Neuroscience letters
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Neuroscience letters · Jun 1996
Sciatic nerve section induces mechanical hyperalgesia in skin adjacent to the deafferented region in rats: lack of correlation with autotomy behavior.
We have studied the development of cutaneous hypersensitivity in the innervation area of the saphenous nerve and autotomy behavior in rats after unilateral sciatic nerve section. Hypersensitivity was assessed by stimulating the saphenous area with mechanical (von Frey hairs and analgesimeter), cold (immersion) or heat (immersion or radiant heat) stimuli 10 days after sciatic nerve section. We did not observe any hypersensitivity to thermal stimulation or weak mechanical stimulation produced by von Frey hairs. ⋯ Eleven of 17 rats had started autotomy at this time, but there was no correlation between the presence of autotomy and mechanical hyperalgesia. It is concluded that in our experimental setting, only mechanical hyperalgesia was present 10 days after axotomy. Moreover, autotomy behavior and adjacent hyperalgesia may be triggered by different mechanisms.
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Neuroscience letters · Apr 1996
Capsaicin blocks tetrodotoxin-resistant sodium potentials and calcium potentials in unmyelinated C fibres of biopsied human sural nerve in vitro.
Topical application of capsaicin has been tested recently for treatment of painful peripheral neuropathy. In the present study, effects of capsaicin were explored on compound action potentials of isolated fascicles from human sural nerve biopsies. Capsaicin reduced the C fibre component by 30-60%; the remaining C fibres were not sensitive to the drug. ⋯ C fibre action potentials recorded in the presence of TTX were completely blocked by capsaicin. Calcium action potentials seen after inhibition of axonal potassium conductances were also completely suppressed. The data indicate that application of capsaicin nearby human peripheral nerves might prevent action potential conduction in specific subtypes of C fibres.
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Neuroscience letters · Jan 1996
Comparative StudyChanges in activity of spinal cells with muscular input in rats with referred muscular hyperalgesia from ureteral calculosis.
In rats with hyperalgesia of the obliquus externus muscle (OE) from artificial calculosis of the ipsilateral upper ureter, changes in cell activity were studied in the ipsilateral spinal cord (T11-T12) versus control animals. In cases of hyperalgesia of high degree, in the dorsal horn (0-900 microns) the following were found: significantly higher percentages of cells driven by OE stimulation (P < 0.03) and of spontaneously active cells with OE input (P < 0.02); significantly higher frequency of background discharge of cells with OE input (P < 0.002); among cells driven by OE stimulation, significantly higher percentages of neurons with exclusively deep input (P < 0.0006) and of neurons with low mechanical threshold of activation (P < 0.03). In the intermediate region of the cord (900-1600 microns), a significantly higher percentage was found of spontaneously active cells with OE input (P < 0.009) while in the ventral horn (1600-2300 microns) no changes were detected. The results indicate that referred muscle hyperalgesia of high degree is accompanied by a state of central sensitization probably triggered by the abnormal afferent input from the visceral focus.
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Neuroscience letters · Jan 1996
Monoaminergic neurotransmitters, their precursors and metabolites in brains of Alzheimer patients.
The catecholamines dopamine (DA), noradrenaline (NA) and adrenaline (A), their aminoacid precursors tyrosine (Tyr), L-3,4-dihydroxyphenylalanine (L-DOPA), two of their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and 4-hydroxy-3-methoxy phenyl glycol (MHPG), serotonin (5-HT) and its precursor tryptophan (Trp), were measured by high pressure liquid chromatography (HPLC) with electrochemical detection in seven regions (globus pallidus, putamen, nucleus amygdalae, nucleus caudatus, substantia nigra, gyrus cinguli and raphe) of postmortem brains from eight histologically verified cases with Alzheimer's disease (AD) and six histologically normal controls. Concentrations of L-DOPA, DA, DOPAC, NA and 5-HT were significantly reduced, while Tyr and MHPG concentrations were significantly increased in AD versus control patients. ⋯ Furthermore, for most brain regions examined, significant negative correlations between Tyr and DA as well as between NA and MHPG levels were found. These data confirm and extend findings of monoaminergic systems disturbances in AD, emphasize the significance of dopaminergic deficit for AD and suggest that in pharmacotherapy of AD, attempts to restore deficits of the transmitter systems should be directed to the monoaminergic, in particular the dopaminergic system.
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Neuroscience letters · Oct 1995
Inhibition by spinal morphine of the tail-flick response is attenuated in rats with nerve ligation injury.
Nerve ligation injury in rats produces increased sensitivity and exaggerated responses to nociceptive stimuli (hyperalgesia) as well as nociceptive responses to normally innocuous stimuli (allodynia) analogous to clinical conditions of neuropathic pain. However, the effect of nerve injury on acute nociception has not been extensively studied. Nerve ligation injury was produced by unilateral ligation of the L5 and L6 spinal roots of the sciatic nerve of male Sprague-Dawley rats. ⋯ Antinociception was readily reversed by naloxone (5 mg/kg, i.p.) in both groups. These data indicate that nerve ligation injury reduces the potency and efficacy of i.th. morphine. While the reasons for this loss of morphine activity in nerve injured animals are unknown, it is possible to speculate that (a) degeneration of primary afferents subsequent to nerve ligation injury might result in a loss of presynaptic opioid (mu?) receptors in the dorsal horn, thereby reducing the antinociceptive activity of morphine at the spinal level; (b) changes in the efficiency of post-receptor transduction may occur following nerve injury which can reduce opioid efficacy; (c) changes in levels of spinal neurotransmitters (e.g., cholecystokinin) may act to diminish opioid action; or (d) sustained afferent input from the site of the injury may be important in limiting the activity of opioids.