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In urethane-anesthetized rats, a membrane potential oscillation (MPO) of up to 30 mV and 0.5-2 Hz (delta frequency range) was found in neurons of the nucleus accumbens. The membrane potential oscillations were of similar frequency and reversed in phase to the extracellular EEG of about 0.5 mV. In freely moving rats, a rhythmic delta EEG of 0.5-3 Hz was found in the nucleus accumbens, and it was of highest amplitude and regularity during awake immobility and face washing, less regular during slow wave sleep, and of the lowest amplitude during body and head movements and rapid eye movement sleep. The behavioural relation of the accumbens EEG was not critically affected after amphetamine, haloperidol, and parachlorophenylalanine, which depleted serotonin, although the accumbens EEG during awake immobility was less regular after blocking muscarinic cholinergic receptors by atropine sulfate. However, stimulation of the ventral tegmental area suppressed the accumbens delta membrane potential oscillations and EEG, and this effect was antagonized by haloperidol, suggesting that endogenous dopamine release may suppress the accumbens delta rhythm. It was concluded that the delta rhythm in the nucleus accumbens may represent a state of bilateral synchrony among accumbens neurons that is perhaps characteristic of an idling system, while desynchronization of the delta rhythm may occur closely with motor action.

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It has been shown that the nucleus accumbens receives input from the amygdala and that mesolimbic dopaminergic projection from the ventral tegmental area (VTA) modulates the response of accumbens neurons to amygdala input. Since the nucleus accumbens projects to the ventral pallidum, the purpose of this study was to investigate, using electrophysiological techniques, whether or not the nucleus accumbens relays the projection from the amygdala to the ventral pallidum and whether or not the mesolimbic dopamine projection interacts with this pathway. Extracellular single-unit recordings were obtained from the ventral pallidum of urethan-anesthetized rats, and the responses of these neurons to electrical stimulation of the amygdala were investigated. Of 392 neurons tested, 36% were inhibited and 11% were excited following amygdala stimulation. Latency of onset of inhibitory responses showed a bimodal distribution with peaks in the ranges of 4-6 ms and 16-18 ms, respectively. Fifty-four percent of inhibitory responses with latencies greater than 12 ms were attenuated by 1) injection of procaine hydrochloride into the nucleus accumbens, or 2) injection of d-amphetamine into the nucleus accumbens, or 3) stimulation of VTA with a train of 10 pulses (10 Hz) prior to stimulation of amygdala. Acute administration of haloperidol intraperitoneally or injection of 6-hydroxydopamine into the ipsilateral VTA, 2 days prior to the recording experiment, reduced the attenuating effects of intra-accumbens injection of d-amphetamine and VTA conditioning stimulations on the inhibitory response of ventral pallidal neurons to amygdala stimulation. These results support the hypothesis that the nucleus accumbens provides a link between the amygdala and the ventral pallidum. Since the amygdala is a limbic structure and the ventral pallidum has possible connections with the extrapyramidal motor system, it is suggested that the amygdala to nucleus accumbens to ventral pallidum projection may be a bridge between the limbic and motor systems. We also suggest that this relay of output from the amygdala to the ventral pallidum via the nucleus accumbens is under the modulating influence of the mesolimbic dopamine projection from the ventral tegmental area.

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