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Journal of Neuroscience, Vol 8, 2087-2100, Copyright © 1988 by Society for Neuroscience
Outgrowth-regulating actions of glutamate in isolated hippocampal pyramidal neurons
MP Mattson, P Dou and SB Kater
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523.
The present study examined the effects of glutamate on the outgrowth of
dendrites and axons in isolated hippocampal pyramidal-like neurons in cell
culture. During the first day of culture the survival and outgrowth of
these neurons was unaffected by high concentrations (up to 1 nM) of
glutamate, quisqualic acid (QA), kainic acid (KA), and N- methyl-D-aspartic
acid. Beginning on day 2 of culture high levels of glutamate, KA and QA
were toxic to the majority of pyramidal neurons, while subtoxic levels of
these agents caused a well-defined, dose- dependent, sequence of effects on
dendritic outgrowth. At increasing concentrations of glutamate, QA, and KA,
the following events were observed: (1) dendritic outgrowth rates were
reduced, while axonal elongation rates were unaffected; (2) dendritic
length was reduced, while axons continued to grow; (3) dendrites regressed
dramatically, and axonal outgrowth rate was reduced. These
dendrite-specific effects of glutamate were apparently mediated at the
growth cones since focal application of glutamate to individual dendritic
growth cones resulted in suppression of growth cone activity and a
regression of the dendrite; axons were unaffected by focal glutamate
application. Pharmacological tests using glutamate receptor agonists and
antagonists demonstrated that receptors of the KA/QA type mediated the
glutamate effects on outgrowth and survival. The calcium channel blocker
Co2+ prevented both glutamate neurotoxicity and glutamate-induced dendritic
regression. Ionophore A23187 and elevations in extracellular K+ levels each
caused a dose-dependent series of outgrowth and survival responses similar
to those caused by glutamate. Taken together, these results indicate that
activation of glutamate receptors leads to the opening of voltage-dependent
calcium channels; the resulting increases in calcium influx lead to the
observed alterations in dendritic outgrowth and neuronal survival.
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