Neuroscience letters
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Neuroscience letters · Feb 2009
Effects of electrolytic lesion of dorsolateral periaqueductal gray on analgesic response of morphine microinjected into the nucleus cuneiformis in rat.
The periaqueductal gray (PAG) and nucleus cuneiformis (CnF), like the rostral ventromedial medulla, have functional roles in descending pain-inhibitory pathway related to morphine antinociception. There is not any evidence concerning the role of different regions of the PAG on antinociceptive effect of morphine administered into the CnF in pain modulatory system. In the present study, we investigate whether electrolytic lesion of dorsolateral periaqueductal gray (dl-PAG) influence the analgesic effect of morphine microinjected into the CnF. 71 adult male Wistar rats weighting 230-280 g cannulated bilaterally into the CnF, concurrently lesion of dl-PAG was done. ⋯ Each rat was given a subcutaneous 50-microl injection of formalin 2.5% into plantar surface of hind paw following morphine administration. The results showed that dl-PAG lesion attenuated the effect of morphine microinjected into the CnF both in tail-flick and formalin tests while dl-PAG lesion solely did not alter basal pain behavior as compared to control group. In conclusion, our results suggest the existence of a direct or indirect projection from CnF to the dl-PAG at least at the level of the morphine antinociception in pain modulation.
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Neuroscience letters · Feb 2009
Case ReportsOculogyric crisis with exacerbation of psychosis: Possible mechanism and clinical implications.
Oculogyric crisis is a distressing acute/chronic side effect of neuroleptic medications. Chronic oculogyric crisis can be considered as a tardive hyperkinetic movement disorder and it may be associated with worsening of psychotic symptoms. Treatment strategies for chronic oculogyric crisis include; high potency antipsychotics and anticholinergics drugs for immediate relief and clozapine as a long-term treatment strategy. Here we are presenting case histories of four patients with oculogyric crisis and associated worsening of psychosis, its possible etiology and various treatment strategies.
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Autophagy is a key pathway for the clearance of damaged organelles. Ischemic preconditioning (IPC) and autophagy are enhanced by mild hypoxic insults, but the association between autophagy and IPC remains unclear. We investigated the existence and role of autophagy in IPC. ⋯ Inhibition of autophagy, especially during reperfusion or lethal oxygen-glucose deprivation periods ameliorated the neuroprotective effects of IPC. Moreover, inhibiting autophagy also attenuated Hsp70 upregulation induced by IPC. These findings imply that autophagy participates in IPC-induced neuroprotection, and that autophagy might provide a means of neuroprotection against cerebral ischemia.
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Neuroscience letters · Feb 2009
Attenuation of opioid analgesic tolerance in p75 neurotrophin receptor null mutant mice.
Repeated exposure to opioid drugs can lead to the development of tolerance, which manifests as a reduction in analgesic potency, and physical dependence, a response indicated by a withdrawal syndrome. Accumulating evidence suggests that the nerve growth factor (NGF) family of neurotrophins may have an important modulatory role in the induction of opioid analgesia and opioid addiction. Because neurotrophins universally bind the p75 neurotrophin receptor (p75NTR), we investigated whether the activity of this receptor is involved in the development of opioid analgesic tolerance and physical dependence. ⋯ In the second part of this study, mice were given escalating doses of systemic (i.p.) morphine over 5 days and subsequently challenged with the opioid receptor antagonist naloxone. This challenge precipitated a robust withdrawal syndrome that was comparable in wild-type mice and p75NTR-/- mice. The findings suggest that p75NTR activity plays a critical role in the development of opioid analgesic tolerance but not in the induction or the expression of opioid physical dependence.