Strategies for studies of neurotoxic mechanisms involving deficient transport of L-glutamate: antisense knockout in rat brain in vivo and changes in the neurotransmitter metabolism following inhibition of glutamate transport in guinea pig brain slices

2000 ◽  
Vol 53 (4) ◽  
pp. 373-381 ◽  
Author(s):  
Caroline Rae ◽  
Megan L Lawrance ◽  
Leonora S Dias ◽  
Tanya Provis ◽  
William A Bubb ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Rat Brain ◽  
Brain Slices ◽  
Glutamate Transport ◽  
Pig Brain ◽  
Guinea Pig Brain ◽  
Neurotransmitter Metabolism

scholarly journals The glial antioxidant network and neuronal ascorbate: protective yet permissive for H2O2 signaling

2004 ◽  
Vol 1 (4) ◽  
pp. 365-376 ◽  
Author(s):  
MARAT V. AVSHALUMOV ◽  
DUNCAN G. MACGREGOR ◽  
LILLY M. SEHGAL ◽  
MARGARET E. RICE
Keyword(s):  
Guinea Pig ◽  
Rat Brain ◽  
Brain Tissue ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Brain Slices ◽  
Edema Formation ◽  
Pig Brain ◽  
The Brain ◽  
Guinea Pig Brain

Increasing evidence implicates reactive oxygen species, particularly hydrogen peroxide (H2O2), as intracellular and intercellular messengers in the brain. This raises the question of how the antioxidant network in the brain can be sufficiently permissive to allow messages to be conveyed yet, at the same time, provide adequate protection against oxidative damage. Here we present evidence that this is accomplished in part by differential antioxidant compartmentalization between glia and neurons. Based on the rationale that the glia-to-neuron ratio is higher in guinea-pig brain than in rat brain, we examined the neuroprotective role of the glial antioxidant network by comparing the consequences of H2O2 elevation in slices of guinea-pig and rat brain. The effects of exogenously applied H2O2 on evoked population spikes in hippocampal slices and on edema formation in forebrain slices were assessed. In contrast to the epileptiform activity observed in rat hippocampal slices after H2O2 exposure, no pathophysiology was seen in guinea-pig hippocampal slices. Similarly, elevated H2O2 caused edema in rat brain slices but not in guinea-pig brain tissue. The resistance of guinea-pig brain tissue to H2O2 challenge was lost, however, when glutathione (GSH) synthesis was inhibited (by buthionine sulfoximine), GSH peroxidase activity was inhibited (by mercaptosuccinate) or catalase was inhibited (by 3-amino-1, 2, 4, -triazole). Strikingly, exogenously applied ascorbate, a predominantly neuronal antioxidant, could compensate for the loss of any other single component of the antioxidant network. Together, these data imply significant roles for glial antioxidants and neuronal ascorbate in the prevention of pathophysiological consequences of the endogenous neuromodulator H2O2.

INCORPORATION OF INORGANIC P32INTO PHOSPHOLIPIDS OF BRAIN SLICES: EFFECT OF CERTAIN TRANQUILLIZING DRUGS

1963 ◽  
Vol 41 (1) ◽  
pp. 1155-1162 ◽  
Author(s):  
W. L. Magee ◽  
R. J. Rossiter
Keyword(s):  
Methylene Blue ◽  
Guinea Pig ◽  
Aerobic Glycolysis ◽  
Brain Slices ◽  
Inorganic P ◽  
Pig Brain ◽  
Low Concentrations ◽  
High Concentrations ◽  
Derivatives Of ◽  
Guinea Pig Brain

Promazine, promethazine, tetrameprazine, and WY 1172, four tranquillizing drugs that are derivatives of phenothiazine, resembled chlorpromazine in that when they were added in a concentration of 0.1 mM to slices of guinea pig brain respiring in a suitable medium they stimulated the incorporation of inorganic P32into the phospholipids of the slices. With one of the drugs, promethazine, this concentration of 0.1 mM was found to cause no significant increase in respiration, in aerobic glycolysis, or in the concentration of phosphocreatine. In higher concentrations (1.0 mM), all of the compounds inhibited the labelling of phospholipid. Promethazine caused a reduction in respiration and in the concentration of phosphocreatine, accompanied by an increase in aerobic glycolysis. Methylene blue, a derivative of phenothiazine with no reported tranquillizing properties, did not stimulate the labelling of phospholipid in brain slices. Azacyclonol, pipradrol, and mepazine, drugs that are derivatives of piperidine, also stimulated phospholipid labelling in low concentrations and inhibited the labelling at higher concentrations. Piperidine and benzhydrol, the two components from which azacyclonol is derived, did not stimulate phospholipid labelling at the concentration which was most effective for azacyclonol. Low concentrations of benzhydrol, however, caused a slight stimulation. Meprobamate and phenaglycodol, two other compounds with reputed tranquillizing action, had either little or no effect. Most of the substances tested inhibited phospholipid labelling when they were added in sufficiently high concentrations.

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