Neuroscience letters
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In the present offering, the authors provide evidence for the role of the hypoglossal motonucleus in causing a cranial nerve hyperactivity syndrome, namely hemilingual spasm. During a microvascular decompression operation to treat hemilingual spasm, transcranial stimulation elicited a delayed electromyographic (EMG) response from the tongue. This late volley of EMG activity occurred with a latency of approximately 40 ms, lasted approximately 50 ms, and disappeared when the offending vessel was displaced away from the exit zone of the hypoglossal nerve root along medulla oblongata. ⋯ This abnormal response, known as the lateral spread response, is a characteristic sign for hemifacial spasm that disappears after the offending vessel is moved off the facial nerve root. The results of the present study indicate that the EMG signs of hemilingual spasm are similar to those of HFS and that the tongue spasms are most likely caused by hyperactivity of the hypoglossal motonucleus. Based on the authors' knowledge, the above detailed electrophysiological findings related to hemilingual spasm have not been previously reported in the literature.
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Neuroscience letters · Sep 2009
Signaling pathway involved in hypoxia-inducible factor-1alpha regulation in hypoxic-ischemic cortical neurons in vitro.
Hypoxia-inducible factor-1alpha (HIF-1alpha) is a key transciptional regulator of cellular and systemic oxygen homeostasis. Previous studies have shown that the regulation of HIF-1alpha is involved in the activation of PI3K/Akt pathway in some cells. However, whether this pathway plays a role in modulating HIF-1alpha in cultured cortical neurons during hypoxia-ischemia (HI) remains unclear. ⋯ Meanwhile, p-Akt increased and peaked at 4h after reperfusion, preceding HIF-1alpha expression. Pretreatment with wortmannin, a PI3K/Akt pathway inhibitor, significantly inhibited p-Akt expression and further attenuated both transcription and translation of HIF-1alpha and VEGF. Collectively, our findings suggested that PI3K/Akt signaling pathway might be involved in HIF-1alpha regulation after OGD in cultured cortical neurons.
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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 · 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.