Fabián Bernal

Learn More
This study investigated the time course of the striatal lesions produced by continuous local injection of the glutamate uptake inhibitor, L-trans-pyrrolidine-2,4-dicarboxylate (PDC) at the rate of 25 nmol/h in rats. The extent of the neurodegeneration area (defined as the lesion area) did not significantly vary with the duration of the PDC treatment between(More)
Activation of excitatory amino acid (EAA) receptors can induce neurodegeneration by two major mechanisms of excitotoxicity, one related to the influx of Na(+), Cl(-) and water, and the other to the increase in intracellular calcium concentration ([Ca(2+)](i)). Thus, acute microinjection of EAAs in several areas of the central nervous system (CNS) has been(More)
Synaptic increase of glutamate level, when not coupled to a heightened energy production, renders neurons susceptible to death. Astrocyte uptake and recycling of synaptic glutamate as glutamine is a major metabolic pathway dependent on energy metabolism, which inter-relationships are not fully understood and remain controversial. We examine how the(More)
The precise immune mechanisms of neuronal death in anti-Hu-associated paraneoplastic encephalomyelitis (PEM) are unclear. We performed an immunohistochemical study on postmortem brain tissue from 11 patients with anti-Hu-associated PEM to further characterize the immune reaction and to ascertain possible mechanisms of neuronal death. To analyze inflammatory(More)
In human brain, nonartherosclerotic calcification is associated with normal aging and several pathological conditions without any clear significance. In all situations, calcification appears predominantly in the basal ganglia, but is also frequent in the hippocampus and cerebral cortex. alpha-Amino-(3-hydroxi-5-methyl-4-isoxazol-4-il)-propionic acid-induced(More)
Activation of glutamate receptors induces an excitotoxic neurodegenerative process characterised in some brain areas by the formation of calcium precipitates. To examine the pathogenesis of basal ganglia calcification (BGC), an improved procedure of X-ray microanalysis was used to study experimental excitotoxic calcification in the rat. Three weeks after(More)
Cellular microcalcification observed in a diversity of human pathologies, such as vascular dementia, Alzheimer's disease, Parkinson's disease, astrogliomas, and posttraumatic epilepsy, also develops in rodent experimental models of central nervous system (CNS) neurodegeneration. Central to the neurodegenerative process is the inability of neurons to(More)
Astroglial participation in the regional differences of vulnerability to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-induced neurodegeneration was investigated in the rat hippocampus and medial septum using L-alpha-aminoadipate (alpha-AA) as a specific astroglial toxin. alpha-AA was microinjected in the hippocampus and the medial septum(More)
This study compares the effects of acute alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) administration in the hippocampus in adult (3 months) and middle-aged (15 months) rats at 15 days postinjection. Injection of 1 and 2.7 mM AMPA produced dose-dependent neurodegeneration, assessed by Nissl staining; a glial reaction shown by glial(More)
Deregulation of intracellular calcium homeostasis is widely considered as one of the underlying pathophysiological mechanisms of hypoxic-ischemic brain injury. Whether this alteration can result in cerebral calcification was investigated in basal ganglia, cerebral cortex, and hippocampus of human premature and term neonates together with glial reaction. In(More)