Neuroscience letters
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Neuroscience letters · Jul 1992
Vasodilator flare due to activation of superficial cutaneous afferents in humans: heat-sensitive versus histamine-sensitive fibers.
Histamine-sensitive nerve endings are assumed to terminate in the superficial epidermis. Heat-sensitive nociceptors that are excited by brief carbondioxide-laser pulses must also terminate within the epidermis, because this infrared radiation has an extinction length of about 10 microns. We now compared laser heat stimuli (10 W, 50 ms, 20 mm2) with intradermal injections of histamine (10(-10) to 10(-8) mol) in their capacity to cause cutaneous vasodilatation (flare) in awake human subjects. ⋯ Although the heat pulses elicited enough nociceptor activity to be perceived as moderately painful, the magnitude of the vasodilatation was smaller and its duration shorter than after the smallest dose of histamine. In contrast, nociceptor activation by heat is usually stronger than by histamine. These data indicate that flare and pain are two different aspects of cutaneous small fiber function.
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Neuroscience letters · Mar 1992
Blood flow increases in the skin of the anaesthetized rat that follow antidromic sensory nerve stimulation and strong mechanical stimulation.
In anaesthetized rats, punctate pressure using forces greater than or equal to 20 mN caused small transient rises in skin blood flow that were similar in normally innervated and chronically denervated skin. A force of 11 mN, sufficient to excite most C-fibres of the polymodal nociceptor class, failed to cause vasodilatation. ⋯ Antidromic vasodilation was unaffected by high frequency stimulation of A alpha beta axons or by simultaneous innocuous mechanical stimulation. The failure of pressure at levels suprathreshold for C-fibre nociceptors to cause neurogenic vasodilatation may mean that antidromic vasodilation in rat skin is due to activity restricted to a mechanically insensitive sub-population of C-fibres.
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Neuroscience letters · Jan 1992
Studies on the spinal interaction of morphine and the NMDA antagonist MK-801 on the hyperesthesia observed in a rat model of sciatic mononeuropathy.
This study evaluated the effects of intrathecally coadministered morphine and the N-methyl-D-aspartate (NMDA) antagonist (+)5-methyl-10,11-dihydro-5H- dibenzocyclohepten-5,10-imine maleate (MK-801) on the thermally evoked hindpaw withdrawal latency (PWL) in rats with one paw (ipsilteral) rendered hyperesthetic by the unilateral application of loose ligatures to the sciatic nerve (delta PWL (+/- S. D.) = PWLhyperesthetic paw - PWLnormal paw = -3.1 +/- 1.2 s). Intrathecal morphine produced a dose-dependent (0.1-10 micrograms; P less than 0.0001) elevation in the thermal response latency of both the contralateral (normal) and ipsilateral (hyperesthetic) paw. delta PWL did not vary with morphine, indicating that the dose-response curves were parallel but shifted to the right for the hyperesthetic paw. ⋯ D.) = -0.067 +/- 2.73). Co-administration of MK-801 with morphine did not alter the effects of morphine in the normal paw, but reduced the delta PWL for each dose of morphine. These results suggest that NMDA antagonism (1) does not alter the thermal sensitivity in the normal paw, (2) selectively abolishes the hypersensitivity of the hypersthetic paw and (3) has a simple additive interaction with the antinociceptive effects of morphine in the hyperesthetic paw.
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Neuroscience letters · Dec 1991
Sympathectomy alleviates mechanical allodynia in an experimental animal model for neuropathy in the rat.
We attempted to determine the effects of surgical sympathectomy on an animal model for neuropathic pain. The L5 and L6 spinal nerves on one side were tightly ligated in anesthetized rats. ⋯ The sympathectomy produced an immediate and almost complete reversal of the increased mechanical sensitivity, whereas sham sympathectomy had no effect. The data suggest that sympathectomy alleviates mechanical allodynia in this experimental animal model.
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Neuroscience letters · Dec 1991
Comparative StudyNon-NMDA antagonists protect against kainate more than AMPA toxicity in the rat hippocampus.
Single focal injection of the excitatory amino acids (EAAs) kainic acid (KA, 1.1 nmol/microliters) and (S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (S)-AMPA, 6 nmol/microliters) into rat dorsal hippocampus resulted in widespread neurodegeneration with 90-100% loss of hippocampal pyramidal cells in CA1, CA2, CA3 and CA4 subfields, and 50-70% loss of dentate granule (DG) cells. Focal injection of NMDA (30 nmol/microliters) under the same conditions resulted in 70-90% loss of CA1 cells with less damage in CA2, CA3, CA4 and DG cells (30-50%, 10-30%, and 30-50%, respectively). The non-NMDA antagonists NBQX (2,3-dihydro-6-nitro-7-sulphamoyl-benzo(f) quinoxaline) and GYKI 52466 (1-(amino)phenyl-4-methyl-7,8-methylendioxy-5H-2,3,benzodiazepine. ⋯ NBQX i.v. protected against (S)-AMPA toxicity in the DG cells but no protection was observed against (S)-AMPA toxicity in hippocampal subfields (CA1, CA2 and CA4). Intravenous administration of NBQX and GYKI 52466 (30 mg/kg/3 h) also failed to protect against NMDA toxicity in the hippocampus. Systemic injections of D(-)-CPPene, (E)-4-(3-phos-phonoprop-2-enyl)-piperazine-2-carboxylic acid, (10 and 5 mg/kg, i.p., 20 min prior and 3 h post EAA injection) protected against NMDA and KA toxicity in the CA1, CA2 and DG subfield with no protective effect against (S)-AMPA toxicity.