Cytotoxic lesion of the medial prefrontal cortex abolishes the partial reinforcement extinction effect, attenuates prepulse inhibition of the acoustic startle reflex and induces transient hyperlocomotion, while sparing spontaneous object recognition memory in the rat

Authors
Citation
Bk. Yee, Cytotoxic lesion of the medial prefrontal cortex abolishes the partial reinforcement extinction effect, attenuates prepulse inhibition of the acoustic startle reflex and induces transient hyperlocomotion, while sparing spontaneous object recognition memory in the rat, NEUROSCIENC, 95(3), 2000, pp. 675-689
Citations number
86
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE
ISSN journal
03064522 → ACNP
Volume
95
Issue
3
Year of publication
2000
Pages
675 - 689
Database
ISI
SICI code
0306-4522(2000)95:3<675:CLOTMP>2.0.ZU;2-V
Abstract
The partial reinforcement extinction effect refers to the increase in resis tance to extinction of an operant response acquired under partial reinforce ment relative to that acquired under continuous reinforcement. Prepulse inh ibition of the acoustic startle response refers to the reduction in startle reactivity towards an intense acoustic pulse stimulus when it is shortly p receded by a weak prepulse stimulus. These two behavioural phenomena appear to be related to different forms of attentional processes. While the prepu lse inhibition effect reflects an inherent early attentional gating mechani sm, the partial reinforcement extinction effect is believed to involve the development of acquired inattention, i.e. the latter requires the animals t o learn about what to and what not to attend. Impairments in prepulse inhib ition and the partial reinforcement extinction effect have been independent ly linked to the neuropsychology of attentional dysfunctions seen in schizo phrenia. The proposed neural substrates underlying these behaviourial pheno mena also appear to overlap considerably: both focus on the nucleus accumbe ns and emphasize the functional importance of its limbic afferents, includi ng that originating from the medial prefrontal cortex, on accumbal output/a ctivity. The present study demonstrated that cytotoxic medial prefrontal co rtex lesions which typically damaged the prelimbic, the infralimbic and the dorsal anterior cingulate areas could lead to the abolition of the partial reinforcement extinction effect and the attenuation of prepulse inhibition . The lesions also resulted in a transient elevation of spontaneous locomot or activity. In contrast, the same lesions spared performance in a spontane ous object recognition memory test, in which the lesioned animals displayed normal preference for a novel object when the novel object was presented i n conjunction with a familiar object seen 10 min earlier within an open fie ld arena. The present results lend support to the hypothesis that medial prefrontal c ortex dysfunction might be related to some forms of attentional abnormality central to the symptomatology of schizophrenia. Relevance of the present f indings in relation to the neural substrates underlying the partial reinfor cement extinction effect and prepulse inhibition is further discussed. (C) 1999 IBRO. Published by Elsevier Science Ltd.