Neuroscience letters
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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
Intrathecal inhibition of calcium/calmodulin-dependent protein kinase II in diabetic neuropathy adversely affects pain-related behavior.
Calcium/calmodulin-dependent protein kinase II (CaMKII) is considered an important enzyme contributing to the pathogenesis of persistent pain. The aim of this study was to test whether intrathecal injection of CaMKII inhibitors may reduce pain-related behavior in diabetic rats. Male Sprague-Dawley rats were used. ⋯ Also, mAIP and KN93 injection significantly increased sensitivity to a mechanical stimulus 24h after i.t. injection. Intrathecal inhibition of CaMKII reduced the expression of total CaMKII and its CaMKII alpha isoform activity in diabetic dorsal horn, which was accompanied with an increase in pain-related behavior. Further studies about the intrathecal inhibition of CaMKII should elucidate its role in nociceptive processes of diabetic neuropathy.
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Neuroscience letters · Oct 2013
Interactive effects of cell therapy and rehabilitation realize the full potential of neurogenesis in brain injury model.
The therapeutic effect of rehabilitation after cell therapy for brain injury remains unclear. Here, we report the neural stem/progenitor cells transplantation into a brain injury mouse model followed by treadmill exercise training. Among all experimental groups, mice that underwent transplantation and treadmill exercise demonstrated significant functional motor and electrophysiological improvement. ⋯ Transplanted cells significantly differentiated into neurons in the mice that underwent transplantation and treadmill exercise compared with those treated with only transplantation. Furthermore, the expression of brain-derived neurotrophic factor and growth-associated protein 43 mRNAs were significantly up-regulated in the mice that underwent transplantation and treadmill exercise than in those in other experimental groups during the early recovery stage. These results suggest that rehabilitation after neural stem/progenitor cell transplantation enhances neurogenesis and promotes the recovery of motor function in brain injury model mice.
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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.