ABSTRACT
Kainate, the analog of the excitatory amino acid L-glutamate, upon binding to non-NMDA glutamate receptors, causes depolarization of neurons followed by severe status epilepticus, neurodegeneration, plasticity and gliosis. These events are best observed in hippocampus, the limbic structure implicated in learning and long-term memory formation. Neurons in all hippocampal structures undergo hyper-activation, however, whereas the cells in the CA subfields degenerate within 2--3 days following the application of kainate, the granule cells of the dentate gyrus are resistant to any form of neurodegeneration and even initiate new synaptic contacts. These physiological and histological changes are modulated by short-term and long-term alterations in gene expression. Perhaps close examination of the changing spatio-temporal patterns of mRNAs of various genes may help in generating a clearer picture of the molecular events leading to complex cognitive functions.
