Is Glutamate a Trigger Factor in Epileptic Hyperactivity?

Abstract

The effects of glutamate and aspartate antagonists were studied on limb-jerk frequency and EEG patterns in rats made epileptic by cobalt implantation in the sensorimotor cerebral cortex. The results of this study were as follows: (1) alpha-Amino-4-phosphonobutyric acid (0.055--1.10 mM) decreased or completely prevented the epileptic manifestations. The effect was reversible 30 min after washing with artificial CSF solution. (2) DL-Pyroglutamic acid completely abolished the myoclonic jerks and EEG spikes. (3) alpha-Amino-5-phosphonovaleric acid and alpha-D-amino-adipic acid significantly reduced the frequency of epileptic spikes and myoclonic jerks. (4) Other analogs, alpha-amino-3-phosphonopropionic acid (0.6 mM), alpha-amino phosphonocaproic acid (0.95), and hydroxy-3-amino pyrrolidone-2 were without effect. (5) Glutamate itself did not decrease the epileptic manifestations.

Enhancing Glutamate Transport: Mechanism of Action of Parawixin1, a Neuroprotective Compound from Parawixia bistriata Spider Venom

“…Because GLT-1/EAAT2 is the predominant CNS glutamate transporter subtype, substances that enhance its activity would be powerful tools for increasing the clearance of glutamate in pathological conditions. Increased extracellular levels of glutamate have been implicated in pathological conditions such as cerebral ischemia (Oechmichen and Meissner, 2006), amyotrophic lateral sclerosis (Rothstein et al, 1992), epilepsy (Coutinho-Netto et al, 1981), schizophrenia (Carlsson et al, 1999), and others.…”

Toxicidade retiniana do gás hexafluoreto de enxofre, líquido perfluorocarbono, ar e solução salina balanceada em olhos de coelhos

“…A análise bioquímica do humor vítreo através da quantificação dos aminoácidos excitatórios feita no presente estudo baseou-se nos princípios de Rothman, Olney (14) que, em 1986, postularam a teoria da toxicidade excitatória (neurotoxicidade) apontando os aminoácidos excitatórios, principalmente o glutamato, como um importante agente causal da morte neuronal. A ocorrência de aumento anormal na liberação do glutamato "in vivo" foi demonstrada pela primeira vez por alguns autores, em ratos (15) . Acredita-se que este aumento nos níveis de glutamato seja proveniente da liberação extracelular deste aminoácido neurotransmissor, presente nos neurônios e células gliais.…”

Anti-Excitotoxic Actions of Taurine in the Rat Hippocampus Studied in Vivo and in Vitro

“…Thus, it was reasonable to conclude that endogenous excitatory amino acids bearing structural similarities to kainate might play pivotal roles in the etiology of seizure disorders. In this regard, glutamate, aspartate, and, more recently, quinolinate (QUIN), endogenous excitants of central nervous tissue, have been suggested as factors involved in initiating events leading to seizures (Lapin, 1978;Coutinho-Netto et al, 1981;Nitsch et al, 1983;Smialowski, 1983;Schwarcz et al, 1984). This conjecture has been indirectly validated by the recent observations that excitatory amino acid antagonists possess anticonvulsant activity in a number of animal models of epilepsy (Croucher et al, 1982;Meldrum et al, 1983;Schwarcz et al, 1984).…”