Neuroscience
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Menopausal women often suffer from hot flashes and sleep disturbances that significantly impact their quality of life. Both human and animal studies suggest that loss of estrogens during menopause contribute to these symptoms. In the female rat, both core body temperature (CBT) and sleep are sensitive to 17β-estradiol (E2) levels, but important differences between the rat and the human patterns limit the interpretation of the results. ⋯ In addition, fewer nighttime arousals were observed under low E2 replacement compared to baseline. Higher delta power was observed under both E2 replacement conditions suggesting enhanced sleep quality. These preliminary results suggest that E2 modulates sleep and thermoregulation in the OVX marmoset, making it a promising model for studying menopausal symptoms.
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The ability to adjust movement timing is essential in daily life. Explorations of the underlying neural mechanisms have reported a gradual increase or decrease in neuronal activity prior to self-timed movements within the cortico-basal ganglia loop. Previous studies in both humans and animals have shown that endogenous dopamine (DA) plays a modulatory role in self-timing. ⋯ Infusion of a small amount of a D1 or D2 antagonist led to early saccades in the self-timed, but not the triggered MS tasks, while infusion of DA agonists produced no consistent effect. We also found that local administration of nicotinic but not muscarinic acetylcholine receptor agonists and antagonists altered the timing of self-initiated saccades. Our data suggest that the timing of self-initiated movements may be regulated by the balance of signals in the direct and indirect basal ganglia pathways, as well as that between both hemispheres of the brain.
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Pur-alpha is a highly conserved sequence-specific DNA and RNA binding protein with established roles in DNA replication, RNA translation, cell cycle regulation, and maintenance of neuronal differentiation. Prior studies have shown that mice lacking Pur-alpha (-/-) display decreased neurogenesis and impaired neuronal differentiation. We sought to examine for the first time, the behavioral phenotype and brain histopathology of mice that are heterozygous (+/-) for Pur-alpha. ⋯ Quantitative immunohistochemical assays of the vermal region of the cerebellum and CA1-3 regions of the hippocampus revealed reduced numbers of neurons in general, as well as reduced numbers of Pur-alpha+-immunopositive neurons and dendrites in heterozygous Pur-alpha mice, compared to wild-type littermates. Past studies have implicated mutations in Pur-alpha in several diseases of brain development and neurodegeneration. When combined with these new findings, the Pur-alpha heterozygous knockout mice may provide an animal model to study mechanisms of and treatments for Pur-alpha-related cognitive deficiencies and neuropathology.
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Motor learning with professional experience leads to cortical reorganization with plasticity. Long-term training facilitates motor cortical excitability. It is not clear how beneficial cortical plasticity is maintained during long-term training. ⋯ In addition, both SICI and LICI were correlated with the slope of MEP input-output curve in athletes but not in novices. The slope of MEP input-output curve, SICI and LICI were also correlated with the training time in athletes. We conclude that both cortical excitation and cortical inhibition are increased, and that the balance between cortical excitation and inhibition is maintained during long-term training.
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Animals use multiple strategies to maintain spatial orientation. Dead reckoning is a form of spatial navigation that depends on self-movement cue processing. During dead reckoning, the generation of self-movement cues from a starting position to an animal's current position allow for the estimation of direction and distance to the position movement originated. ⋯ Disruptions in exploratory behavior associated with medial frontal lesions were consistent with impaired motor coordination, response inhibition, or egocentric reference frame. These processes are necessary for spatial orientation; however, they are not sufficient for self-movement cue processing. Therefore it is possible that the medial frontal cortex provides processing resources that support dead reckoning in other brain structures but does not of itself compute the kinematic details of dead reckoning.