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Abstract

A dysfunction in the brain reward circuitry is implicated in several psychiatric disorders including drug abuse; alcohol dependence and depression. Previous work with psychophysically based studies suggests that destruction of the habenula which lies in the dorsal diencephalic conduction system (DDC) degrades the intracranial self-stimulation. In this work, we investigated the contribution of the dorsal diencephalic conduction system (DDC) in the brain reward circuitry. Rats were implanted with stimulating electrodes at the level of the dorsal raphe (DR) and the lateral hypothalamus (LH) and lesioning electrodes in the medial forebrain bundle (MFB) and the DDC. They were then trained daily to obtain an electrical stimulation at three different current intensities. Electrolytic lesions were made in the medial forebrain bundle (MFB) and the DDC and the reward induced by the stimulation was monitored daily for two weeks before and after the lesions. Results show that lesions of both the MFB and the DDC produce larger and longer-lasting attenuation in reward than lesions of either pathway alone. Moreover, the lesions had little appreciable effect on the rewarding nature of DR stimulation compared to when LH was stimulated. This study validates the existence of two parallel pathways that could constitute a viable route for the reward signal triggered by the electrical brain stimulation.

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