Glutamate selectively increases the high-threshold Ca2+ channel current in sensory and hippocampal neurons.
Previous studies resulted in conflicting conclusions that glutamate application either decreases or increases the activity of Ca2+ channels in hippocampal neurons. We studied whole-cell Ca2+ currents (ICa) in chick dorsal root ganglion neurons and rat hippocampal cells. For both cell types glutamate (1-30 microM) increased high-threshold Ca2+ current. It was independent of the charge carriers, Ca2+ or Ba2+. Low-threshold Ca2+ channel current and the fast sodium current were not changed with glutamate application. The effect developed within 1-2 min and then further facilitated after washout of the agonist. A second application of glutamate produced no additional increase in ICa. No changes in the time-course of whole-cell currents were observed, suggesting that glutamate recruits 'sleepy' Ca2+ channels. Whatever its mechanism, overlasting increase of ICa by glutamate may be important in neuronal plasticity.
Max-Planck-Institute for Psychiatry, Planegg-Martinsried, FRG.
S L
SL
Mironov
H D
HD
Lux
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects*; D002642:Chick Embryo; D005971:Glutamates / Q000494:pharmacology*; D018698:Glutamic Acid; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects*; D009475:Neurons, Afferent / Q000187:drug effects*; D051381:Rats
D015220:Calcium Channels; D005971:Glutamates; D018698:Glutamic Acid