Navegando por Palavras-chave "brainstem"
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- ItemSomente MetadadadosAltered Balance of gamma-Aminobutyric Acidergic and Glutamatergic Afferent Inputs in Rostral Ventrolateral Medulla-Projecting Neurons in the Paraventricular Nucleus of the Hypothalamus of Renovascular Hypertensive Rats(Wiley-Blackwell, 2010-03-01) Biancardi, Vinicia Campana; Campos, Ruy Ribeiro [UNIFESP]; Stern, Javier Eduardo; Med Coll Georgia; Universidade Federal de São Paulo (UNIFESP)An imbalance of excitatory and inhibitory functions has been shown to contribute to numerous pathological disorders. Accumulating evidence supports the idea that a change in hypothalamic gamma-aminobutyric acid (GABA)-ergic inhibitory and glutamatergic excitatory synaptic functions contributes to exacerbated neurohumoral drive in prevalent cardiovascular disorders, including hypertension. However, the precise underlying mechanisms and neuronal substrates are still not fully elucidated in the present study, we combined quantitative immunohistochemistry with neuronal tract tracing to determine whether plastic remodeling of afferent GABAergic and glutamatergic inputs into identified RVLM-projecting neurons of the hypothalamic paraventricular nucleus (PVN-RVLM) contributes to an imbalanced excitatory/inhibitory function in renovascular hypertensive rats (RVH). Our results indicate that both GABAergic and glutamatergic innervation densities increased in oxytocin-positive, PVN-RVLM (OT-PVN-RVLM) neurons in RVH rats. Despite this concomitant increase, time-dependent and compartment-specific differences in the reorganization of these inputs resulted in an altered balance of excitatory/inhibitory inputs in somatic and dendritic compartments. A net predominance of excitatory over inhibitory inputs was found in OT-PVN-RVLM proximal dendrites. Our results indicate that, along with previously described changes in neurotransmitter release probability and postsynaptic receptor function, remodeling of GABAergic and glutamatergic afferent inputs contributes as an underlying mechanism to the altered excitatory/inhibitory balance in the PVN of hypertensive rats. J. Comp. Neurol. 518:567-585, 2010. (C) 2009 Wiley-Liss, Inc
- ItemSomente MetadadadosLeukoencephalopathy With Brainstem and Spinal Cord Involvement and Normal Lactate: A New Mutation in the DARS2 Gene(Sage Publications Inc, 2010-11-01) Lin, Jaime [UNIFESP]; Faria, Eliete Chiconelli; Da Rocha, Antonio Jose; Masruha, Marcelo Rodrigues; Pereira Vilanova, Luiz Celso; Scheper, Gert C.; Van der Knaap, Marjo S.; Universidade Federal de São Paulo (UNIFESP); Fac Ciencias Med Santa Casa São Paulo; Vrije Univ AmsterdamLeukoencephalopathy with brainstem and spinal cord involvement and elevated brain lactate diagnosis is based on its highly characteristic pattern of abnormalities observed by magnetic resonance imaging and spectroscopy. Clinically, affected patients develop slowly progressive cerebellar ataxia, spasticity, and dorsal column dysfunction, sometimes with a mild cognitive deficit or decline. in 2007, the pathophysiology of this disorder was elucidated with the discovery of mutations in the DARS2 gene, which encodes mitochondrial aspartyl-tRNA synthetase, in affected individuals. Here, the authors present a case of leukoencephalopathy with brainstem and spinal cord involvement with normal brain lactate, in which genetic analysis revealed a new mutation in the DARS2 gene not previously described.
- ItemSomente MetadadadosRapid eye movement sleep deprivation-induced down-regulation of beta-adrenergic receptors in the rat brainstem and hippocampus(Elsevier B.V., 2004-09-01) Pedrazzoli, M.; Venditti, Marco Antonio Campana [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Rapid eye movement (REM) sleep deprivation induces a cortical down-regulation of beta-adrenergic receptors. Down-regulation of cortical beta-adrenergic receptors is consistently observed after a number of different chronic antidepressant treatments (drugs and electroconvulsive shock). REM sleep deprivation has an antidepressant effect in humans, and in rats, it decreases immobility in the behavioral despair test, an effect also produced by antidepressant treatments. To verify whether REM sleep deprivation also affects hippocampal beta-adrenergic receptors, we carried out the binding of [H-3]-dihydroalprenolol ([H-3]-DHA) to hippocampal membranes from rats deprived of REM sleep for 96 h. We also determined the binding of [H-3]-DHA to brainstem membranes, a brain region where noradrenergic nuclei are located. Rats were deprived of REM sleep using a water tank with multiple small platforms. [H-3-DHA] saturation conditions (concentrations ranging from 0.15 to 6 nM) were obtained in a crude hippocampus and brainstem membrane preparation. Nonspecific binding was determined using DL-propranolol in hippocampus homogenates. in the brainstem homogenates, nonspecific binding was determined in the presence of DL-propranolol or L-isoproterenol. the results obtained showed statistically significant down-regulation of beta-adrenergic receptors in both the hippocampus and the brainstem after REM sleep deprivation. in the hippocampus, there was also a significant decrease in the dissociation constant (K-D). in the brainstem, a significant decrease in K-D was observed when DL-propranolol was used to determine nonspecific binding. the down-regulation of beta-adrenergic receptors in the hippocampus and brainstem suggests the involvement of these brain areas in the antidepressant effect of REM sleep deprivation. (C) 2004 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosRepeated electroconvulsive shock induces changes in high-affinity [H-3]-ouabain binding to rat striatal membranes(Springer, 2006-04-01) Bignotto, Magda [UNIFESP]; Venditti, Marco Antonio Campana [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)Repeated electroconvulsive shock is an effective treatment for affective disorders. Striatum, hippocampus and brainstem are involved in affective disorders. Sodium-potassium/ATPase is of paramount importance for the proper functioning of the brain and its involvement in the affective disorders has been claimed for a long time. Sodium-potassium/ATPase has an extracellular regulatory binding site to which cardiotonic glycosides, such as ouabain, bind to, thus regulating the activity of the enzyme. Endogenous ouabain-like substances exist in the brain and their actions on the sodium-potassium/ATPase resemble ouabain biological properties. the aim of this work was to determine if electroconvulsive shock (ECS) would induce changes in the high-affinity binding of ouabain to the sodium-potassium/ATPase from rat brain regions. Adult, male Wistar rats received one (ECSx1 group) or seven electroshocks (ECSx7 group) delivered daily through ear-clips electrodes. Control rats received the same manipulations; however, no current was delivered through the electrodes (SHAMx1 and SHAMx7 groups). All groups were sacrificed 24 h after the last ECS session. the B-max and K-D of high-affinity [3H]-ouabain binding were determined in crude membrane preparations from the striatum, hippocampus and brainstem. the results obtained showed a statistically significant increase in the affinity of [H-3]-ouabain (lower K (D)) to striatal membranes in those rats receiving seven ECS. in the striatum there was no change in the K (D) after one ECS; as well as there was no change in the B-max after a single or seven ECS. High-affinity [H-3]-ouabain binding to hippocampus and brainstem did not reveal any significant differences either in K (D) or B-max after one or seven ECS. the increased affinity of ouabain to the striatal sodium-potassium/ATPase induced by repeated ECS suggests an increased interaction in vivo of the endogenous ouabain-like substances with the enzyme and the involvement of the extracellular regulatory allosteric ouabain binding site in the striatal sodium-potassium/ATPase in the effects of electroconvulsive shock.