Neuroscience letters
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Neuroscience letters · Nov 1993
NMDA receptor antagonists attenuate mechanical hyperalgesia in rats with unilateral inflammation of the hindpaw.
The effects of N-methyl-D-aspartate (NMDA) receptor antagonists on mechanical hyperalgesia associated with tissue inflammation were studied. Following an injection of the inflammatory agent, complete Freund's adjuvant, into the rat hindpaw, there was a significant decrease in threshold and an increase in response duration to mechanical stimuli, suggesting that a state of mechanical hyperalgesia was induced. The intrathecal administration of the NMDA receptor antagonists, dizocilpine maleate and (+/-)-2-amino-5-phosphonopentanoic acid, significantly increased mechanical threshold and reduced response duration in the inflamed hindpaw, but had no effect on the non-injected paw. The results suggest that NMDA receptor activation may contribute to the mechanical hyperalgesia that follows peripheral tissue inflammation.
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Neuroscience letters · Sep 1993
Capsaicin-induced central facilitation of a nociceptive flexion reflex in humans.
The effect of selective activation of nociceptive primary afferent fibers by capsaicin on a nociceptive lower limb flexion reflex was studied in healthy human subjects. Capsaicin (1%) applied topically to the skin produced a burning spontaneous pain sensation and allodynia in the treated region and in its immediate vicinity. Capsaicin applied to the distal innervation area of the sural or saphenous nerve produced a significant decrease of the threshold for the nociceptive limb flexion reflex induced by electric stimulation of the proximal sural nerve trunk, and this threshold decrease was rapidly attenuated by a cool compress concomitantly with the attenuation of the capsaicin-induced spontaneous pain. ⋯ The non-nociceptive H-reflex was not modified by capsaicin. It is concluded that a selective activation of nociceptive primary afferent fibers of the skin by capsaicin produces a central facilitation of a nociceptive flexion reflex in humans. This facilitation is selective on the nociceptive reflex and depends, at least partly, on the on-going afferent barrage in C-fibers.
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Neuroscience letters · Sep 1993
MK-801, an N-methyl-D-aspartate receptor antagonist, blocks quinolinic acid-induced lipid peroxidation in rat corpus striatum.
In this study, we evaluate the possible participation of lipid peroxidation (LP) in the neurotoxic events that follow after quinolinic acid (QUIN) microinjection into the rat corpus striatum. Two hours after QUIN (240 nmol/microliters) intrastriatal administration, lipid peroxidation was found increased by 32% vs. control as measured by thiobarbituric acid-reactive substances (TBARS). ⋯ The increase of QUIN-induced lipid peroxidation was completely abolished by pretreatment of rats with an N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801 (10 mg/kg, i.p.), 60 min before QUIN microinjection. Results suggest an NMDA receptor involvement in the QUIN-induced oxidative processes.
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Neuroscience letters · Aug 1993
The noradrenergic innervation density of the monkey paraventricular nucleus is not altered by early social deprivation.
A series of neuroanatomic analyses have been undertaken to identify potential neuropathological changes seen in monkeys exposed to early social deprivation, which leads to psychopathology, inappropriate responses to stress and appetitive disorders. The animals used in this study were either socially reared or maternal- and peer-deprived. ⋯ Quantitative analysis of dopamine-beta-hydroxylase-immunoreactive varicosity density within magnocellular and parvicellular regions revealed no significant differences between rearing conditions, suggesting that this chemically identified afferent input to the paraventricular nucleus was not affected by the early environmental insult of social deprivation. The apparent lack of vulnerability of the paraventricular nucleus to differential rearing conditions contrasts with the neuropathological changes observed in several discrete brain regions.
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Neuroscience letters · Aug 1993
Fos induction in brainstem neurons by intravenous hypertonic saline in the conscious rat.
Experiments were done in conscious rats to investigate the effect of intravenous infusion of hypertonic saline on the induction of the protein Fos, in brainstem neurons. Neurons containing Fos-like immunoreactivity were observed in the caudal nucleus of the solitary tract (NTS), the caudal and rostral ventrolateral medulla, and parabrachial nucleus after an infusion of solutions containing 1.4 M NaCl. Little or no expression of Fos was detected in brainstem neurons after intravenous infusions of either physiological (143 mM) or hypotonic (106 mM) NaCl solutions. These data provide evidence for the involvement of brainstem structures in osmoregulatory functions and suggest that brainstem neuronal circuits that function in cardiovascular regulation may also be shared by those involved in body fluid homeostasis.