Abstract
Gamma-aminobutyric acid ( GABA) receptor-mediated modification of omasal spiking activity ( SA) was studied in six conscious ewes at rest, chronically fitted with electrodes implanted in the reticular and omasal walls and a cannula placed in the left cerebral lateral ventricle. Intracerebroventricular (0·1 μg kg −1) but not intravenous (25 μg kg −1) administration of muscimol increased both the duration of omasal SA and the frequency of groups of spiking bursts ( GSB) from the reticulum and oral omasum; the frequency of GSB from the aboral omasum decreased. These responses were antagonised by intracerebroventricular pretreatment with bicuculline (0·5 μg kg −1). Both intravenous (500 μg kg −1) and intracerebroventricular (1 μg kg −1) administration of baclofen inhibited reticular SA; in both the oral and aboral omasum, while the duration of SA increased, the frequency of GSB decreased. Reticuloomasal responses to intravenous or intracerebroventricular baclofen were greatly antagonised or abolished, respectively, by a previous intracerebroventricular injection of phaclofen (80 μg kg −1). The main conclusion which could be drawn from these results is that exclusively central GABA A and mainly central GABA B receptors mediate a prolongation of omasal body motility in sheep.
Published Version
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