University of Louisville

cFos/FosB and µ-Opioid Receptors in the MPOA of Postpartum Rats.

Institution

University of Louisville

Abstract

cFos and FosB are immediate-early gene proteins whose expression increases in the medial preoptic area in brains of postpartum rats exposed to pups and may be necessary for expression of maternal behavior. Activation of µ-opioid receptors in the medial preoptic area represses maternal behavior in postpartum rats, raising the possibility that µ-opioid receptors act via suppression of cFos/FosB neuron activity. On the day of parturition we removed pups from one group of Sprague-Dawley rats, while another group was allowed to interact with their pups for one day. All females were euthanized one day after parturition and their brains assessed for colocalization of µ-opioid receptors with either cFos or FosB in medial preoptic area neurons using double-label fluorescent immunohistochemistry. Our detection of colocalized neurons supports the hypothesis that µ-opioid receptors inhibit maternal behavior by interfering with cFos/FosB neuron output.

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cFos/FosB and µ-Opioid Receptors in the MPOA of Postpartum Rats.

cFos and FosB are immediate-early gene proteins whose expression increases in the medial preoptic area in brains of postpartum rats exposed to pups and may be necessary for expression of maternal behavior. Activation of µ-opioid receptors in the medial preoptic area represses maternal behavior in postpartum rats, raising the possibility that µ-opioid receptors act via suppression of cFos/FosB neuron activity. On the day of parturition we removed pups from one group of Sprague-Dawley rats, while another group was allowed to interact with their pups for one day. All females were euthanized one day after parturition and their brains assessed for colocalization of µ-opioid receptors with either cFos or FosB in medial preoptic area neurons using double-label fluorescent immunohistochemistry. Our detection of colocalized neurons supports the hypothesis that µ-opioid receptors inhibit maternal behavior by interfering with cFos/FosB neuron output.