Neuroscience
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On- and off-cells of the rostral ventromedial medulla are thought to be involved in bulbospinal inhibition of ascending nociceptive information. Experiments were carried out in lightly anaesthetized rats to assess the effects of prefrontal cortex stimulation on the responses of neurons in the rostral ventromedial medulla. For comparison purposes, effects of periaqueductal gray stimulation were also investigated. ⋯ Short-train stimulation of the ventrolateral orbital cortex (100-400 microA) excited eight of 25 on-cells and inhibited the ongoing activity of 10 of 14 off-cells. Long-train ventrolateral orbital cortex stimulation (5-15 s, 100-200 microA, 200-300 Hz) enhanced the noxious evoked responses of 10 of 11 on-cells, prolonged the noxious heat-evoked pause of all of four off-cells and decreased the tail-flick latency (pronociception). The results of this study support the proposed role of on- and off-cells in descending inhibition of nociception from the periaqueductal gray and implicate the ventrolateral orbital cortex in the control of this pathway.
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Many chemicals including nicotine, capsaicin and piperine (pungent chemicals in red and black peppers, respectively) evoke oral pain and irritation via largely unknown neural mechanisms. As a first step in defining the central pathway for oral chemical irritation, we have used an immunohistochemical method to map locations of brainstem neurons expressing the nuclear protein, c-Fos (a putative nociceptive marker), following application of various irritants to the tongue. In barbiturate-anesthetized rats, one of the following was applied to the dorsal surface of the tongue: nicotine (0.5%), capsaicin (0.1%), histamine (2 or 20%), piperine (0.2%), acetylcholine (10%) or vehicle control (0.9% saline, dH2O, 70% ethanol). ⋯ Fos-immunoreactivity was also seen consistently in the ventrolateral medulla dorsal to the lateral reticular nucleus, and vestibular and cochlear nuclei, and less consistently in nucleus raphe pallidus and inferior olive, in both irritant and in control groups, indicating that it was not stimulus-evoked. These results have identified a population of neurons in the dorsomedial trigeminal nucleus caudalis likely to be involved in signaling chemical irritation of the tongue. Increases in Fos-immunoreactivity observed in the nucleus of the solitary tract, area postrema, and ventrolateral trigeminal caudalis also suggest roles for these areas in autonomic responses consequent to oral irritation.
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The effect intracerebroventricular injections of angiotensin II (0.1 nm), angiotensin-(1-7) (1 or 100 nm) and carbachol (500 ng) on c-fos expression was examined in the forebrain of Lister hooded rats. Intense staining of the c-Fos protein was found in the median preoptic nucleus, organum vasculosum of the lamina terminalis, subfornical organ, paraventricular nucleus and supraoptic nucleus after angiotensin II and carbachol Angiotensin II caused significantly more c-fos expression in the ventral median preoptic nucleus and organum vasculosum of the lamina terminalis than carbachol, whereas in the paraventricular and supraoptic nuclei this was reversed, with carbachol having a greater effect on c-fos expression in these areas. Angiotensin-(1-7), however, only induced c-Fos protein in the organum vasculosum of the lamina terminalis and median preoptic nucleus with the number and the intensity of staining of the nuclei significantly less in both areas than after angiotensin II or carbachol. ⋯ Angiotensin II and carbachol caused an approximate five-fold increase in plasma vasopressin levels compared to cerebrospinal fluid-injected rats, but angiotensin-(1-7) had no effect on vasopressin release. Therefore, three compounds with widely differing effects on thirst, sodium appetite and vasopressin release induce distinctive patterns of c-fos protein expression in the forebrain. By combining experimental approaches in this way it is possible to determine areas of the brain which are involved in certain behavioural and endocrine responses.
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[3H]Noradrenaline release was studied in cultured sympathetic neurons derived from superior cervical ganglia of neonatal rats. Acetylcholine elicited a concentration- and time-dependent increase in 3H outflow which was half-maximal at about 300 microM and within 5 s. The overflow induced by 10 s exposure to 300 micro A acetylcholine was reduced by the nicotinic antagonist hexamethonium, but increased by the muscarinic antagonist atropine. ⋯ The acetylcholine-induced transmitter release is based on two mechanisms, one involving and the other one bypassing voltage-dependent Ca2+ channels. alpha2-Adrenoceptor activation reduces voltage-activated Ca2+ currents and effects exclusively the component of acetylcholine-induced release which involves voltage-dependent Ca2+ channels. These results support the hypothesis that voltage-activated Ca2+ channels are the sole site of autoinhibitory alpha2-adrenergic effects on transmitter release from rat sympathetic neurons. The inhibitory effects of alpha2-adrenoceptor agonists and antagonists on currents through nicotinic acetylcholine receptors are not mediated by an alpha2-adrenoceptor.
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While B2 receptors mediate pain and hyperalgesia induced by bradykinin, in normal rats, recent reports indicate that, in the setting of inflammation, B1 receptors also mediate pain and hyperalgesia. Since bradykinin-induced hyperalgesia in normal rats is mediated by prostaglandins released from the postganglionic sympathetic neurons, we have evaluated the contribution of the sympathetic nervous system to the hyperalgesia induced by bradykinin, a preferential B2-receptor agonist, and des-Arg9-bradykinin, a major metabolite of bradykinin and a selective B1-receptor agonist. Mechanical hyperalgesia was quantified by the Randall-Selitto paw-withdrawal method. ⋯ These results are consistent with the suggestions that B2 receptors mediate bradykinin-induced cutaneous hyperalgesia in the normal rat hindpaw. The hyperalgesia induced by bradykinin, 48 h post injection of complete Freund's adjuvant is mediated by both B1 and B2 receptors, that by des-Arg9-bradykinin is mediated by B1 receptors. The hyperalgesia induced by both agents is dependent on the presence of intact sympathetic postganglionic neurons.