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This Article Full Text Full Text (PDF) All Versions of this Article: 555/1/71    most recent jphysiol.2003.056739v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kombian, S. B. Articles by Matowe, W. C. Search for Related Content PubMed PubMed Citation Articles by Kombian, S. B. Articles by Matowe, W. C.

Departments of ¹ Applied Therapeutics ² Pharmacy Practice, Faculty of Pharmacy, Health Science Centre, Kuwait University, PO Box 24923, Safat 13110, Kuwait

The peptide cholecystokinin (CCK) is abundant in the rat nucleus accumbens (NAc). Although it is colocalized with dopamine (DA) in afferent terminals in this region, neurochemical and behavioural reports are equally divided as to whether CCK enhances or diminishes DA's actions in this nucleus. To better understand the role of this peptide in the physiology of the NAc, we examined the effects of CCK on excitatory synaptic transmission and tested whether these are dependent on DA and/or other neuromodulators. Using whole-cell recording in rat forebrain slices containing the NAc, we show that sulphated CCK octapeptide (CCK-8S), the endogenously active neuropeptide, consistently depolarized cells and depressed evoked excitatory postsynaptic currents (EPSCs) in the rostral NAc. It caused a reversible, dose-dependent decrease in evoked EPSC amplitude that was accompanied by an increase in the decay constant of the EPSC but with no apparent change in paired pulse ratio. It was mimicked by unsulphated CCK-8 (CCK-8US), a CCK_B receptor-selective agonist, and blocked by LY225910, a CCK_B receptor-selective antagonist. Both CCK-8S and CCK-8US induced an inward current with a reversal potential around -90 mV that was accompanied by an increase in input resistance and action potential firing. The CCK-8S-induced EPSC depression was slightly reduced in the presence of SCH23390but not in the presence of sulpiride or 8-cyclopentyltheophylline. By contrast, it was completely blocked by CGP55845 a potent GABA_B receptor-selective antagonist. These results indicate that CCK excites NAc cells directly while depressing evoked EPSCs indirectly, mainly through the release of GABA.

(Received 12 October 2003; accepted after revision 9 December 2003; first published online 12 December 2003)
Corresponding author S. B. Kombian: Department of Applied Therapeutics, Faculty of Pharmacy, Health Science Centre, Kuwait University, PO Box 24923, Safat 13110, Kuwait. Email: kombian{at}hsc.kuniv.edu.kw

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