Neurochemical research
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Neurochemical research · Apr 2006
Neuroprotective effects of N-acetylcysteine on experimental closed head trauma in rats.
N-acetylcysteine (NAC) is a precursor of glutathione, a potent antioxidant, and a free radical scavenger. The beneficial effect of NAC on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of NAC on nervous system trauma remains less understood. ⋯ The morphology of neurons in the NAC treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+NAC treatment groups. In conclusion, the NAC treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications.
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Neurochemical research · Mar 2006
Glial activation and segmental upregulation of interleukin-1beta (IL-1beta) in the rat spinal cord after surgical incision.
The present study investigated the expression patterns of glial cells and interleukin-1beta (IL-1beta) in the rat spinal cord after a surgical incision, which is closely related with clinical postoperative pain. Microglia and astrocytes became activated in the spinal cord following incision. Real-time polymerase chain reaction (PCR) and immunohistochemisty showed that IL-1beta mRNA and protein level in the spinal cord was transiently upregulated after surgical incision. ⋯ Although obvious increase in IL-1beta-IR could be observed in the lumbar segments of the spinal cord ipsilateral to a hind paw incision, significant upregulation of IL-1beta was not detected in the lumbar segments following thoracic incision. The present study indicated that surgical incision could induce glial activation and segmental upregulation of IL-1beta in the spinal cord. The activated glial cells and upregulated IL-1beta, in turn, may be involved in the incision-induced pain hypersensitivity.
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Neurochemical research · Dec 2005
ReviewEpileptogenesis after experimental focal cerebral ischemia.
Cerebrovascular diseases are one of the most common causes of epilepsy in adults, and the incidence of stroke-induced epileptogenesis is increasing as the population ages. The mechanisms that lead to stroke-induced epileptogenesis in a subpopulation of patients, however, are still poorly understood. ⋯ Here we summarize data from models in which epileptogenesis has been studied after focal ischemia; photothrombosis, middle cerebral artery (MCA) occlusion with filament, and endothelin-1-induced MCA occlusion. Analysis of the data indicates that neurobiologic changes occurring during stroke-induced epileptogenesis share some similarities to those induced by status epilepticus or traumatic brain injury.
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Neurochemical research · Mar 2005
Neuroprotective effects of ebselen on experimental spinal cord injury in rats.
Spinal cord injury (SCI) results in rapid and significant oxidative stress. This study was aimed to investigate the possible beneficial effects of Ebselen in comparison with Methylprednisolone in experimental SCI. Thirty six Wistar albino rats (200-250 g) were divided in to six groups; A (control), B (only laminectomy), C (Trauma; laminectomy + spinal trauma), D (Placebo group; laminectomy + spinal trauma + serum physiologic), E (Methylprednisolone group; laminectomy + spinal trauma + Methylprednisolone treated), F (Ebselen group; laminectomy + spinal trauma + Ebselen treated), containing 6 rats each. ⋯ The morphology of neurons in groups E and F were very well protected, but not as good as the control group. The number of neurons in the spinal cord tissues of the groups C and D were significantly less than the groups A, B, E and F. We concluded that the use of Ebselen treatment might have potential benefits in spinal cord tissue damage on clinical grounds.
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Neurochemical research · Nov 2004
NMDA receptor in nucleus accumbens is implicated in morphine withdrawal in rats.
The purpose of the present study is to elucidate whether ketamine, a non-competitive antagonist of the NMDA receptor, can suppress the morphine withdrawal syndrome in rats at a dose without affecting motor functions and to identify its site of action in the central nervous system. Rats were made dependent on morphine by multiple injections of morphine hydrochloride for 5 days. They were then given ketamine at the following doses and routes of administration: (a) intraperitoneal (i.p.) injections (2-16 mg/kg), (b) intracerebroventricular (i.c.v.) injections (4-100 microg), and (c) intra-nucleus accumbens (NAc) or intra-amygdalar microinjections (0.4-10 microg). ⋯ Results showed that some of the precipitated withdrawal signs were dose-dependently suppressed by repeated injections of ketamine at 8 and 16 mg/kg, i.p. or 100 microg, i.c.v. Dose-dependent suppression was observed by repeated microinjections (0.4-10 microg) of ketamine to NAc, but not to amygdala. These results indicate that the NMDA receptor antagonist ketamine has the ability to suppress morphine withdrawal syndrome in experimental settings without motor interference, and NAc could be the critical CNS site mediating such effect.