Neuroscience letters
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Neuroscience letters · May 1994
Effects of sympathectomy on the cutaneous temperature abnormalities in rats with chronic constriction injury of the sciatic nerve.
Effects of surgical sympathectomy on the cutaneous temperature abnormalities of plantar surface evoked by the chronic constriction injury (CCI) of the sciatic nerve were investigated in the rat. In normal animals, there were very small temperature differences between both plantar surfaces. ⋯ Surgical sympathectomy prior to and just after CCI significant suppressed the temperature abnormalities during the first week, but no effect was observed after 2 weeks following CCI. These observations indicate that sympathetic vasoconstriction may contribute to the cutaneous temperature abnormalities evoked by CCI during the early stage, but does not affect the abnormalities at later stages.
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Neuroscience letters · Apr 1994
Coexistence of oxytocin and NADPH-diaphorase in magnocellular neurons of the paraventricular and the supraoptic nuclei of the rat hypothalamus.
Nitric oxide (NO), which was firstly identified as an endothelium-derived relaxing factor, has recently been demonstrated to be a neurotransmitter in the central and peripheral nervous systems. In the hypothalamus, abundant nitric oxide synthase (NOS) immunoreactivity and its histochemical marker, NADPH-diaphorase activity, have been demonstrated in the hypothalamo-neurohypophyseal system. ⋯ Most oxytocin-immunoreactive neurons in the paraventricular and supraoptic nuclei expressed NADPH-diaphorase activity, but virtually no vasopressin-immunoreactive neurons contained NADPH-diaphorase activity. This suggests that oxytocin neurons are the main source of NO production in the hypothalamic-pituitary system.
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Neuroscience letters · Mar 1994
Activated human platelets in plasma excite nociceptors in rat skin, in vitro.
Extravascular activation of thrombocytes may contribute to nociceptor excitation and pain, since platelets store and, upon stimulation, release potential algogenic substances such as serotonin, histamine and precursor molecules of bradykinin. To test this hypothesis, a skin-nerve preparation of rat hairy skin, in vitro, was used that allows to record and characterize single afferent nerve fibers. In a first protocol, receptive fields of nociceptive C-fibers, at the corium side of the skin patch, were exposed to adenosine diphosphate (ADP), to heparinized human platelet-rich plasma (PRP) and to PRP activated by ADP. ⋯ Frey) and thermal thresholds of the CMH units were not significantly altered. The findings demonstrate that nociceptors can indeed be driven and sensitized by activated platelets. This pain inducing mechanism may be relevant to certain clinical conditions, and it appears promising to scrutinize the chemical factors involved.
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Neuroscience letters · Jan 1994
Paradoxical timing of the circadian rhythm of sleep propensity serves to consolidate sleep and wakefulness in humans.
The contribution of the circadian pacemaker and the sleep homeostat to sleep tendency and consolidation was quantified by forced desynchrony of the sleep-wake cycle from the circadian pacemaker in eight men who lived in time-isolation for 33-36 days. Analysis of 175 polygraphically recorded sleep episodes revealed that the circadian pacemaker and the sleep homeostat contribute about equally to sleep consolidation, and that the phase relationship between these oscillatory processes during entrainment to the 24-h day is uniquely timed to facilitate the ability to maintain a consolidated bout of sleep at night and a consolidated bout of wakefulness throughout the day.
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Neuroscience letters · Jan 1994
Streptozotocin-induced diabetes selectively reduces antinociception mediated by mu 1-opioid receptors, but not that mediated by mu 2-opioid receptors.
We assessed the effect of naloxonazine, a selective mu 1-opioid receptor antagonist, on antinociception produced by intrathecal or intracerebroventricular injections of morphine in streptozotocin-induced diabetic mice. The antinociceptive effect of morphine (10 micrograms), administered i.c.v., was significantly less in diabetic mice than in non-diabetic mice. The antinociceptive effect of i.c.v. morphine was significantly reduced in both diabetic and non-diabetic mice following pretreatment with naloxonazine. ⋯ Furthermore, naloxonazine had no significant effect on the antinociceptive effect of i.t. morphine in either diabetic or non-diabetic mice. On the other hand, the antinociceptive effects of i.c.v. and i.t. morphine were significantly reduced following pretreatment with beta-funaltrexamine, a selective mu-opioid receptor antagonist, in both diabetic and non-diabetic mice. In conclusion, mice with diabetes are selectively hyporesponsive to supraspinal mu 1-opioid receptor-mediated antinociception, but are normally responsive to activation of spinal mu 2-opioid receptors.