Neuroscience
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Review
New Perspectives for the Modulation of Mind-Wandering Using Transcranial Electric Brain Stimulation.
When our attention is decoupled from an ongoing task and becomes coupled to thoughts and feelings not being subject to task engagement, we are mind-wandering. This transient and pervasive mental process can occupy a considerable amount of our waking hours. Mind-wandering is understood to exert both positive and negative effects on well-being, and has been shown to play a role in mood disorders and depression. ⋯ For instance, tDCS effects on deliberate versus undeliberate mind-wandering should be disentangled. The hippocampus as an important hub for mind-wandering-related processes may be targeted. Most importantly, research efforts related to mind-wandering and rumination should be integrated.
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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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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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We established hypoglycemic rat models and divided them into three groups (the sham group, the acute hypoglycemia group and the recovery group). The brain water diffusion was examined using DWI. Thereafter, neuropathologic examinations were performed in order to evaluate the distribution of brain damage. ⋯ Our work revealed that hypoglycemia significantly influenced the water diffusion of the brain. The decrease of AQP4 was associated with the formation of cytotoxic edema in acute hypoglycemia. Hypoglycemia primarily tends to damage the cerebral cortex, hippocampus and hypothalamus and may result in permanent injury to the brain.
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Estrogen receptor-alpha (ERα) and -beta (ERβ) occur in key elements of the brain gluco-homeostatic network in both sexes, including the hindbrain dorsal vagal complex (DVC), but the influence of distinct receptor populations on this critical function is unclear. The ventromedial hypothalamic nucleus (VMN) maintains glucose balance by integrating nutrient, endocrine, and neurochemical cues, including metabolic sensory information supplied by DVC A2 noradrenergic neurons. Current research utilized the selective ERα and ERβ antagonists MPP and PHTPP to characterize effects of DVC ERs on VMN norepinephrine (NE) activity and metabolic neurotransmitter signaling in insulin-induced hypoglycemic (IIH) male rats. ⋯ Both ERs regulate corticosterone, but not glucagon secretion during IIH and oppose hypoglycemic diminution of circulating free fatty acids. These findings identify distinguishing versus common VMN functions targeted by DVC ERα and -β. Sex differences in hypoglycemic VMN NE accumulation, glycogen metabolism, and transmitter signaling may involve, in part, discrepant regulatory involvement or differential magnitude of impact of these hindbrain ERs.