Brain research
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(1) Unitary extracellular recordings were made from 92 lumbar dorsal horn neurones in urethane-anaesthetised rats. These neurones were classed as 'noxious-only' (4), 'non-noxious-only' (33) or 'convergent' (55) by their responses to stimulation of their cutaneous receptive fields on the ipsilateral hindpaw. (2) Distension of abdominal viscera (colon, urinary bladder) depressed the activities of the vast majority (93%) of the convergent neurones but of only one other cell (a non-noxious-only neurone). ⋯ There were however, some small differences in the extent and temporal evolution of the inhibitory effects of the visceral and of the somatic stimuli--the visceral stimuli generally producing weaker inhibitions with slower rates of onset and recovery. It is proposed that these differences may have reflected different amounts and patterns of activity in the relevant primary afferent fibres rather than being due to different central neural mechanisms. (4) These results and the likely explanation that the effects of the visceral stimuli were mediated by a diffuse mechanism should be taken into account when interpreting the results of other studies in which inhibitory effects are produced by visceral stimulation.
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Prostaglandin E2 (PGE2) microinjection (25 ng, 250 nl) into the preoptic area of the anterior hypothalamus (POAH) stimulated heat production in brown adipose tissue (BAT) and increased core temperature in urethane-anesthetized rats. These thermogenic and hyperthermic effects were attenuated by co-injection of NG-monomethyl-L-arginine (NMMA, 25 micrograms), a competitive inhibitor of nitric oxide (NO) production from L-arginine. ⋯ Intra-POAH injection of NMMA (25 micrograms) or L-arginine (50 micrograms) alone had no effect on IBAT and core temperatures. The results suggest that the effect on thermoregulation induced by action of PGE2 in the POAH is modulated by a local L-arginine-dependent and NMMA-sensitive NO-generating system.
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Two physiologically and pharmacologically distinct classes of putative nociceptive modulatory neurons have been identified in the rostral ventral medulla (RVM) of the lightly anesthetized rat: on-cells and off-cells. We have previously shown that administration of morphine either systemically or by microinjection into the periaqueductal gray (PAG) produces an increase in the activity of all off-cells and a depression of the activity of all on-cells concomitant with inhibition of the tail flick reflex. We now demonstrate that morphine applied intrathecally has effects on RVM neurons that are indistinguishable from those of systemic or PAG administration. This may contribute to the known multiplicative effects of concurrent administration of opioids at spinal and supraspinal sites.
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Alpha 2-adrenoceptor agonists such as clonidine are sedatives and enhance the effectiveness of several different kinds of anesthetics. This study was performed to quantitate the effect of dexmedetomidine, a novel alpha 2-adrenoceptor agonist, on the action of the volatile anesthetic agent isoflurane in rats in vivo. ⋯ In hippocampal CA1 neurons, on the other hand, there was a relatively small potentiation of the effects of isoflurane at the maximally effective dexmedetomidine concentration (1 nM). The hippocampal CA1 area, at least in the slice preparation, may thus not be representative of the CNS site(s) at which alpha 2 adrenoceptor agonists lessen anesthetic requirement in vivo.
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The mechanisms of the antinociceptive, depressor and bradycardic responses produced by intravenous (i.v.) administration of morphine were examined in rats lightly anesthetized with pentobarbital sodium. Intravenous administration of 0.1, 0.25, 0.5, 1.0 or 2.5 mg/kg of morphine produced dose-dependent inhibition of the nociceptive tail flick (TF) reflex, hypotension, and bradycardia. Bilateral cervical vagotomy (CVAG) significantly attenuated the antinociception produced by i.v. morphine and the degree of attenuation was inversely related to drug dose. ⋯ These intrathecal doses of naloxone also antagonized the depressor and bradycardic responses produced by morphine. However, the antagonism produced by 1.5 micrograms of intrathecal naloxone was not due to spread to the systemic circulation, since i.v. administration of 1.5 micrograms of naloxone did not significantly affect either the antinociceptive or cardiovascular responses produced by morphine. These findings indicate that vagal afferents play a significant role in the antinociception produced by i.v. administration of morphine.(ABSTRACT TRUNCATED AT 400 WORDS)