The Journal of neuroscience : the official journal of the Society for Neuroscience
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Intraperitoneal administration of hypertonic saline is a potent stimulus to the "stress" responsive hypophysiotrophic parvicellular neurons of the hypothalamic paraventricular nucleus (PVN), as well as to magnocellular neurons of the hypothalamo-neurohypophysial system. Precise identification of the pathways gating information about the "stress" of intraperitoneal hypertonic saline to the PVN has not been ascertained earlier. In this study we demonstrate that intraperitoneal injection of hypertonic saline induces increased expression of c-fos immunoreactivity within neurons of the medial parvicellular division of the PVN, within the circumventricular organs surrounding the anteroventral tip of the third ventricle, and within the magnocellular neurons of the PVN and supraoptic nucleus. ⋯ In the brainstem, the "stressor" induced expression of c-fos-IR nuclei in almost all of the retrogradely labeled cells of the ventrolateral part of the medulla oblongata (A1 and C1), while only about 25% of the ChB-labeled cells of the caudal part of the nucleus of the solitary tract (A2) were concomitantly immunoreactive to c-fos. Within the parabrachial nucleus, only 20% of the ChB-labeled cells were also immunoreactive for c-fos. The present results provide evidence that information about the "stress" of intraperitoneal hypertonic saline is conveyed to both magnocellular neurons projecting to the neurohypophysis and hypophysiotrophic parvicellular neurons the PVN via afferent projections from a variety of neurons in the osmosensitive anteroventral tip of the third ventricle and visceromotor neurons of the parabrachial nucleus, the ventrolateral medulla and the nucleus of the solitary tract.
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Studies in mice and rats have shown that antinociception produced by intrathecal (i.t.) administration of opioids can be partially inhibited by intracerebroventricular (i.c.v.) administration of naloxone. In this study we tested the hypothesis that this inhibition by i.c.v. naloxone results from antagonism of supraspinal endogenous opioid-mediated antinociception produced by the action of i.t. opioids on an ascending antinociceptive pathway. In rats lightly anesthetized with urethane/alpha-chloralose, i.t. ⋯ Microinjection of naloxone methiodide into nucleus accumbens but not into the rostral ventral medulla (RVM) or the periaqueductal gray matter (PAG) antagonized the suppression of the JOR produced by i.t. DAMGO or lidocaine. The possibility that this ascending pathway may represent a source of spinal input to mesolimbic circuitry involved in setting the state of sensorimotor reactivity to noxious stimuli is discussed.