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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Age-related hearing loss (presbycusis) is caused mainly by the hypofunction of the inner ear, but recent findings point also toward a central component of presbycusis. We used MR morphometry and diffusion tensor imaging (DTI) with a 3T MR system with the aim to study the state of the central auditory system in a group of elderly subjects (>65years) with mild presbycusis, in a group of elderly subjects with expressed presbycusis and in young controls. Cortical reconstruction, volumetric segmentation and auditory pathway tractography were performed. ⋯ A trend toward a decrease of L1 on the left side, which was more pronounced in the elderly groups, was observed. The effect of hearing loss was present in subjects with expressed presbycusis as a trend toward an increase of the radial vectors (L2L3) in the white matter under Heschl's gyrus. These results suggest that in addition to peripheral changes, changes in the central part of the auditory system in elderly subjects are also present; however, the extent of hearing loss does not play a significant role in the central changes.
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The study describes for the first time the colocalization pattern of calbindin (CB) and cocaine- and amphetamine-regulated transcript (CART) in the mammillary body (MB) and anterior thalamic nuclei (ATN) - structures connected in a topographically organized manner by the mammillothalamic tract (mtt). Immunohistochemical study was performed on fetal (E40, E50, E60), newborn (P0) and postnatal (P20, P80) brains of the guinea pig, but the coexistence pattern of the substances was invariable throughout the examined developmental stages. CB and CART colocalized in the perikarya of the lateral part of the medial mammillary nucleus (MMl), whereas in its medial part (MMm) only CB was detected. ⋯ In the ventral part of AV, CB and CART colocalized vastly in the neuropil. The lateral mammillary nucleus and anterodorsal thalamic nucleus were virtually devoid of CB- and CART-positive structures. Based on the known connections between the MB and ATN, we conclude that the studied substances may cooperate in the MMl-AV part of the axis and CB plays a significant role in the MMm-AM part.
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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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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.