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Kainic acid-induced seizures and brain damage in the rat: Role of calcium homeostasis by M. Berg; T. Bruhn; Aa. Frandsen; A. Schousboe; N. H. Diemer is a Neuroscience article available to read on EtoBox.

What is Kainic acid-induced seizures and brain damage in the rat: Role of calcium homeostasis about?

Seizure activity induced by kainic acid (KA) and subsequent neuronal death are thought to be associated with an increase in cytoplasmic free calcium ([Ca2+li) and can be prevented by N-methyl-D-aspartate (NMDA) antagonists. In addition to influx through receptor operated Ca2+ channels the increase in [Ca2+Ii may be the result of an increased influx through voltage-operated calcium channels and/or release from intracellular deposits. It was therefore investigated whether compounds other than NMDA antagonists with known actions on the intracellular Ca2+ homeostasis had any protective effect against KA-induced neuronal death. Voltage-operated calcium channels in the cell membrane were blocked with the L-type ion channel antagonist, Nimodipine (1.0 mglkg), and release of Ca" from internal stores was prevented with Dantrolene (10 mg/kg). Animals from two control groups injected with kainate (8 mg/ kg) exhibited a survival rate of 67 and 539'6, respectively. Countings of neurons in dorsal hippocampus showed subtotal or total loss in the CA1 and CA3 subregions. There were no significant differences concerning seizure and survival rates in the groups injected with kainate and treated with

Who reads Kainic acid-induced seizures and brain damage in the rat: Role of calcium homeostasis?

Author

M. Berg; T. Bruhn; Aa. Frandsen; A. Schousboe; N. H. Diemer

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

1995

Language

EN

Field

Neuroscience (Life Sciences)