Abstract
Interoreceptors in the central nervous system elicit compensatory behavioral and physiological responses to cellular glucopenia. Antagonism of μ and κ opioid receptors attenuates glucoprivic hyperphagia, findings that implicate these peptidergic receptors in the central processing of metabolic regulatory signals. Several hypothalamic structures of critical importance for the regulation of energy balance exhibit one or both of these receptors. The following studies investigated the role of these opioid receptors in glucoprivic induction of immediate-early gene expression in these brain sites. Male rats were pretreated with β-funaltrexamine (μ antagonist), Mr-1452 MS (κ antagonist), or vehicle prior to intraperitoneal injection of the glucose antimetabolite, 2-deoxy-D-glucose (2DG), then sacrificed by transcardial perfusion 2 h later. Nuclear immunolabeling for the transcription factor, Fos, was observed in several preoptic and hypothalamic sites following 2DG administration. Rats pretreated with the μ antagonist exhibited significantly fewer Fos-positive neurons in the medial preoptic area and dorsomedial hypothalamic nucleus in response to 2DG, compared to vehicle-pretreated controls. Blockade of κ receptors diminished 2DG and induced Fos staining in the paraventricular and supraoptic nuclei. Numbers of Fos-positive cells in the arcuate nucleus and ventrolateral hypothalamic area were not altered by either antagonist. The present data implicate μ and κ opioid receptors in neural mechanisms underlying glucoprivic induction of the Fos stimulus-transcription pathway by local neurons in discrete hypothalamic sites.
Published Version
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