Neuroscience
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Comparative Study
Glucocorticoids, hippocampal corticosteroid receptor gene expression and antidepressant treatment: relationship with spatial learning in young and aged rats.
The emergence of cognitive deficits in a subgroup of aged rats is associated with increased hypothalamic-pituitary-adrenal axis activity, decreased hippocampal mineralocorticoid and/or glucocorticoid receptor gene expression and neuronal loss. Short-term treatment with antidepressant drugs in young rats increases hippocampal corticosteroid receptor gene expression. In this study, the effects of chronic antidepressant administration on hippocampal mineralocorticoid and glucocorticoid receptor gene expression and spatial memory in young and aged rats were investigated. ⋯ Our data support the notion that corticosterone exerts a concentration-dependent biphasic influence, via selective activation of hippocampal mineralocorticoid and glucocorticoid receptor, on spatial memory. Amitriptyline improves spatial memory in young rats and increases hippocampal mineralocorticoid receptor gene expression. The lack of amitriptyline effect on spatial memory in aged rats may reflect decreased plasticity of both the synaptic processes underlying spatial memory and the regulation of hippocampal mineralocorticoid/glucocorticoid receptor expression, with mineralocorticoid receptors fully occupied due to elevated basal plasma corticosterone levels (in part a consequence of inadequate glucocorticoid receptor function).
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Viscerofugal neurons are enteric neurons in the myenteric plexus of the stomach and intestine that project to the prevertebral ganglia as the afferent limb of intestino-intestinal reflexes. This study characterizes viscerofugal projections to the inferior mesenteric ganglion and investigates the possibility of similar projections to the major pelvic ganglia in the male rat. The colon and rectum were examined for retrogradely labelled neurons following the injection of retrograde tracer into the inferior mesenteric or major pelvic ganglia, or following the application of tracer to the caudal end of the cut intermesenteric nerves, or either end of the cut hypogastric nerves. ⋯ Very few viscerofugal neurons project to the neurons of the major pelvic ganglia via the rectal nerves, and no viscerofugal neurons project caudally in the hypogastric nerves to these ganglia. The majority of labelled neurons resembled Dogiel type I morphology. Thus the inferior mesenteric ganglion receives a substantial innervation from viscerofugal neurons of the large intestine, with the greatest supply from the distal colon and rectum.(ABSTRACT TRUNCATED AT 250 WORDS)
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Several indices of peptidergic, primary afferent neural transmission in rat at the level of the lumbar spinal cord exhibited differential changes over time in response to adjuvant-induced inflammation of the hindpaw. The indices were measurements of the production of messenger RNA encoding the precursors for substance P and calcitonin gene-related peptide in dorsal root ganglia, the storage of substance P and calcitonin gene-related peptide in the dorsal spinal cord and the release of the peptides evoked by application of capsaicin to the dorsal spinal cord. A 47% decrease in the content of immunoreactive substance P in the dorsal half of the lumbar spinal cord, as determined by radioimmunoassay, was measured at 6 h following the injection of complete Freund's adjuvant into the hindpaw. ⋯ Radioimmunoassay of the superfusate of the dorsal half of the lumbar spinal cord was used to measure the release of immunoreactive substance P and immunoreactive calcitonin gene-related protein in vitro. Although the basal release of immunoreactive substance P and immunoreactive calcitonin-gene related protein from the dorsal spinal cord was constant throughout the time points examined, changes occurred in the release of peptide evoked by 10 microM capsaicin. The capsaicin-evoked release of immunoreactive substance P was decreased at 6 h and eight days post-injection of adjuvant.(ABSTRACT TRUNCATED AT 400 WORDS)
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Randomized Controlled Trial Clinical Trial
Enhancement of morphine analgesia by the alpha 2-adrenergic antagonist yohimbine.
Although interactions between opioids and adrenergic agonists in the treatment of pain have been demonstrated in humans, the contribution of specific adrenergic receptors in this interaction remains to be clarified. In a double-blind, placebo-controlled study in male patients with postoperative dental pain, we investigated the effect of preoperative administration of the alpha 2-adrenergic antagonist, yohimbine, on analgesia produced by postoperative intravenous morphine. Although yohimbine by itself did not affect the pain, the overall analgesic effect of morphine was significantly enhanced in the presence of yohimbine. This report is the first to demonstrate that an alpha 2-adrenergic antagonist enhances opiate analgesia in humans.
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Physiological studies were conducted to examine the effects of noxious stimulation of one hindpaw or one forepaw on the latency of the withdrawal reflex in the tail-flick test in lightly anesthetized spinally intact or transected rats. Male Sprague-Dawley rats were anesthetized with an intraperitoneal injection of a mixture of Na-pentobarbital (20 mg/kg) and chloral hydrate (120 mg/kg). After baseline readings were taken in the tail-flick test, the effects of various noxious stimuli applied to remote body regions were assessed. ⋯ The antinociceptive effect of noxious thermal stimulation was attenuated or absent in chronically spinalized animals (T6/7) following hindpaw or forepaw immersion, respectively. Noxious mechanical stimulation had no effect on tail-flick latency. The data provide evidence that a noxious thermal or chemical stimulus produces a heterosegmental antinociceptive effect which is mediated in part via a supraspinal mechanism and in part via a local spinal mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)