oxadiazoles and Learning-Disabilities

oxadiazoles has been researched along with Learning-Disabilities* in 1 studies

Other Studies

1 other study(ies) available for oxadiazoles and Learning-Disabilities

Article	Year
Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead. FEBS letters, 1990, Feb-12, Volume: 261, Issue:1 The effect of Pb2+ on glutamate receptor activity in rat hippocampal neurons was investigated with a view of explaining the cognitive and learning deficits produced by this heavy metal. Pb2+ (2.5-50 microM) selectively inhibited N-methyl-D-aspartate (NMDA)-induced whole-cell and single-channel currents in a concentration-dependent but voltage-independent manner, without significantly altering currents induced by either quisqualate or kainate. The frequency of NMDA-induced channel activation was decreased by Pb2+. Neither glycine (10-100 microM), nor Ca2+ (10 mM) reversed the effect of Pb2+. Pb2+ also inhibited the [3H]MK-801 binding to rat hippocampal membranes in vitro. The elucidation of the actions of Pb2+ on the NMDA receptor ion channel complex provides important insights into the clinical and toxic effects of this cation. Topics: Animals; Aspartic Acid; Calcium; Dibenzocycloheptenes; Dizocilpine Maleate; Electric Conductivity; Glycine; Hippocampus; Ion Channels; Kainic Acid; Lead; Learning Disabilities; Male; N-Methylaspartate; Oxadiazoles; Quisqualic Acid; Rats; Rats, Inbred Strains; Receptors, Glutamate; Receptors, N-Methyl-D-Aspartate; Receptors, Neurotransmitter	1990

Article

Year

Selective blockade of NMDA-activated channel currents may be implicated in learning deficits caused by lead.

FEBS letters, 1990, Feb-12, Volume: 261, Issue:1

The effect of Pb2+ on glutamate receptor activity in rat hippocampal neurons was investigated with a view of explaining the cognitive and learning deficits produced by this heavy metal. Pb2+ (2.5-50 microM) selectively inhibited N-methyl-D-aspartate (NMDA)-induced whole-cell and single-channel currents in a concentration-dependent but voltage-independent manner, without significantly altering currents induced by either quisqualate or kainate. The frequency of NMDA-induced channel activation was decreased by Pb2+. Neither glycine (10-100 microM), nor Ca2+ (10 mM) reversed the effect of Pb2+. Pb2+ also inhibited the [3H]MK-801 binding to rat hippocampal membranes in vitro. The elucidation of the actions of Pb2+ on the NMDA receptor ion channel complex provides important insights into the clinical and toxic effects of this cation.

Topics: Animals; Aspartic Acid; Calcium; Dibenzocycloheptenes; Dizocilpine Maleate; Electric Conductivity; Glycine; Hippocampus; Ion Channels; Kainic Acid; Lead; Learning Disabilities; Male; N-Methylaspartate; Oxadiazoles; Quisqualic Acid; Rats; Rats, Inbred Strains; Receptors, Glutamate; Receptors, N-Methyl-D-Aspartate; Receptors, Neurotransmitter

1990