Neuroscience
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White matter lesions due to cerebral hypoperfusion may be an important pathophysiology in vascular dementia and stroke, although the inherent mechanisms remain to be fully elucidated. The present study, using a mouse model of chronic cerebral hypoperfusion, examined the white matter protective effects of levetiracetam, an anticonvulsant, via the signaling cascade from the activation of cAMP-responsive element binding protein (CREB) phosphorylation. Mice underwent bilateral common carotid artery stenosis (BCAS), and were separated into the levetiracetam group (injected once only after BCAS [LEV1] or injected on three consecutive days [LEV3]), the vehicle group, or the anti-epileptic drugs with different action mechanisms phenytoin group (PHT3; injected on three consecutive days with the same condition as in LEV3). ⋯ The activation of microglia and astrocytes was markedly suppressed, although the number of oligodendrocyte precursor cells (OPCs) and GST-pi-positive-oligodendrocytes was markedly higher in the cerebral white matter. Moreover, oxidative stress was significantly reduced. We found that 3-day treatment with levetiracetam maintained SV2A protein expression via interaction with astrocytes, which influenced the OPC lineage through activation of CREB to protect white matter from ischemia.
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The incidental acquisition of a succession of tasks is termed implicit task sequence learning. Patients with dorsolateral prefrontal cortex (DLPFC) lesions are strongly impaired in this ability. However, recent results of conventional transcranial direct current stimulation (tDCS) above the prefrontal cortex showed no modulation of implicit task sequence learning and consolidation. ⋯ Furthermore, consolidation was robust. However, both sequence learning and consolidation were not modulated by stimulation. Thus, this study corroborates previous findings by showing that even focal HD-tDCS is not sufficient to modulate implicit task sequence learning and consolidation.
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Neonatal treatment with monosodium glutamate causes profound deficits in place learning and memory in adult rats evaluated in the Morris maze. Theta activity has been related to hippocampal learning, and increased high-frequency theta activity occurs through efficient place learning training in the Morris maze. We wondered whether the place learning deficits observed in adult rats that had been neonatally treated with monosodium glutamate (MSG), were related to altered theta patterns in the hippocampus and prelimbic cortex, which were recorded during place learning training in the Morris maze. ⋯ Learning-related changes were observed in the relative power distribution in control and MSG-treated groups in the hippocampal EEG, but not in the prelimbic cortex. Increased prefrontal and reduced hippocampal absolute power that appeared principally during the final days of training, and reduced coherence between regions throughout the training (4-12 Hz), were observed in the MSG-treated rats, thereby suggesting a misfunction of the circuits rather than a hyperexcitable general state. In conclusion, neonatal administration of MSG, which caused a profound deficit in place learning at the adult age, also altered the theta pattern both in the hippocampus and prelimbic cortex.
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The topographic map of motor cortical representation, called the motor map, is not invariant, but can be altered by motor learning, neurological injury, and functional recovery from injury. Although much attention has been paid to short-term changes of the motor map, robust measures have not been established. The existing mapping methods are time-consuming, and the obtained maps are confounded by time preference. ⋯ Although the motor threshold of the hotspot was not changed, the area in which it was decreased appeared caudally to the hotspot, which may be in the somatosensory cortex. The present study demonstrated rapid enlargement of the forelimb motor map in the order of a few minutes induced by skin stimulation. This helps to understand the spatial dynamism of motor cortical representation that is modulated rapidly by somatosensory input.