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Influence of 5,7-dihydroxytryptamine lesions of the rat fornix—fimbria and cingulum bundles on spontaneous activity in an aversive maze

Section of Psychiatry, Division of Pathology and Neuroscience, University of Dundee Medical School, Ninewells Hospital, Dundee, UK, d.robertson{at}chester.ac.uk

JE Beattie

Section of Psychiatry, Division of Pathology and Neuroscience, University of Dundee Medical School, Ninewells Hospital, Dundee, UK

IC Reid

Section of Psychiatry, Division of Pathology and Neuroscience, University of Dundee Medical School, Ninewells Hospital, Dundee, UK

DJK Balfour

Section of Psychiatry, Division of Pathology and Neuroscience,University of Dundee Medical School, Ninewells Hospital, Dundee, UK

Exposure to aversive environmental stimuli stimulates the serotonergic neurones that project to the forebrain and inhibit spontaneous activity when studied in a simple maze. This study explored the putative role of the principal 5-hydroxytryptamine (5-HT) neurones that project to the hippocampus from the median raphe nucleus in this response to an aversive environment by lesioning the 5-HT fibres that project through the fornix/fimbria and cingulum bundles. The effects of the lesions were investigated in independent groups of animals tested in an enclosed four-arm maze and a more aversive elevated maze of the same dimensions composed entirely of four open arms. The rats were significantly less active in the open maze, the principal effect of maze design being observed during the first 5 min sub-trial of a 15 min trial. This response to the more aversive environment was totally abolished by the lesion. It is concluded that exposure to an explicitly aversive environment elicits a brief stimulation of the 5-HT neurones that project to the hippocampus from the median raphe nucleus and that this stimulation inhibits the initial burst of exploratory activity that is observed in animals placed in a less aversive novel environment.

Key Words: hippocampus • 5-HT • locomotor activity • 5,7-dihydroxytryptamine

This version was published on May 1, 2008

Journal of Psychopharmacology, Vol. 22, No. 3, 285-289 (2008)
DOI: 10.1177/0269881107083841


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