Neuroscience
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Randomized Controlled Trial
The neural substrate of the ideomotor principle revisited: evidence for asymmetries in action-effect learning.
Ideomotor theory holds that the perception or anticipatory imagination of action effects activates motor tendencies toward the action that is known to produce these effects, herein referred to as ideomotor response activation (IRA). IRA presupposes that the agent has previously learned which action produces which effects, and that this learning process has created bidirectional associations between the sensory effect codes and the motor codes producing the sensory effects. Here, we refer to this process as ideomotor learning. ⋯ We replicated earlier findings of a hand asymmetry in ideomotor processing with significantly stronger IRA by left-hand than right-hand action effects. Crucially, we traced this effect back to more pronounced associative learning for action-contingent effects of the left hand compared with effects of the right hand. In this context, our findings point to the caudate nucleus and the angular gyrus as central structures of the neural network underlying ideomotor learning.
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Diffusion tensor imaging (DTI) provides information regarding white matter microstructure; however, macroscopic fiber architectures can affect DTI measures. A larger brain (fiber tract) has a 'relatively' smaller voxel size, and the voxels are less likely to contain more than one fiber orientation and more likely to have higher fractional anisotropy (FA). Previous DTI studies report left-to-right differences in the white matter; however, these may reflect true microscopic differences or be caused purely by volume differences. ⋯ Voxel-wise analysis with adjustment for volume asymmetry revealed many white matter FA asymmetries, including leftward asymmetry of the arcuate fasciculus and cingulum. The voxel-wise analysis showed a reduced number of regions with significant FA asymmetry compared with analysis performed without adjustment for volume asymmetry; however, the overall trend of the results was unchanged. The results of the present study suggest that these FA asymmetries are not caused by volume differences and reflect microscopic differences in the white matter.
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Better treatment of status epilepticus (SE), which typically becomes refractory after about 30 min, will require new pharmacotherapies. The effect of sec-butyl-propylacetamide (SPD), an amide derivative of valproic acid (VPA), on electrographic status epilepticus (ESE) was compared quantitatively to other standard-of-care compounds. Cortical electroencephalograms (EEGs) were recorded from rats during ESE induced with lithium-pilocarpine. ⋯ SPD has a faster onset and greater efficacy than DZP and VPA, and is similar to propofol and pentobarbital. SPD and structurally similar compounds may be useful for the treatment of refractory ESE. Further development and use of automated analyses of ESE may facilitate drug discovery for refractory SE.
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The elderly have comparatively worse cognitive impairments from traumatic brain injury (TBI) relative to younger adults, but the molecular mechanisms that underlie this exacerbation of cognitive deficits are unknown. Experimental models of TBI have demonstrated that the cyclic AMP-protein kinase A (cAMP-PKA) signaling pathway is downregulated after brain trauma. Since the cAMP-PKA signaling pathway is a key mediator of long-term memory formation, we investigated whether the TBI-induced decrease in cAMP levels is exacerbated in aged animals. ⋯ Rolipram rescued the LTP deficits after mild TBI for young adult animals and caused a partial recovery for aged animals. However, rolipram did not rescue LTP deficits after moderate TBI in either young adult or aged animals. These results indicate that the exacerbation of cognitive impairments in aged animals with TBI may be due to decreased cAMP levels and deficits in hippocampal LTP.
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Loss of function mutations in THAP1 has been associated with primary generalized and focal dystonia in children and adults. THAP1 encodes a transcription factor (THAP1) that harbors an atypical zinc finger domain and plays a critical role in G(1)-S cell cycle control. Current thinking suggests that dystonia may be a neurodevelopmental circuit disorder. ⋯ In contrast, it was more diffusely distributed throughout the dendritic arbor of adult Purkinje cells producing a moderate diffuse staining pattern in the molecular layer. At all time points, nuclear IR was weaker than cytoplasmic IR. The prominent cytoplasmic and developmentally regulated expression of THAP1 suggests that THAP1 may function as part of a cell surface-nucleus signaling cascade involved in terminal neural differentiation.