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  • Title: Modulation of intracranial self-stimulation behaviour by local perfusions of dopamine, noradrenaline and serotonin within the caudate nucleus and nucleus accumbens.
    Author: Redgrave P.
    Journal: Brain Res; 1978 Oct 27; 155(2):277-95. PubMed ID: 688018.
    Abstract:
    In order to examine the possible role of dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) in the control of intracranial self-stimulation behaviour (ICSS) a push-pull perfusion system was used to administer different consecutive doses of DA, NA and 5-HT to discrete regions within the caudate nucleus (CN) and nucleus accumbens (NAC) of rats during ICSS. Electrode placements supporting ICSS were in both the medial forebrain bundle (MFB) and the ventral mesencephalic tegmentum (VMT). Animals were allowed to determine the ICSS pulse train duration thereby permitting three measures of ICSS behaviour: (1) mean presses/min; (2) mean duration/press and (3) mean time pressed/min. Eleven electrode/cannula combinations were found to be responsive to both DA and 5-HT. The DA response profile was typified by a significant increase in mean presses/min, a significant decrease in mean duration/press and no significant change in the mean time pressed/min. The response profile for 5-HT was the converse of the DA pattern for the first two measures of ICSS, however, again there was no significant change in the mean time pressed/min. In addition, 8 electrode/cannula combinations were sensitive to NA; for 5 combinations the response pattern was similar to that of DA, however, the changes in ICSS were generally larger and of longer duration. For the remaining 3 combinations sensitive to NA there was no major change in mean presses/min but a dramatic increase in the mean duration/press and consequently, an increase in the mean time pressed/min. It is suggested that the central control of ICSS behaviour might depend, in part, upon a relative balance between DA and 5-HT systems within the CN and NAC. The operational characteristics of this balance may be subject to additional modulation by the activation of an adrenergic receptor.
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