Neuroscience
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The dystonias are a group of disorders defined by sustained or intermittent muscle contractions that result in involuntary posturing or repetitive movements. There are many different clinical manifestations and causes. ⋯ The new network model for the pathogenesis of dystonia has raised many questions, particularly regarding the role of the cerebellum. For example, if dystonia may arise from cerebellar dysfunction, then why are there no cerebellar signs in dystonia? Why are focal cerebellar lesions or degenerative cerebellar disorders more commonly associated with ataxia rather than dystonia? Why is dystonia more commonly associated with basal ganglia lesions rather than cerebellar lesions? Can answers obtained from animals be extrapolated to humans? Is there any evidence that the cerebellum is not involved? Finally, what is the practical value of this new model of pathogenesis for the neuroscientist and clinician? This article explores potential answers to these questions.
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Enkephalin (ENK) has been postulated to play important roles in modulating nociceptive transmission, and it has been proved that ENKergic neurons acted as a critical component of sensory circuit in the adult spinal cord. Revealing the developmental characteristics of spinal ENKergic neurons will be helpful for understanding the formation and alteration of the sensory circuit under pain status. However, the relationship between the embryonic birth date and the adult distribution of ENKergic neurons has remained largely unknown due to the difficulties in visualizing the ENKergic neurons clearly. ⋯ Further comparative analysis revealed that spinal ENKergic neurons underwent heterogeneous characteristics. Our study also indicated that the laminar arrangement of ENKergic neurons in the superficial spinal dorsal horn depended on the neurogenesis stages. Taken together, the present study suggested that the birth date of ENKergic neurons is one determinant for their arrangement and function.
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We aimed to determine the effect of distinctly different cognitive tasks and walking speed on cognitive-motor interference of dual-task walking. ⋯ Results show that the motor and cognitive cost of dual-task walking depends heavily on the type and perceived complexity of the cognitive task being performed. Cognitive cost for the STR task was low irrespective of walking speed, suggesting that at preferred-speed individuals prioritize complex cognitive tasks requiring higher attentional and processing resources over walking. While performing VMRT task, individuals preferred to prioritize more complex walking task over VMRT task resulting in lesser motor cost and increased cognitive cost for VMRT task. Furthermore, slow walking can assist in diverting greater attention towards complex cognitive tasks, improving its performance while walking.
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α-Tocopherol (vitamin E) is an essential dietary antioxidant with important neuroprotective functions. α-Tocopherol deficiency manifests primarily in neurological pathologies, notably cerebellar dysfunctions such as spinocerebellar ataxia. To study the roles of α-tocopherol in the cerebellum, we used the α-tocopherol transfer protein for the murine version (Ttpa(-/)(-)) mice which lack the α-tocopherol transfer protein (TTP) and are a faithful model of vitamin E deficiency and oxidative stress. When fed vitamin E-deficient diet, Ttpa(-/)(-) mice had un-detectable levels of α-tocopherol in plasma and several brain regions. ⋯ Concomitantly, vitamin E deficiency precipitated cellular atrophy and diminished dendritic branching of Purkinje neurons, the predominant output regulator of the cerebellar cortex. The anatomic decline induced by vitamin E deficiency was paralleled by behavioral deficits in motor coordination and cognitive functions that were normalized upon vitamin E supplementation. These observations underscore the essential role of vitamin E and TTP in maintaining CNS function, and support the notion that α-tocopherol supplementation may comprise an effective intervention in oxidative stress-related neurological disorders.
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Extinction is a well-known and important behavioral phenomenon that allows an organism to adapt its behavior to its environment. Previous studies have shown that the expression of extinction is highly context dependent, meanwhile, conditioning context, as part of fear memory, might have influence on extinction formation. To this end, we have conducted four different extinction paradigms in this study: extinction conducted in the conditioning context but tested in another, novel context (AAB); conditioning in one context and extinction and testing in the second (ABB); conditioning in context A, extinction training in context B, but test back to context A (ABA); and extinction training in a third context, context C (ACB). ⋯ Our results showed that rats under the AAB, but not the ACB or ABA condition, showed a similar level of freezing compared with the typical ABB extinction paradigm. Moreover, muscimol infused into CA1 before extinction training resulted in impaired extinction and down-regulation of NR2B activity and phosphorylated GluR1 (at Ser845) in CA1, and the expression levels of NR2B and GluR1 were decreased significantly in the basolateral amygdala (BLA). Thus, CA1 may play an important role in the context-specific expression of fear extinction, and Ser845 may be a phosphorylation site in GluR1 in CA1, triggering the context-specific response of extinction memory.