Neuroscience
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The K(+)-dependent Na(+)/Ca(2)-exchanger (NCKX) family is encoded by five related genes, of which NCKX2 (solute carrier family 24, member 2) is the most abundant member present in the brain. Nckx2 knockout mice display profound loss of hippocampal long-term potentiation, and selective deficits in motor learning and spatial working memory. However, the molecular mechanisms underlying these changes have not been established. ⋯ In the molecular layer, a greater fraction of NCKX2 is associated with axon terminals and, in addition, a fraction of NCKX2 is found not associated with the plasma membrane but located in the cytoplasm. These studies describe for the first time the exact location of NCKX2 in the hippocampus of adult mice and suggest that the function of NCKX2 in neuronal plasticity in hippocampal CA1 neurons may be mediated by its kinetic effect on the local Ca(2+) concentration that influences dendritic integration. At other hippocampal locations NCKX2 has a somewhat different spatial distribution, consistent with published reports of NCKX2 expression in other brain regions, suggesting that NCKX2 contributes to Ca(2+) homeostasis in distinct ways in different brain neurons.
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Arm movement control takes advantage of multiple inputs, including those originating from the contralateral arm. In the mirror paradigm, it has been suggested that control of the unseen arm, hidden by the mirror, is facilitated by the reflection of the other, moving arm. Although proprioceptive feedback originating from the moving arm, (the image of which is reflected in the mirror), is always coupled with visual feedback in the mirror paradigm, the former has received little attention. ⋯ Next (in Experiment 2), we masked proprioceptive afferents of the passively moved arm and specifically evaluated mirror feedback. We found that interlimb coupling through mirror feedback (though significant) was weaker than interlimb coupling through proprioceptive feedback. Overall, the present results show that in the mirror paradigm, proprioceptive feedback is stronger and more consistent than visual-mirror feedback in terms of the impact on interlimb coupling.
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Previous contributions in younger cohorts have revealed that reallocation of cerebral resources, a crucial mechanism for working memory (WM), may be disrupted by parallel demands of background acoustic noise suppression. To date, no study has explored the impact of such disruption on brain activation in elderly individuals with or without subtle cognitive deficits. We performed a functional Magnetic Resonance Imaging (fMRI) study in 23 cases (mean age=75.7y.o., 16 men) with mild cognitive impairment (MCI) and 16 elderly healthy controls (HC, mean age=70.1y.o., three men) using a 2-back WM task, under two distinct MRI background acoustic noise conditions (louder vs. lower noise echo-planar imaging). ⋯ Our results suggest that background acoustic noise has a differential impact on WMN activation in normal aging as a function of the cognitive status. Only louder noise has a disruptive effect on the usually observed DMN deactivation during WM task performance in HC. In contrast, MCI cases show altered DMN reactivity even in the presence of lower noise.
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High-intensity sound can induce seizures in susceptible animals. After repeated acoustic stimuli changes in behavioural seizure repertoire and epileptic EEG activity might be seen in recruited limbic and forebrain structures, a phenomenon known as audiogenic kindling. It is postulated that audiogenic kindling can produce synaptic plasticity events leading to the spread of epileptogenic activity to the limbic system. ⋯ These findings show that repeated high-intensity sound stimulation prevent LTP of Schaffer-CA1 synapses from Wistar rats, without affecting spatial memory. This effect was not seen in hippocampi from audiogenic seizure-prone WARs. In WARs the link between auditory stimulation and hippocampal LTP seems to be disrupted which could be relevant for the susceptibility to seizures in this strain.
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Transcranial magnetic stimulation (TMS) can be applied to modulate cortical phenomena. The modulation effect is dependent on the applied stimulation frequency. Repetition suppression (RS) has been demonstrated in the motor system using TMS with short suprathreshold 1-Hz stimulation trains repeated at long inter-train intervals. ⋯ The effects of the two stimulation intensities exhibited a similar trend; however, the SPT30 evoked a more profound inhibitory effect compared to that achieved by rMT. Moreover, the resting MEP amplitudes and SP durations correlated (rho⩽-0.674, p<0.001) and the pre-TMS EMG level did not differ between stimuli in resting MEPs (F=0.0, p⩾0.999). These results imply that the attenuation of response size seen in resting MEPs might originate from increasing activity of inhibitory GABAergic interneurons which relay the characteristics of SPs.