Neuroscience letters
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Neuroscience letters · Oct 2016
Suppressed GABAergic signaling in the zona incerta causes neuropathic pain in a thoracic hemisection spinal cord injury rat model.
Suppression of the gamma-aminobutyric acid (GABA)ergic activity of the zona incerta (ZI) reportedly plays a role in neuropathic pain after spinal cord injury (SCI). A reduction in GABAergic signaling in the ZI of a thoracic hemisection-SCI rat model has been suggested, but not clearly demonstrated. Accordingly, our objective was to investigate whether GABAergic signals influence SCI-induced neuropathic pain. ⋯ These data provide evidence that neuropathic pain after SCI is caused by decreased GABAergic signaling in the ZI. Furthermore, our data demonstrate that infusion of a GABAergic drug into the ZI could restore its inhibitory action and improve neuropathic pain behaviors.
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Neuroscience letters · Oct 2016
Post-ischemia mdivi-1 treatment protects against ischemia/reperfusion-induced brain injury in a rat model.
When given prior to brain ischemia, mitochondrial division inhibitor-1 (mdivi-1) attenuates the brain damage caused by ischemia. Here, we investigated the potential effects of post-ischemia mdivi-1 treatment (1mg/kg, i.p., administered immediately after 2h of ischemia and prior to reperfusion) using a MCAO rat model. Mdivi-1 treatment decreased infarct volume and improved neurological function. ⋯ Mdivi-1 treatment augmented the increases in the mRNA expression of peroxisome proliferator-activated receptor coactivator-1α, nuclear respiratory factor-1, and mitochondrial transcriptional factor A. In conclusion, when given after ischemia and prior to reperfusion, mdivi-1 can protect against brain damage by inhibiting the mitochondria-mediated apoptosis induced by mitochondrial fission. Post-ischemia mdivi-1 treatment might promote I/R-induced mitochondrial biogenesis.
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Neuroscience letters · Oct 2016
Differential patterns of regional cerebral hypometabolism according to the level of cerebral amyloid deposition in patients with amnestic mild cognitive impairment.
Although amnestic mild cognitive impairment (aMCI) with high cerebral deposition of amyloid-beta proteins (Aβ) could be classified as a prodromal state of Alzheimer's disease (AD) dementia, aMCI with the absence of or very little cerebral Aβ deposition is likely related to other pathophysiological processes. Thus, the present study aimed to investigate the differential patterns of regional cerebral glucose metabolism (rCMglu) according to the level of Aβ burden in the brains of patients with aMCI. This study included 25 patients with aMCI and 33 cognitively normal (CN) elderly individuals who underwent a comprehensive clinical examination, (11)C-labelled Pittsburgh Compound B (PiB) positron emission tomography (PET) scans, and (18)F-fluorodeoxyglucose (FDG) PET scans. ⋯ Compared with the CN group, rCMglu was decreased in the bilateral medial temporal regions of the aMCI- subgroup and in the medial temporal cortices as well as the right precuneus of the aMCI+ subgroup. Additionally, rCMglu was lower in the right precuneus of the aMCI+ subgroup compared with the aMCI- subgroup. The present findings indicate that, even though both aMCI subgroups were phenomenologically very similar, the patients with aMCI- exhibited a markedly different regional pattern of functional neurodegeneration compared with the aMCI+ patients.
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Neuroscience letters · Oct 2016
Association of DYRK1A polymorphisms with sporadic Parkinson's disease in Chinese Han population.
α-Synuclein plays important roles in the development of Parkinson's disease (PD) pathologies. The dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) has a wide range of phosphorylation targets including α-synuclein. Posphorylated α-synuclein is more neurotoxic to dopamine (DA) neurons, but little is known about the genetic variation of DYRK1A in patients with PD. ⋯ Results revealed TT genotype in SNP rs8126696 denoted a significant difference between PD patients and controls (OR=1.710, 95% CI=1.116-2.619, P=0.014), and the frequency of rs8126696 TT genotype was significantly higher in male PD patients than male controls (OR=2.012, 95%CI: 1.125-3.599, p=0.018). The genotypes in rs2835740 and rs1137600 showed no significant difference between PD patients and controls. These results suggest that TT genotype derived from SNP rs8126696 of DYRK1A gene is a possible risk factor for sporadic PD, especially for males in this Chinese Han population.
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Neuroscience letters · Sep 2016
Inhibition of HCN channel activity in the thalamus attenuates chronic pain in rats.
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate neuronal excitability in both peripheral and central nerve systems. Emerging evidence indicates that HCN channels are involved in the development and maintenance of chronic pain. However, the impact of HCN channel activity in the thalamus on chronic pain has not been examined. ⋯ We show that ZD7288 dose-dependently attenuated mechanical allodynia and thermal hyperalgesia in rats with chronic pain. In the thalamus, immunoreactivity of both HCN1 and HCN2 subunits was increased in both rat models. These results suggest that the increased HCN channel activity in the thalamus of the ascending nociceptive pathway contributes to both chronic neuropathic and inflammatory pain conditions.