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Accumulation of Extracellular Glutamate by Inhibition of Its Uptake Is Not Sufficient for Inducing Neuronal Damage: An In Vivo Microdialysis Study
An increased extracellular glutamate level in vivo due to dysfunction of its transporter is not sufficient for inducing neuronal damage, and the neurotoxic effects of dihydrokainate could be explained by direct activation of glutamate postsynaptic receptors. Expand
Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of glutamate- and GABA-mediated neurotransmission and of ion channels
It is concluded that 4-aminopyridine stimulates the release of glutamate from nerve endings and that the resultant augmented extracellular glutamate is directly related to the neurodegeneration and is involved in the generation of epileptiform discharges through the concomitant overactivation of glutamate receptors. Expand
Biochemical Pharmacology of GABA in CNS
The numerous pharmacological studies of GABA in brain described in the literature have been carried out mainly with the purpose of investigating the possible role of this amino acid as an inhibitoryExpand
Relationships Among Seizures, Extracellular Amino Acid Changes, and Neurodegeneration Induced by 4‐Aminopyridine in Rat Hippocampus: A Microdialysis and Electroencephalographic Study
It is concluded that the glutamate release‐inducing effect of 4‐aminopyridine results in excitotoxicity because it occurs at the level of nerve endings, thus permitting the interaction of glutamate with its postsynaptic receptors, which is probably not the case after K+ depolarization. Expand
Ruthenium red as a tool to study calcium channels, neuronal death and the function of neural pathways
The in vitro and in vivo effects of RuR are reviewed and discussed in terms of the usefulness of the dye as an interesting tool to study calcium channels linked to transmitter release, neuronal death mechanisms and the function of neural pathways. Expand
Vascular Endothelial Growth Factor Prevents Paralysis and Motoneuron Death in a Rat Model of Excitotoxic Spinal Cord Neurodegeneration
The finding that VEGF protected motoneurons from this AMPA receptor-mediated excitotoxic death suggests that it may be a therapeutic agent in sporadic ALS. Expand
VEGF protects spinal motor neurons against chronic excitotoxic degeneration in vivo by activation of PI3‐K pathway and inhibition of p38MAPK
J. Neurochem. (2010) 115, 1090–1101.
Glutamate Uptake Impairment and Neuronal Damage in Young and Aged Rats In Vivo
The present results suggest that age appears not to be a significant factor in the sensitivity of neurons to the toxic effect of extracellular glutamate increase via blockade of its transport system. Expand
Seizures and wet-dog shakes induced by 4-aminopyridine, and their potentiation by nifedipine.
Nifedipine-treated rats showed long-lasting (greater than 60 min) continuous discharges in all structures studied (status epilepticus), which is discussed in the light of the possible participation of Ca2+ channels in the convulsant effect of 4-AP and its potentiation by nifEDipine. Expand
Binding of Lanthanum Ions and Ruthenium Red to Synaptosomes and Its Effects on Neurotransmitter Release
It is concluded that La3+ and RuR share at least one type of binding site, which is probably the high‐affinity La3+, related to the voltage‐dependent Ca2+ entry involved in neurotransmitter release. Expand