Carmen Cucarella

Instituto de Biomedicina de Valencia

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Carmina Montoliú

Universitat de València

Vicente Felipo

Centro de Investigacion Principe Felipe

Carlos Hermenegildo

Universitat de València

Marta Llansola

Centro de Investigacion Principe Felipe

Marı́a-Dolores Miñana

Hospital General Universitario De Valencia

Luigi Manzo

University of Naples Federico II

Rosana Sáez

Universitat de València

Santiago Grisolı́a

Generalitat Valenciana

ЕK

Еlena Kosenko

Institute of Theoretical and Experimental Biophysics

Santiago Grisolía

Instituto de Biomedicina de Valencia

Cooperative Institutions

Instituto de Biomedicina de Valencia

Universitat de València

Centro de Investigacion Principe Felipe

INCLIVA Health Research Institute

Hospital Clínico Universitario de Valencia

Instituto Valenciano de Investigaciones Agrarias

Consejo Superior de Investigaciones Científicas

University of Naples Federico II

University of Salerno

University of Pavia

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Glutamate and Muscarinic Receptors in the Molecular Mechanisms of Acute Ammonia Toxicity and of Its Prevention

Advances in experimental medicine and biology (1997)

María‐Dolores Miñana Marta Llansola Carlos Hermenegildo Carmen Cucarella Carmina Montoliú

Hyperammonemia

Brain Function

10.1007/978-1-4615-5945-0_3

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Chronic Exposure to Aluminum Impairs Neuronal Glutamate‐Nitric Oxide‐Cyclic GMP Pathway

Journal of Neurochemistry (1998)

Carmen Cucarella Carmina Montoliú Carlos Hermenegildo Rosana Sáez Luigi Manzo

Abstract: Humans are exposed to aluminum from environmental sources and therapeutic treatments. However, aluminum is neurotoxic and is considered a possible etiologic factor in Alzheimer's disease and other neurological disorders. The molecular mechanism of aluminum neurotoxicity is not understood. We tested the effects of aluminum on the glutamate‐nitric oxide‐cyclic GMP pathway in cultured neurons. Neurons were exposed to 50 µ M aluminum in culture medium for short‐term (4 h) or long‐term (8–14 days) periods, or rats were prenatally exposed, i.e., 3.7% aluminum sulfate in the drinking water, during gestation. Chronic (but not short‐term) exposure of neurons to aluminum decreased glutamate‐induced activation of nitric oxide synthase by 38% and the formation of cyclic GMP by 77%. The formation of cyclic GMP induced by the nitric oxide‐generating agent S ‐nitroso‐ N ‐acetylpenicillamine was reduced by 33%. In neurons from rats prenatally exposed to aluminum but not exposed to it during culture, glutamate‐induced formation of cyclic GMP was inhibited by 81%, and activation of nitric oxide synthase was decreased by 85%. The formation of cyclic GMP induced by S ‐nitroso‐ N ‐acetylpenicillamine was not affected. These results indicate that chronic exposure to aluminum impairs glutamate‐induced activation of nitric oxide synthase and nitric oxide‐induced activation of guanylate cyclase. Impairment of the glutamate‐nitric oxide‐cyclic GMP pathway in neurons may contribute to aluminum neurotoxicity.

Neurotoxicity

10.1046/j.1471-4159.1998.70041609.x

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Activation of the Metabotropic Glutamate Receptor mGluR5 Prevents Glutamate Toxicity in Primary Cultures of Cerebellar Neurons

Journal of Pharmacology and Experimental Therapeutics (1997)

Carmina Montoliú Marta Llansola Carmen Cucarella Santiago Grisolía Vicente Felipo

1-Aminocyclopentane-trans-1,3-dicarboxylic acid, an agonist of the metabotropic glutamate receptors 1, 2, 3 and 5, prevents neurotoxicity of glutamate and of N-methyl-D-aspartate in primary cultures of cerebellar neurons. The aim of this work was to assess which of the metabotropic glutamate receptors (mGluRs) is responsible for the protective effect. We tested the protective effects of selective agonists for each type of receptor. It is shown that glutamate and N-methyl-D-aspartate neurotoxicity are prevented by the following compounds: 1-amino-cyclo-pentane-trans-1,3-dicarboxylic acid, agonist of mGluR1, 2, 3 and 5; 3,5-dihydroxyphenylglycine, agonist of mGluR1 and 5; S-4-carboxy-3-hydroxyphenylglycine, agonist of mGluR5 and antagonist of mGluR1; trans-azetidine-2,4-dicarboxylic acid, agonist of mGluR5. Glutamate neurotoxicity is not prevented by (2S,1'S,2'S)-2(2'-carboxycyclopropyl)glycine, an agonist of mGluR2 and mGluR3. Moreover, the protective effect of 1-aminocyclo-pentane-trans-1,3-dicarboxylic acid is prevented by alpha-methyl-4-carboxyphenylglycine, an antagonist of mGluR1 and 5, but not by alpha-methyl-4-tetrazoylphenylglycine, an antagonist of mGluR2 and 3. A protective effect of activation of mGluR1 can not be ruled out because of the limitations imposed by the lack of specificity of the agonists and antagonists currently available. The results shown clearly indicate that activation of mGluR5 prevents glutamate and N-methyl-D-aspartate neurotoxicity in primary cultures of cerebellar neurons.

10.1016/s0022-3565(24)36656-x

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Citations (28)