Neuroscience
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Studies involving therapeutic combinations reveal an important benefit in the rehabilitation of neglect patients when compared to single therapies. In light of these observations our present work examines, in healthy individuals, sensorimotor and cognitive after-effects of prism adaptation and neck muscle vibration applied individually or simultaneously. We explored sensorimotor after-effects on visuo-manual open-loop pointing, visual and proprioceptive straight-ahead estimations. ⋯ This is the first demonstration of cognitive after-effects following neck muscle vibration in healthy individuals. The simultaneous application of both methods did not produce significant greater after-effects than prism adaptation alone in both sensorimotor and cognitive tasks. These results are discussed in terms of transfer of sensorimotor plasticity to spatial cognition in healthy individuals.
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Astrocytes are plastic cells that play key roles in brain physiology and pathology, including via their glutamate transporters, excitatory amino acid transporter (EAAT)1 and EAAT2, maintaining low extracellular glutamate concentrations and protecting against excitotoxic neuronal injury. Alterations in cell surface expression of EAATs and astrocytic cytoskeleton are important for regulating transporter activity. This study employed the actions of rottlerin, to interrogate the regulation of EAAT activity, expression and localization, and interfaces with Na(+)/K(+)-ATPase and astrocytic morphology. ⋯ Removal of rottlerin rapidly elevated Na(+)/K(+)-ATPase activity beyond control levels, while co-treatment with monensin failed to stimulate the Na(+)/K(+)-ATPase. These data reveal inhibition of EAAT activity by rottlerin is not associated with loss of EAATs at the cell surface, but rather linked to cytoskeletal rearrangement, and inhibition of the Na(+)/K(+)-ATPase. Rapid recovery of Na(+)/K(+)-ATPase activity, and subsequent restoration of glutamate uptake indicates that astrocytic morphology and EAAT activity are co-regulated by a tightly coupled, homeostatic relationship between l-glutamate uptake, the electrochemical gradient and the activity of the Na(+)/K(+)-ATPase.
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Lateral lemniscus, a relay nucleus of auditory sensation, is involved in the control of phonatory movements such as human speech and vocalization of animals. The present study was designed to test whether neurons in the lateral lemniscus contributed to the control of swallowing, one of non-phonic oro-pharyngolaryngeal movements. In acutely decerebrated cats (n=15), swallowing was induced by electrical stimulation (20-80μA at 10Hz for 20s with rectangular pulses of 0.2ms duration) delivered to the superior laryngeal nerve (SLN). ⋯ An injection of baclofen did not alter the swallowing. These results suggest the presence of functional topography in the lateral lemniscus and the paralemniscal area in relation to the control of swallowing. The facilitatory LLD-effects on swallowing are modulated by glutamatergic and GABAergic receptors on neurons in the LLD.
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The Kv7/M current is one of the major mechanisms controlling neuronal excitability, which can be modulated by activation of the G protein-coupled receptor (GPCR) via distinct signaling pathways. Membrane microdomains known as lipid rafts have been implicated in the specificity of various cell signaling pathways. The aim of this study was to understand the role of lipid rafts in the specificity of Kv7/M current modulation by activation of GPCR. ⋯ The increase of B2R-induced intracellular Ca(2+) was also greatly reduced after MβCD treatment. Finally, B2R but not M1R was found to interact with the IP3 receptor. In conclusion, the present study implicates an important role for lipid rafts in mediating specificity for GPCR-mediated inhibition of the Kv7/M current.
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In the present study, we investigated the effects of lesions of A2 neurons of the commissural nucleus of the solitary tract (cNTS) alone or combined with the blockade of angiotensinergic mechanisms on the recovery of arterial pressure (AP) to hemorrhage in conscious rats. Male Holtzman rats (280-320g) received an injection of anti-dopamine-beta-hydroxylase-saporin (12.6ng/60nl; cNTS/A2-lesion, n=28) or immunoglobulin G (IgG)-saporin (12.6ng/60nl, sham, n=24) into the cNTS and 15-21days later had a stainless steel cannula implanted in the lateral ventricle. After 6days, rats were submitted to hemorrhage (four blood withdrawals, 2ml/300g of body weight every 10min). ⋯ Losartan (angiotensin type 1 receptor antagonist) injected intracerebroventricularly (100μg/1μl) or intravenously (i.v.) (10mg/kg of body weight) impaired the recovery of AP in cNTS/A2-lesioned rats (-24±6 and -35±7mmHg at 30min, respectively). In sham rats, only i.v. losartan affected the recovery of AP (-39±6mmHg at 60min). The results suggest that lesion of the A2 neurons in the cNTS facilitates the activation of the angiotensinergic pressor mechanisms in response to hemorrhage.