Neuroreport
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The present study aimed to investigate the effects of changes in motor-evoked potential (MEP) amplitude on short-latency afferent inhibition (SAI) and short-interval intracortical inhibition (SICI). MEPs in response to transcranial magnetic stimulation (TMS) of the left primary motor cortex were measured from the right first dorsal interosseous muscle of 10 healthy participants. SAI was evaluated by measuring MEPs in response to variable-intensity test TMS pulses delivered 22 ms following electrical stimulation of the right ulnar nerve (intensity fixed at the motor threshold). ⋯ Significant positive correlations were detected between the unconditioned and conditioned MEP amplitudes at both SAI and SICI. This study demonstrated that SAI and SICI are highly sensitive to the MEP amplitude and SAI decreases with increasing MEP amplitude, whereas SICI does not change. The different responses for SAI and SICI to the increasing MEP amplitude is interpreted as evidence that different inhibitory neural circuits may be involved in SAI and SICI.
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Absence seizures are known to originate from disruptions within the corticothalamocortical network; however, the precise underlying cellular and molecular mechanisms that induce hypersynchronicity and hyperexcitability are debated and likely to be complex and multifactorial. Recent studies implicate impaired thalamic GABAergic inhibition as a common feature in multiple animal models of absence epilepsy, including the well-established stargazer mouse model. Recently, we demonstrated region-specific increases in the whole tissue and synaptic levels of GABAA receptor (GABAAR) subunits α1 and β2, within the ventral posterior region of the thalamus in adult epileptic stargazer mice compared with nonepileptic control littermates. ⋯ Semiquantitative western blotting was used to analyze the relative tissue level expression of GABAAR α1 and β2 subunits in the thalamus of juvenile stargazer mice compared with their nonepileptic control littermates at three different time points before the initiation of seizures. We show that there is a statistically significant increase in the expression of α1 and β2 subunits in the thalamus of stargazer mice, at the PN7-9 stage, compared with the control littermates, but not at PN10-12 and PN13-15 stages. These results suggest that an aberrant expression of GABAAR subunits α1 and β2 in the stargazers does not occur immediately before seizure onset and therefore is unlikely to directly contribute to the initiation of absence seizures.
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Anesthesia neurotoxicity in developing brain has gained increasing attention. However, knowledge regarding its mitigating strategies remains scant. Sevoflurane, a commonly used anesthetic, is responsible for learning and memory deficits in neonates. ⋯ The data showed that the spatial recognition memory and fear memory of the rats treated with sevoflurane decreased compared with the control, and the cognitive function of the rats treated with sevoflurane and hydrogen gas significantly increased in comparison with treatment with sevoflurane alone. Moreover, hydrogen gas suppressed NF-κB phosphorylation and nuclear translocation and reduced the production of interleukin-1β, interleukin-6, and tumor necrosis factor-α following sevoflurane administration. Thus, the results proposed that hydrogen gas might protect against sevoflurane neurotoxicity by inhibiting NF-κB activation and proinflammatory cytokine release, providing a novel therapeutic strategy for anesthesia neurotoxicity.