Selective nucleus accumbens core lesions enhance dizocilpine-induced but not apomorphine-induced disruption of prepulse inhibition in rats

Prepulse inhibition refers to the reduction in startle reaction to a startle-eliciting ‘pulse’ when it is shortly preceded by a weak ‘prepulse’ stimulus. The nucleus accumbens plays a pivotal role in the regulation of prepulse inhibition in rats, but the relative contributions of its subregions rema...

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Bibliographic Details
Published in:	Behavioural pharmacology Vol. 17; no. 2; pp. 107 - 117
Main Authors:	Pothuizen, Helen H.J, Neumann, Ken R, Feldon, Joram, Yee, Benjamin K
Format:	Journal Article
Language:	English
Published:	England Lippincott Williams & Wilkins, Inc 01-03-2006
Subjects:	Animals Apomorphine - pharmacology Dizocilpine Maleate - pharmacology Dopamine Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology Habituation, Psychophysiologic - drug effects Male Nucleus Accumbens - physiology Rats Rats, Wistar Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Reflex, Startle - drug effects
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Summary:	Prepulse inhibition refers to the reduction in startle reaction to a startle-eliciting ‘pulse’ when it is shortly preceded by a weak ‘prepulse’ stimulus. The nucleus accumbens plays a pivotal role in the regulation of prepulse inhibition in rats, but the relative contributions of its subregions remain unclear. Here, we investigated the effects of selective excitotoxic lesion restricted to the nucleus accumbens core on prepulse inhibition and its sensitivity to dopaminergic and glutamatergic manipulations known to disrupt prepulse inhibition. We first assessed the effects of selective core lesions on prepulse inhibition, before going on to evaluate whether the lesions affect the sensitivity to the prepulse inhibition-disruptive effects of systemic treatment of the dopamine agonist, apomorphine (0.025 mg/kg, subcutaneous) and of the non-competitive N-methyl-D-aspartate receptor antagonist, dizocilpine (0.1 mg/kg, subcutaneous). Contrary to our expectations, core lesions failed to disrupt prepulse inhibition. The lesions, however, enhanced the disruptive effect of dizocilpine, but not of apomorphine, on prepulse inhibition. Our results thus suggest that nucleus accumbens core can indeed lead to deregulation of prepulse inhibition, perhaps via a disturbance of normal glutamatergic activity.
ISSN:	0955-8810 1473-5849
DOI:	10.1097/01.fbp.0000190683.00232.ec