Brain research
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It is unclear whether spinal cord stimulation (SCS) at higher frequencies induces further increases in vasodilation and enhances clinical efficacy. ⋯ SCS at 500 Hz significantly increased SCS-induced vasodilation without influencing MT. Furthermore, effects of SCS at 500 Hz are mediated via activation of TRPV1-containing fibers and a release of CGRP.
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In the present study, the effects of intra-hippocampal CA1 injections of l-arginine, a nitric oxide (NO) precursor and N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on morphine-induced antinociception in rat formalin test were investigated. To induce inflammation pain, formalin (50 microl at 2.5%) was injected into the right hind-paw of male Wistar rats prior to testing. Morphine (3-9 mg/kg) was injected intraperitoneally (i.p.) 10 min before injection of formalin. ⋯ The present study reveals an expression of NADPH-diaphorase in the rat brain samples administered by L-arginine. Expression of NADPH-d is decreased in the samples which were pre-injected with L-NAME. This study suggests NO participation in the rat hippocampal CA1 area in morphine-induced antinociception.
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Neuropathic pain is usually persistent and there is no effective treatment. Activation of P2X(3) receptor subtype in primary sensory neurons is involved in neuropathic pain. Sodium ferulate (SF) is an active principle from Chinese herbal medicine and has anti-inflammatory activities. ⋯ The expression of P2X(3) receptor in DRG neurons was increased after CCI. In CCI rats treated with SF, the up-regulated expression of P2X(3) receptor in DRG neurons was reduced. SF may reduce the thermal and mechanical hyperalgesia in CCI rat model by decreasing the pain transmitted by primary afferant neurons mediated by P2X(3) receptor during the chronic neuropathic pain injury.
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Using a fully implanted cortical electrical stimulation (CES) device with low-frequency burst impulse train, we investigated the effects of CES alone on behavioral recovery and surface density of dendritic structure in a rat model of middle cerebral artery occlusion (MCAO). After MCAO in rats, magnetic resonance imaging (MRI) was used to confirm cortex infarction and to identify a location for implantation of stimulating electrode over the peri-infarct cortex. The device was implanted on the 6th day after MCAO with CES then lasting for 16 days. ⋯ In behavioral tests, the rats in the CES group showed greater functional recovery compared to the NS group. Moreover, the functional improvement coincided with an increase in surface density of dendritic processes immunoreactive to microtubule-associated protein 2 (MAP2) in peri-infarct cortex. These results suggest the feasibility of the fully implanted CES device and the efficacy of the new stimulation protocol alone to improve functional outcome and cortical neuronal structural plasticity following focal cerebral ischemia in rats.
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The role of noradrenergic depletion of the locus coeruleus (LC) in the pathophysiology of Parkinson's disease (PD) is still unclear. In the present study, apomorphine-induced circling behavior and extracellular firing activity of substantia nigra pars reticulata (SNr) neurons were examined in rats with unilateral 6-hydroxydopamine lesions of the LC, substantia nigra pars compacta (SNc) and with combined SNc and LC lesions. A moderate contralateral circling was observed in rats with LC lesions after apomorphine. ⋯ However, the firing rate of SNr neurons in rats with combined LC and SNc lesions increased significantly when compared to that of rats with simple lesions of the SNc, although the firing pattern was not altered. Furthermore, SNc lesions in rats increased the firing rate of SNr neurons with irregular firing pattern, and additional LC lesions in SNc-lesioned rats increased the firing rate of SNr neurons with regular and irregular firing pattern. These results indicate that lesions of the LC intensify apomorphine-induced circling behavior and lead to a further hyperactivity of SNr neurons in a rat model of PD, suggesting that LC-noradrenergic system is involved in the motor dysfunction of PD.