Neuroscience letters
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Neuroscience letters · Sep 2015
Structured movement representations of a phantom limb associated with phantom limb pain.
The relation between phantom limb pain (PLP) and the movement representation of a phantom limb remains controversial in several areas of neurorehabilitation, although there are a few studies in which the representation of phantom limb movement was precisely evaluated. We evaluated the structured movement representation of a phantom limb objectively using a bimanual circle-line coordination task. We then investigated the relation between PLP and the structured movement representation. ⋯ When the OI neared 100%, the trajectory changed toward becoming more circular. A significant negative correlation was observed between the intensity of PLP and the OI (r=-0.66, p<0.05). Our findings directly suggest that structured movement representations of the phantom limb are necessary for alleviating PLP.
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Neuroscience letters · Sep 2015
Acute nicotine treatment attenuates lipopolysaccharide-induced cognitive dysfunction by increasing BDNF expression and inhibiting neuroinflammation in the rat hippocampus.
Although nicotine has been shown to improve cognitive function in various studies, the mechanisms underlying acute nicotine treatment-induced neuroprotection remain incompletely understood. In this study, we evaluated the effect of acute nicotine treatment on the cognitive impairment induced by lipopolysaccharide (LPS) and explored the underlying mechanism. ⋯ Furthermore, nicotine administration led to a significant increase in BDNF mRNA expression at 4 and 24h and in BDNF protein expression at 24h after LPS injection in the dorsal hippocampus. Taken together, acute nicotine administration attenuated LPS-induced cognitive dysfunction, and this neuroprotective effect may be related to the up-regulation of BDNF and the inhibition of neuroinflammation and apoptosis-related proteins in the dorsal hippocampus.
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Neuroscience letters · Sep 2015
Cerebellar vermis contributes to the extinction of conditioned fear.
The cerebellum is known to contribute to the acquisition and retention of conditioned motor and emotional responses. Eyeblink conditioning and fear conditioning have been studied in greatest detail. Whereas a considerable number of studies have shown that the cerebellum is also involved in extinction of conditioned eyeblink responses, the likely contribution of the cerebellum to extinction of conditioned fear responses has largely been ignored. ⋯ During the acquisition phase, the fMRI signal related to the CS+ was significantly higher in hemispheric lobule VI in early compared to late acquisition (p<.05, permutation corrected). During the extinction phase, the fMRI signal related to the contrast CS+>CS- was significantly higher within the anterior vermis in early compared to late extinction (p<.05, permutation corrected). The present data show that the cerebellum is not only associated with the acquisition but also with the extinction of conditioned fear.
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Neuroscience letters · Sep 2015
Comparative StudyManipulating neuronal activity in the mouse brain with ultrasound: A comparison with optogenetic activation of the cerebral cortex.
Low-intensity focused ultrasound induces neuronal activation via mechanisms that remain to be elucidated. We recorded local field potential fluctuations in the motor cortex in response to ultrasound stimulation of the somatosensory barrel cortex, comparing them to those recorded in response to optogenetic stimulation of interneurons and pyramidal neurons of the somatosensory cortex in the same animals. ⋯ Comparison of post mortem evoked responses to responses in living tissue confirmed the necessity for excitable tissue in the evoked response. Collectively, these experiments demonstrate an excitation-dependent response to low-frequency transdural ultrasound stimulation of cerebral cortical neuronal activity.
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Neuroscience letters · Sep 2015
Early treatment with UR13870, a novel inhibitor of p38α mitogenous activated protein kinase, prevents hyperreflexia and anxiety behaviors, in the spared nerve injury model of neuropathic pain.
Microglia cell activation plays a role in the development of neuropathic pain partly due to the activation of the p38α MAPK signaling pathway after nerve injury. In this study we assessed the effect of UR13870, a p38α MAPK inhibitor, in the "spared nerve injury" (SNI) model, to study its effects on modulation of spinal microglial activation and to test behavioral hyperreflexia responses and cerebral-mediated pain behavior. The effect of daily administration of UR13870 (10mg/kg p.o.) and Pregabalin (50mg/kg p.o.) on reflex hypersensitivity to mechanical and cold test stimuli and on affective related pain responses measured with the place escape avoidance paradigm and the open field-induced anxiety test, were evaluated after SNI in Sprague Dawley rats. ⋯ UR13870 treatment significantly decreased hindlimb hyperreflexia to both mechanical and cold stimuli after SNI without loss of general motor function, in addition to a reduction in pain-related anxiety behavior at day 21 after SNI, accompanied by normalization of OX-42 immunoreactivity within the ipsilateral lumbar dorsal horn. Pregabalin treatment only reduced mechanical hyperreflexia and affected general motor function. Oral administration of the p38α MAPK inhibitor, UR13870, mediates antinociception to both mechanical and cold stimuli, and significantly restored inner-zone exploration in the open field test, accompanied by normalization in dorsal horn microglial activation in the SNI model.