Neuroscience letters
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Neuroscience letters · Sep 2009
Peripheral and spinal antihyperalgesic activity of najanalgesin isolated from Naja naja atra in a rat experimental model of neuropathic pain.
Snake venoms are a rich source of various compounds that have applications in medicine and biochemistry. Recently, it has been demonstrated that najanalgesin isolated from the venom of Naja naja atra exerts analgesic effects on acute pain in mice. The objective of this study was to evaluate the antinociceptive effect of najanalgesin in a rat model of neuropathic pain, induced by L5 spinal nerve ligation and transaction. ⋯ These results demonstrate that najanalgesin has antinociceptive effects on the central and peripheral system in the rat neuropathic pain model. The opioid receptor and muscatinic receptor are involved in najanalgesin-induced antinociception in the spinal cord. This research supports the possibility of using najanalgesin as a novel pharmacotherapeutic agent for neuropathic pain.
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Neuroscience letters · Sep 2009
Neuroprotection (and lack of neuroprotection) afforded by a series of noble gases in an in vitro model of neuronal injury.
Xenon-induced neuroprotection has been well studied both in vivo and in vitro. In this study, the neuroprotective properties of the other noble gases, namely, krypton, argon, neon and helium, were explored in an in vitro model of neuronal injury. Pure neuronal cultures, derived from foetal BALB/c mice cortices, were provoked into injury by oxygen and glucose deprivation (OGD). ⋯ Helium had a detrimental effect on the cells. In the absence of OGD, krypton reduced the reducing ability of uninjured cells to 0.84+/-0.09 (p<0.01), but argon showed an improvement in reducing ability to 1.15+/-0.11 (p<0.05). Our data suggest that the cheap and widely available noble gas argon may have potential as a neuroprotectant for the future.
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Neuroscience letters · Aug 2009
Changes of functional connectivity of the motor network in the resting state in Parkinson's disease.
We used functional MRI (fMRI) and a network model based on graph theory to measure functional connectivity of brain motor network in the resting state in patients with Parkinson's disease (PD). FMRIs were acquired in 22 PD patients before and after levodopa administration, and in age- and sex-matched normal controls. The total connectivity degree of each region within the motor network was calculated and compared between patients and controls. ⋯ Our findings demonstrate that the pattern of functional connectivity of the motor network in the resting state is disrupted in PD. This change is secondary to dopamine deficiency, and related to the severity of the disease. We postulate that this abnormal functional connectivity of motor network in the baseline state is possibly an important factor contributing to some motor deficits in PD, e.g. akinesia.
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Neuroscience letters · Aug 2009
Deficits in ERK and CREB activation in the hippocampus after traumatic brain injury.
Traumatic brain injury (TBI) activates several protein kinase signaling pathways in the hippocampus that are critical for hippocampal-dependent memory formation. In particular, extracellular signal-regulated kinase (ERK), a protein kinase activated during and necessary for hippocampal-dependent learning, is transiently activated after TBI. However, TBI patients experience hippocampal-dependent cognitive deficits that occur for several months to years after the initial injury. ⋯ We found that activation of ERK (p<0.05) and CREB (p<0.05) after 30s of glutamate stimulation or KCl depolarization was decreased in hippocampal slices from animals at 2, 8, or 12 weeks after TBI as compared to sham animals. Basal levels of phosphorylated or total ERK were not significantly altered at 2, 8, or 12 weeks after TBI, although basal levels of phosphorylated CREB were decreased 12 weeks post-trauma. These results suggest that TBI results in chronic signaling deficits through the ERK-CREB pathway in the hippocampus.
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Neuroscience letters · Jul 2009
Involvement of increased expression of transient receptor potential melastatin 8 in oxaliplatin-induced cold allodynia in mice.
Oxaliplatin is a chemotherapy drug and induces peripheral neuropathy which is aggravated by exposure to cold, the mechanism of which is unclear. In the present study, we investigated in mice whether transient receptor potential melastatin 8 (TRPM8), which is activated by cooling temperature, would be involved in cold allodynia induced by oxaliplatin. Mice were given an intraperitoneal injection of oxaliplatin. ⋯ Oxaliplatin increased wet-dog shake and jumping behaviors evoked by the TRPM8 agonist icilin. An injection of oxaliplatin increased the expression level of TRPM8 mRNA at day 3 after injection and the expression was decreased to the near-normal level on days 10 and 25. These results suggest that cold allodynia induced by oxaliplatin is at least partly due to the increased expression of TRPM8 in the primary afferents.