Locomotor and learning deficits in adult rats exposed to monosodium-L-glutamate during early life.

Neonatal administration of neurotoxic doses of monosodium-L-glutamate (MSG) to rats causes neuronal necrosis of the hypothalamus along with behavioral abnormalities. In the present study the behavioral effects in rats treated with subneurotoxic doses of MSG (2 mg/g, p.o., for 10 days) at the weaned stage were investigated at day 90 post-dosing. The MSG-treated rats did not show significant changes in any of the components of spontaneous locomotor activity but, after apomorphine challenge, marked decreases in the distance travelled, ambulatory and stereotypic times, and the number of stereotypic movements with an increase in the resting time were observed. Significant decrease in the active avoidance learning performance was observed in the MSG-treated rats in the learning (acquisition) phase without any changes in the extinction and relearning phases. The results indicate that exposure to MSG in early life in rats could lead to subtle behavioral aberrations in late adulthood.

Blood glutamate levels in patients with motor neuron disease.

This study was undertaken to evaluate the role of excitatory amino acid glutamate (Glu) in the pathophysiology of motor neuron disease (MND). It was observed that blood Glu levels were significantly higher in MND patients with respect to healthy controls. The data indicate that Glu homeostasis is altered in the patients with MND.

Single microinjection of L-glutamate induces oxidative stress in discrete regions of rat brain.

Glutamate (Glu) is a major excitatory amino acid neurotransmitter in the mammalian brain. Under Certain Circumstances Glu can also exert toxic effects on neuronal Cells. To unravel the biochemical mechanisms of Glu-induced acute neuronal injury, Glu 1 mumol/1 mul was microinjected into cerebral Cortex, striatum and hippocampus of adult rats and oxidative stress and antioxidant parameters were evaluated. The results show that the rate of lipid peroxidation was significantly increased in the above brain regions following Glu administration suggesting neuronal membrane damage and also the total and free sulfhydryl groups were significantly depleted, indicating altered red-ox status of the cells. There was also alteration in the activity of antioxidant enzyme catalase in cerebral cortex. Some of the above Glu-induced effects were reversed or modified by NMDA receptor antagonist MK-801.

Effect of neonatal monosodium glutamate on lipid peroxidation in adult rat brain.

Glutamate (glu), an excitatory amino acid (EAA) abundantly present in the brain of mammals, is also a neurotoxin. We examined lipid peroxidation (LPO) potential and antioxidant parameters of midbrain region (MBR) and frontal cortex of adult rats following treatment with monosodium glutamate (MSG) during postnatal day (PND) 1 through PND 10 at a daily dose of 4 mg g-1 body weight. In PND 90 rats MSG increased LPO by 56% and altered antioxidant status of MBR. This indicates that oxidative stress produced by glu in vulnerable brain regions may persist for prolonged periods and could be one of the mechanisms of EAA neurotoxicity resulting in chronic neurodegeneration.

Effect of neonatal monosodium glutamate on the activities of glutamate dehydrogenase and aminotransferases in the circumventricular organs of rat brain.

Glutamate (Glu) the major amino acid in mammalian brain and most dietary proteins possesses neurotransmitter as well as neurotoxic properties. We administered monosodium glutamate (MSG) 4 mg/g bwt, sc on postnatal day (PND) 1 through 10 to rats on alternate days or daily and sacrificed them on PND 45 or PND 90 respectively. The activities of glutamate dehydrogenase and aminotransferases were evaluated in the circumventricular organs of brain. Results show that neonatal MSG produces alterations in glutamate metabolism in blood-brain-barrier deficient regions.

Lipid peroxidation potential and antioxidant status of circumventricular organs of rat brain following neonatal monosodium glutamate.

Glutamate (glu), an excitatory aminoacid neurotransmitter is abundantly present in the brain of mammals, as well as in dietary protein. Earlier studies with glu mostly involved histopathological and neuroendocrine changes in the blood-brain-barrier deficient areas of brain following its systemic administration. The present study examined lipid peroxidation potential and anti-oxidant parameters of immature rat mid-brain region which include arcuate nucleus, hypothalamus, and other circumventricular organs (CVO) following their exposure to monosodium glutamate (MSG) neonatally. This compound was administered at a dose of 4 mg/g bwt, sc, for the first ten days of postnatal period. Animals were sacrificed on postnatal day 25, and the lipid peroxidation potential was evaluated. The treatment of MSG significantly increased lipid peroxidation (P < 0.01) as well as the activity of anti-oxidant enzyme catalase (P < 0.025) and significantly depleted total and free sulfhydryl groups (P < 0.05) in the CVO. These results indicate that neonatal MSG treatment produces neuronal damage in the CVO by increasing lipid peroxidation and is in agreement with the hypothesis that excitotoxins may generate free radicals in causing neurotoxicity.

Lactate dehydrogenase and glutamate dehydrogenase activities in the circumventricular organs of rat brain following neonatal monosodium glutamate.

Glutamate (glu) an excitatory neurotransmitter amino acid, is present in high concentrations in the mammalian central nervous system and is the most abundant amino acid in our daily diet. In the present study the activities of lactate dehydrogenase (LDH) and glutamate dehydrogenase (GDH) were evaluated in the circumventricular organs (CVO) of the brain in 25-day-old rats following MSG administration at a dose of 4 mg/g b.wt during the first ten days of life. The results show the LDH activity increased to 265% of that in the control (p < 0.001), whereas GDH activity was significantly decreased (p < 0.05). The great elevation in LDH, a cytoplasmic marker enzyme, is apparently due to cytoskeletal changes brought about as a consequence of glu toxicity, whereas lowered GDH activity indicates altered glu homostasis in the blood-brain-barrier deficient areas following neonatal exposure to glu.