Neuroreport
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Bile duct ligation (BDL) in young rats can cause impaired liver function and cognition deficits. Nitric oxide is implicated in hepatic encephalopathy and is also involved in cognition. In this study, we examined the role of brain asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, in young BDL rats with spatial deficits. ⋯ In addition, melatonin maintained brain-derived neurotrophic factor in the dorsal hippocampus at a level comparable with controls. We concluded that melatonin is effective in preventing spatial deficits and decreasing ADMA levels in the plasma, prefrontal cortex, and dorsal hippocampus in young BDL rats. Brain ADMA levels might play a role in BDL-induced spatial deficits.
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There are still some controversies that attentional bias to negative emotions in individuals with high-trait anxiety (HTA), as compare with those with low-trait anxiety (LTA), occurs in the engagement or disengagement facet of attentional selectivity and whether this attentional bias is affected by negative emotional types. In this study, we explored the different attentional selectivity mechanisms for threatening emotions of anger and disgust between individuals with HTA and LTA using the variant attentional-probe paradigm. The results showed that under the engagement condition, the HTA group's attentional bias index of the anger mood was negative and was significantly less than the disgusting mood (positive) and that the P1 was smaller with angry faces as compared with neutral faces, which was separate from the results of the disgusted faces, having a significant difference with neutral faces on P1 component. ⋯ The results suggested that there were different mechanisms of selective attentional bias for threatening emotions of anger and disgust in individuals with HTA. HTA individuals were characterized by facilitated attentional engagement with angry faces and impaired attentional engagement with disgusted faces. LTA individuals had different neural underpinnings and had impaired attentional disengagement with disgusted faces.
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Laboratory studies suggested that general anesthetics induce neuroapoptosis and inhibit neurogenesis in developing brains of animals. Minocycline exerts neuroprotection against a wide range of toxic insults in neurodegenerative diseases models. Here, we investigate whether minocycline can alleviate neurogenetic damage and improve cognition following midazolam exposure in neonatal rats. ⋯ Compared with the control, midazolam reduced cell proliferation both in the SVZ and in the SGZ of the hippocampus of neonatal rats, and decreased spatial learning and memory ability of rats in adulthood significantly. Pretreatment with minocycline increased cell proliferation both in the SVZ and in the SGZ of the hippocampus and improved spatial learning and memory ability compared with midazolam, but it did not mitigate the changes to the normal levels compared with the controls. Our results indicated that pretreatment with minocycline can alleviate midazolam-induced damage in neural stem cell proliferation of neonatal rats and improve spatial learning and memory ability of rats in adulthood.
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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.