Neuroscience letters
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Neuroscience letters · Oct 2013
Carvacrol alleviates cerebral edema by modulating AQP4 expression after intracerebral hemorrhage in mice.
Carvacrol is a natural compound extracted from many plants of the family Lamiaceae. Previous studies have demonstrated that carvacrol has potential neuroprotective effects in central nervous system diseases such as Alzheimer's disease and cerebral ischemia. In this study, we investigated the preclinical effect of carvacrol on cerebral edema after intracerebral hemorrhage (ICH) using a bacterial collagenase-induced ICH mouse model. ⋯ We also found that carvacrol treatment decreased AQP4 mRNA in a dose-dependent manner at 24h. Furthermore, AQP4 protein expression in the perihematomal area was reduced by carvacrol significantly at day 3 after ICH (p<0.05). Our findings suggest that carvacrol may exert its protective effect on ICH injury by ameliorating AQP4-mediated cerebral edema.
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Neuroscience letters · Oct 2013
Modulation of thermal somatosensory thresholds within local and remote spinal dermatomes following cervical repetitive magnetic stimulation.
Repetitive magnetic stimulation (rMS) modulates thermal somatosensory function at both low (0.2-1.0Hz) and high (5.0-20.0Hz) frequencies within the conditioned dermatome. However the effects of 1Hz and 20Hz cervical (C6-C7) rMS on thermosensory thresholds and contact heat evoked potentials (CHEPs) tested within local and remote spinal dermatomes are not known. ⋯ Both 1 and 20Hz cervical rMS modulated warm detection threshold within the locally conditioned C6 dermatome. The concomitant increase in warm detection threshold within the T10 dermatome following 1Hz rMS provides evidence for remote neuromodulation of thermosensory function via intraspinal control mechanisms.
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Pain processing has been poorly studied in multiple system atrophy (MSA), notwithstanding these subjects complaint pain very frequently. We hypothesized that, as observed in other basal ganglia neurodegenerative disorders involving the striatonigral projections, also in MSA with predominant parkinsonian signs could be detected an abnormal pain processing. ⋯ We demonstrated a facilitated temporal processing of pain in MSA subjects paralleling findings from PD. We hypothesize that the abnormal pain processing detected in both MSA and PD, could represent a consequence of the striatonigral neurodegeneration which in turn make these subjects more prone to develop pain conditions.
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Neuroscience letters · Oct 2013
Up-regulation of spinal microglial Iba-1 expression persists after resolution of neuropathic pain hypersensitivity.
Spinal microglial activation plays a major role in the development of neuropathic pain following peripheral nerve injury. We here provide evidence for an elevated expression of the microglial marker Iba-1 in the lumbar dorsal horn ipsilateral to L5 spinal nerve transection that persists for at least 14 weeks, a time at which mechanical hypersensitivity had fully resolved. ⋯ We therefore conclude that microglia remain partly activated beyond the phase of pain hypersensitivity. Thus, the relation between microglial cells and neuropathic pain outcome is subject to change over time after nerve injury.
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Neuroscience letters · Oct 2013
Contribution of muscarinic M1 receptors to the cholinergic suppression of synaptic responses in layer II of the entorhinal cortex.
The entorhinal cortex is thought to play roles in sensory and mnemonic function, and the cholinergic suppression of the strength of synaptic inputs is likely to have important impacts on these processes. Field excitatory postsynaptic potentials (fEPSPs) in the medial entorhinal cortex evoked by stimulation of the piriform cortex are suppressed during theta EEG activity in behaving animals, and cholinergic receptor activation suppresses synaptic responses both in vivo, and in layer II entorhinal neurons in vitro. ⋯ The M2/M4 preferring receptor blocker methoctramine, or the M4 receptor blocker PD102807, did not prevent the cholinergic suppression. However, the M1/M4 receptor blocker pirenzepine and the M1 receptor blocker VU0255035 reduced the suppression, suggesting that the cholinergic suppression of synaptic responses in the entorhinal cortex is dependent in large part on activation of M1 receptors.