Neuroscience letters
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Neuroscience letters · Aug 2004
Comparative StudyPersistent hindpaw inflammation produces coeruleospinal antinociception in the non-inflamed forepaw of rats.
In a rat model of unilateral hindpaw inflammation, it is unclear whether the coeruleospinal modulation system is active at spinal segments distant from the inflamed plantar region, such as the cervical segments. To clarify this query, in the present study we measured paw withdrawal latency (PWL) to thermal stimuli on four paws (both forepaws and both hindpaws) following induction of inflammation and compared PWLs between rats with bilateral lesions of the locus coeruleus/subcoeruleus (LC/SC) and rats with sham operation. Unilateral hindpaw inflammation was produced by a subcutaneous injection of carrageenan (2 mg in 0.15 ml saline). ⋯ These phenomena which were observed in the inflamed left hindpaw were also observed in the non-inflamed left forepaws. In the right forepaws and the right hindpaws, no significant change in PWL was observed between before and 4 h after injection in both the sham-operated and the LC/SC-lesioned rats. These results suggest that unilateral hindpaw inflammation activates the coeruleospinal modulation system and that this modulation system is active not only at the lumbar segments but also at the cervical level where spinal segments are distant from the inflamed plantar region.
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Neuroscience letters · Aug 2004
Comparative StudyAcute and chronic ethanol exacerbates formalin pain in neonatal rats.
We have previously reported that withdrawal from acute ethanol (EtOH) exposure lowers mechanical thresholds in post-natal day 7 (P7) and post-natal day 21 (P21) rats. The present study tested the hypothesis that daily administration of 4 g/kg 15% EtOH for 5 days in rats during the human developmental equivalent of the third trimester, but not at a later time in development, would alter mechanical thresholds and formalin-induced pain behaviors. A transient decrease in mechanical thresholds (allodynia) was observed in P7 rats upon withdrawal from repeated EtOH between P3 and P7. ⋯ In contrast to chronic EtOH administration to rats between P3 and P7, prolonged mechanical allodynia was observed in P21 rats upon withdrawal from chronic EtOH between P17 and P21. Formalin responses were unchanged in P25 rats exposed to acute or chronic EtOH. The affects of EtOH on somatosensory processing are dependent upon the age at which exposure occurs.
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Neuroscience letters · Aug 2004
Comparative StudyRegulation of calcitonin gene-related peptide release from rat trigeminal nucleus caudalis slices in vitro.
Calcitonin gene-related peptide (CGRP) released from trigeminal primary afferents has been implicated in the pathophysiology of migraine. Here, we have used an in vitro slice preparation to investigate its release from nerve terminals in the rat trigeminal nucleus caudalis. ⋯ The capsaicin (1 microM)-evoked CGRP release was blocked by capsazepine and was also attenuated in the presence of the cyclooxygenase inhibitor, indomethacin, an effect that was reversed when slices were stimulated with capsaicin in the presence of the cyclooxygenase metabolite, prostaglandin E(2). Taken together, these data further highlight the importance of prostaglandins as enhancers of neuropeptide release and suggest that CGRP released from the central terminals of trigeminal neurones has the potential to be involved in the transmission of nociceptive information of relevance to migraine headache.
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Neuroscience letters · Aug 2004
Assessment of Nurr1 nucleotide variations in familial Parkinson's disease.
Parkinson's disease (PD) is characterised by the death of dopaminergic neurons of the substantia nigra. As Nurr1 seems to regulate the development and maintenance of these neurons, we evaluated its potential role in Parkinson's disease using genetic methods. ⋯ Our results failed to replicate the association initially observed and none of the mutations were present in our familial Parkinson's disease cases. These observations suggest that this gene is unlikely to play a major effect in French familial Parkinson disease.
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Neuroscience letters · Aug 2004
NGF-mediated sensitization of the excitability of rat sensory neurons is prevented by a blocking antibody to the p75 neurotrophin receptor.
Nerve growth factor (NGF) can play a causal role in the initiation of hyperalgesia. Recent work demonstrates that NGF can act directly on nociceptive sensory neurons to augment their sensitivity to a variety of stimuli. Based on the existing literature, it is not clear whether this sensitization is mediated by the high-affinity TrkA receptor or the low-affinity p75 neurotrophin receptor. ⋯ In this report, pretreatment with the p75 blocking antibody completely prevents the NGF-induced increase in the number of action potentials evoked by a ramp of depolarizing current as well as the suppression of a delayed rectifier-type of potassium current(s) in these neurons. Although the sensitization by NGF was blocked, the antibody had no effect on the capacity of ceramide, a putative downstream signaling molecule, to either enhance the excitability or inhibit the potassium current. These results indicate that NGF can increase the excitability of nociceptive sensory neurons through activation of the p75 neurotrophin receptor and its consequent liberation of ceramide from neuronal sphingomyelins.