Brain research
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Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. ⋯ AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.
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Sympathetic preganglionic neurons (SPN) are responsible for the control of many autonomic targets including the heart and blood vessels. Previous intracellular studies have examined the morphology of SPN in the thoracic spinal cord, but there are no intracellular studies of SPN in the lumbar spinal cord. In this study we identified lumbar SPN using intracellular recording and dye-filling so that we could study their entire soma-dendritic tree, as well as their axons. ⋯ Dendrites ramified in the intermediolateral cell column, the dorsolateral white matter and the ventral and medial gray matter. Axons arose either from cell bodies or from primary dendrites and did not bifurcate or have varicose intraspinal collaterals. This is the first report of the morphology of intracellularly filled SPN in the lumbar spinal cord.
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Comparative Study
Effect of lactic and CO2 acidosis on neuronal function following glucose-oxygen deprivation in rat hippocampal slices.
The present study was designed to determine whether lactate changes the critical pH point at which the recovery of rat population spike is inhibited following glucose-oxygen deprivation and second, which degree of lactic acidosis is similar to the effect of CO2 acidosis. The population spike was recorded from the hippocampal CA1 region after stimulation of the Schaffer collaterals. Slices were randomly perfused with various acidotic solutions for 30 min. ⋯ In the control acidotic solution, the critical pH point was 5.0. When 15 mM or 30 mM lactate were added to the control solution, the critical pH point changed to 5.5 or 6.0, suggesting that the inhibition of the population spike was enhanced by lactate in a dose-dependent fashion. The recovery of the population spike was inhibited by exposing the slices to CO2 of 25% or above (pH was 5.76 or below) and this inhibition of recovery associated with CO2 acidosis was the same degree as occurred with 30 mM, namely severe lactic acidosis.
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Recent data have suggested that adrenal medullary tissue allografts in the spinal cord subarachnoid space, by releasing catecholamines and opioid peptides, attenuate responses to various acute noxious stimuli and chronic pain-related behaviors. However, the application of this approach is limited by the low availability of allogeneic donor material. Alternatively, chromaffin cells from xenogeneic sources such as the bovine adrenal medulla are plentiful and simple to extract. ⋯ The analgesic effects of chromaffin cell grafts were partially attenuated following i.t. injection of naloxone and phentolamine separately and in combination, suggesting involvement of spinal opioid and alpha-adrenergic receptors. Following termination of behavioral studies, immunocytochemical analysis revealed robust survival of chromaffin cells in the implants. These results demonstrate that chromaffin cell xenografts may be effective in alleviating pain of neurogenic origin.
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The effects of N-methyl-D-aspartic acid (NMDA; 100 fmol-1 nmol) or quisqualic acid (QA; 10 pmol-10 nmol) on visceromotor and pressor responses to noxious colorectal distention (CRD; 40 mmHg, 20 s duration, interstimulus interval: 4 min) were studied in awake rats. Lesser doses of NMDA (100 fmol-1 pmol) administered intrathecally (i.t.) to the lumbar spinal cord produced a dose-dependent facilitation of visceromotor as well as pressor responses to CRD (maximum with 1 pmol NMDA at 1 min). The greatest dose tested (1 nmol) attenuated these responses (maximum at 1 min) and also produced a caudally-directed biting and scratching behavior accompanied by vocalizations. ⋯ In contrast, 3 nmol QA inhibited visceromotor responses to CRD at all intensities tested. In summary, these data suggest that activation of NMDA and non-NMDA receptors in the spinal cord differentially modulates visceral nociceptive input. Spinal segmental NMDA receptor activation produces selective facilitation of visceral nociceptive processing at noxious intensities of stimulation and may thereby contribute to central mechanisms underlying visceral hyperalgesia.