Reexamination of the Effects of MCPG on Hippocampal LTP, LTD, and
Depotentiation.
Selig, David K., Hey-Kyoung Lee, Mark F. Bear, and Robert C. Malenka.
Dept.'s of Psychiatry and Physiology, Center for Neurobiology and
Psychiatry, University of California, San Francisco, 94143, Dept. of
Neuroscience and Howard Hughes Medical Institute, Brown University,
Providence, Rhode Island, 02912.
APStracts 2:0134N, 1995.
SUMMARY AND CONCLUSIONS
1. We examined the effects of the metabotropic glutamate receptor (mGluR)
antagonist (RS)--methyl-4-carboxyphenylglycine (MCPG) on the induction of
long-term potentiation (LTP), long-term depression (LTD), and depotentiation
in CA1 hippocampal neurons using extracellular recording techniques. 2. MCPG
(500 M) strongly antagonized the presynaptic inhibitory action of the mGluR
agonist 1-aminocyclopentane-(1S, 3R)-dicarboxylate (ACPD) yet failed to block
LTP induced with either tetanic stimulation (100 Hz, 1 sec) or theta burst
stimulation. 3. To test the possibility that our failure to block LTP was due
to prior activation of a "molecular switch" that in its "on"
state obviates the need for mGluR activation to generate LTP (Bortolotto et
al. 1994), we gave repeated periods of prolonged low frequency stimulation (1
Hz, 10 min; LFS), a manipulation reported to turn the switch "off".
Although this stimulation saturated LTD, subsequent application of MCPG still
failed to block LTP. 4. MCPG did not block LFS-induced depotentiation in older
slices (4-6 weeks), or LFS-induced LTD in older, young (11-18 day) or neonatal
(3-7 day) slices. 5. These results demonstrate that MCPG-sensitive mGluRs are
not necessary for the induction of either LTP, LTD, or depotentiation in
hippocampal CA1 pyramidal cells. The possibility remains, however, that their
activation may modify the threshold for the induction of these long-term
plastic changes.
Received 14 March 1994; accepted in final form 18 April 1995.
APS Manuscript Number J164-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 2 May 1995.