Neuroscience
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Spinal intrathecal administration of nicotine inhibits bradykinin-induced plasma extravasation, a component of the inflammatory response, in the knee joint of the rat in a dose-related fashion. Nociceptors contain nicotinic receptors and activation of a nociceptor at its peripheral terminal, by capsaicin, also produces inhibition of inflammation. ⋯ Conversely, intrathecal administration of an alpha-adrenoceptor antagonist, phentolamine or an opioid receptor antagonist, naloxone, to block descending antinociceptive controls, which provide inhibitory input to primary afferent nociceptors, enhanced the action of both nicotine and capsaicin. These findings support the hypothesis that the central terminal of the primary afferent nociceptor is a CNS target at which nicotine acts to inhibit inflammation.
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Environmental thermal stimuli result in specific and coordinated thermoregulatory response in homeothermic animals. Warm exposure activates numerous brain areas within the cortex, hypothalamus, pons and medulla oblongata. We identified these thermosensitive cell groups in the medulla and pons that were suggested but not outlined by previous physiological studies. ⋯ Among several brain regions, warm exposure elicited c-fos expression specifically in the ventrolateral part of the medial preoptic area, the central subdivision of the lateral parabrachial nucleus and the caudal part of the peritrigeminal nucleus, whereas cold stress resulted in c-fos expression in the ventromedial part of the medial preoptic area, the external subdivision of the lateral parabrachial nucleus and the rostral part of the peritrigeminal nucleus. These neurons are part of a network coordinating specific response to warm or cold exposure. The topographical differences suggest that well-defined cell groups and subdivisions of nuclei are responsible for the specific physiological (endocrine, autonomic and behavioral) changes observed in different thermal environment.
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While the acute physiological effects of brain-derived neurotrophic factor (BDNF) have been well demonstrated, little is known regarding possible morphological effects that occur within a short period of time. The acute effects of BDNF on dendritic spine morphology were examined in granule cells in cultured main olfactory bulb slices. Organotypic slices prepared from 7-day-old rats were cultured for 1 day, and BDNF was applied at varying time points prior to fixation. ⋯ The changes became detectable as early as 30 min when 50 ng of BDNF was applied. The pretreatment with tetanus toxin or an N-methyl-D-aspartate receptor antagonist abolished the acute effects of BDNF on spine morphology. These results indicate that BDNF can alter spine morphology within a shorter period of time than previously observed and that the effects are mediated by enhanced glutamatergic signaling.
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This experiment tested the effect of cortical spreading depression on the sympathetic and thermogenic effects induced by orexin A. The firing rates of the sympathetic nerves to interscapular brown adipose tissue (IBAT), along with IBAT and colonic temperatures and heart rate were monitored in urethane-anesthetized male Sprague-Dawley rats before and 5 h after an injection of orexin A (1.5 nmol) into the lateral cerebral ventricle. The same variables were monitored in rats with cortical spreading depression, induced by an application of cotton pellets soaked with 2 M KCl to the frontal cortex. ⋯ The increases in firing rate, IBAT and colonic temperatures are blocked by cortical spreading depression, while the increase in heart rate is not affected by cortical spreading depression. These findings suggest that the cerebral cortex is involved in the control of the orexin A-induced hyperthermia. Furthermore, we suggested the name "hyperthermine A," as additional denomination of "orexin A."
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The aim of the present study was to investigate the effect of a micro-opioid receptor agonist DAMGO (Tyr-d-Ala-Gly-NMe-Phe-Gly-ol) on the excitability of trigeminal root ganglion (TRG) neurons, projecting onto the superficial layer of the cervical dorsal horn, by using the perforated-patch technique and to determine whether TRG neurons show the expression of mRNA or functional protein for micro-opioid receptors by using reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. TRG neurons projecting onto the superficial layer of the cervical dorsal horn were retrogradely labeled with Fluorogold (FG). The cell diameter of FG-labeled TRG neurons was small (<30 microm). ⋯ The micro-opioid receptor immunoreactivity was expressed in the small diameter FG-labeled TRG neurons. These results suggest that the activation of micro-opioid receptors inhibits the excitability of rat small diameter TRG neurons projecting on the superficial layer of the cervical dorsal horn and this inhibition is mediated by potentiation of voltage-dependent K(+) currents. We therefore concluded that modulation of nociceptive transmission in the trigeminal system, resulting in the functional activation of micro-opioid receptors, occurs at the level of small TRG cell bodies and/or their primary afferent terminals, which contribute to opioid analgesia in the trigeminal pain.