Neuroscience
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Voltage-gated Ca2+ channels (VGCCs) play key roles in auditory perception and information processing within the inner ear and brainstem. Pharmacological inhibition of low voltage-activated (LVA) T-type Ca2+ channels is related to both age- and noise induced hearing loss in experimental animals and may represent a promising approach to the treatment of auditory impairment of various etiologies. Within the LVA Ca2+ channel subgroup, Cav3.2 is the most prominently expressed T-type channel entity in the cochlea and auditory brainstem. ⋯ Our results, based on a self-programmed automated wavelet approach, demonstrate that both heterozygous and Cav3.2 null mutant mice exhibit age-dependent increases in hearing thresholds at 5 months of age. In addition, complex alterations in WI-IV amplitudes and latencies were detected that were not attributable to alterations in the expression of other VGCCs in the auditory tract. Our results clearly demonstrate the important physiological role of Cav3.2 VGCCs in the spatiotemporal organization of auditory processing in young adult mice and suggest potential pharmacological targets for interventions in the future.
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The ability to track multiple objects is important for daily life activities such as driving, but it is subject to some restrictions. One limitation concerns the hemifields in which objects move. A previous study showed that when subjects were restricted to the use of one hemifield, both the maximum number of tracked objects and the tracking accuracy were lower than when they were permitted to use both hemifields. ⋯ In the SSVEP experiment, SSVEP amplitudes for target and distractor frequencies differed under the Within condition but did not differ under the Crossover condition. However, phase synchronization between the left and right hemifields exhibited the opposite trend. This study provides evidence that attention to objects moving between hemifields is suppressed relative to attention to objects moving within hemifields and that Crossover tracking diminishes attentional modulation at an early sensory processing level while modulating interhemispheric functional connectivity.
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Glucose metabolism and serotonergic neurotransmission have been reported to play an important role in epileptogenesis. We therefore aimed to use neuroimaging to evaluate potential alterations in serotonin 5-HT1A receptor and glucose metabolism during epileptogenesis in the rat electrical kindling model. To achieve this goal, we performed positron emission tomography (PET) imaging in a rat epileptogenesis model triggered by electrical stimulation of the hippocampus using 2-deoxy-2-[18F]fluoro-D-glucose (18F-FDG), a radiolabeled analog of glucose, and 2'-methoxyphenyl-(N-2'-pyridinyl)-p-18F-fluoro-benzamidoethylpiperazine (18F-MPPF), a radiolabeled 5-HT1A receptor ligand, to evaluate brain metabolism and 5-HT1A receptor functionality. ⋯ Importantly, astroglial activation was detected in the hippocampus of kindled rats. Overall, electrical kindling induced hypometabolism, astrogliosis and serotonergic alterations in epilepsy-related regions. Furthermore, the present findings point to 5-HT1A receptor as a valuable epileptogenesis biomarker candidate and a potential therapeutic target.
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Before movement onset, during the reaction time, excitability of M1 is selectively modulated by somatosensory inputs, only in the movement-related muscle. If a similar mechanism operates before the onset of mental movements, then somatosensory afferent inputs are exploited during cognitive representation of movement. We assessed sensorimotor modulation through short latency afferent inhibition (SAI) paradigm before the onset of executed and imagined movements. ⋯ There was a positive correlation between the individual degree of sensorimotor modulation during executed and mental movements and between the sensorimotor modulation during mental movements and motor imagery ability. Sensorimotor modulation operates during the cognitive representation of movement with selective disinhibition of the cortical representation of the muscle involved in the task. Sensorimotor modulation mechanisms prior to mental and executed movements likely share overlapping circuits.
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ALG13 (asparagine-linked glycosylation 13 homolog) encodes a crucial protein involved in the process of N-linked glycosylation, and abnormal N-linked glycosylation is considered an important risk factor that leads to neurological deficits and disorders. However, the causal relationship between ALG13 and epilepsy remains unknown. This study applied a kainic acid (KA)-induced epileptic mouse model to determine whether ALG13 deficiency resulted in increased susceptibility to and severity of epileptic seizures. ⋯ Furthermore, KA-induced epilepsy-related pathological changes of the brain were predominantly exacerbated in Alg13 KO mice. This study also preliminarily explored the possible mechanisms of ALG13-involved epilepsy by showing hyperactive mTOR signaling pathways in the cortex and hippocampus of Alg13 KO mice. To the best of our knowledge, this report is the first evidence of the association between ALG13 and epilepsy in experimental animals.