhythm2, a parsimonious hypothesis to account for these common effects is that tranquillisers affect behaviour by altering septal control of this rhythm.

Sodium amylobarbitone (SA) has been shown to block the behavioural effects of frustrative non-reward1, as do septal3 and hippocampal4 lesions. Rats exposed to non-reward in the runway show a

characteristic hippocampal θ response at 7.7 Hz (ref. 1) (the θ frequency range in the rat is about 6–12 Hz). Higher and lower frequencies occur during forms of behaviour which are

unaffected by the drug. It has therefore been proposed1 that the behavioural effects of SA arise by virtue of an impairment of septal control of the hippocampal θ rhythm specifically in a

frequency band centred on 7.7 Hz. In support of this, it has been demonstrated5 that this drug raises the threshold for septal driving of the hippocampal θ rhythm selectively at 7.7 Hz,

frequencies both above and below this value being minimally affected. Here we show that this kind of frequency-specific effect on septal driving of the hippocampal θ rhythm is also produced

by other drugs with similar effects on behaviour1 (ethanol, chlordiazepoxide and Δ9-tetrahydro-cannabinol (Δ9-THC)), by drugs which impair noradrenergic neural transmission, and by

destruction of the dorsal ascending noradrenergic bundle by intracerebral injection of 6-hydroxydopamine (6-OHDA)6.

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