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Journal of Neuroscience, Vol 15, 87-98, Copyright © 1995 by Society for Neuroscience
Inhibition of long-term potentiation in the dentate gyrus of freely moving rats by the metabotropic glutamate receptor antagonist MCPG
G Riedel, G Casabona and KG Reymann
Department of Neurophysiology, Institute for Neurobiology, Magdeburg, Germany.
Metabotropic glutamate receptors (mGluRs) are critically involved in the
maintenance of long-term potentiation (LTP) (Reymann and Matthies, 1989;
Behnisch et al., 1991; Izumi et al., 1991; Bashir et al., 1993). In order
to assess further the physiological role of MGluRs in LTP, we injected
freely moving rats with the recently available, competitive mGluR
antagonist (R,S)-alpha-methyl-4-carboxyphenylglycine (MCPG)
intraventricularly and recorded extracellularly the population spike (PS)
as well as the field excitatory postsynaptic potential (fEPSP) of the
granule cells of the dentate gyrus in response to stimulation of fibers of
the perforant path. MCPG was administered in two concentrations (A = 20
mM/5 microliters; B = 200 mM/5 microliters) either 30 min prior to or 5 min
after LTP induction. Sodium chloride infusion served as a control. Normal
synaptic transmission was not altered by MCPG. However, the mGluR
antagonist inhibited LTP in a concentration-dependent manner. Concentration
A did not influence the potentiation shortly after the tetanus. In the PS,
short-term potentiation (STP), which is decremental in its time course,
occurred normally, but in contrast to controls the potentiation declined
back to baseline values after 2-3 hr. This dose also reduced the
posttetanic increase in the slope function of the fEPSP, and led to a time
course of potentiation similar to that for the PS. Concentration B
completely abolished the tetanus-induced potentiation. This block was
similar to that obtained for the NMDA antagonist
2-amino-5-phosphonopentanoate (AP5). Both MCPG concentrations had no
influence on the time course of preestablished LTP. These effects seem to
be due to the action of the (+)-isomer of MCPG, since
intracerebroventricular application of the (- )-isomer was without effect
on the duration and magnitude of LTP. In addition, we were interested in
the mGluR subtypes involved in the blocking mechanism of MCPG.
1S,3R-aminocyclopentane-1,3-dicarboxic acid (ACPD)-activated PPI hydrolysis
in hippocampal slices was competitively inhibited by MCPG at a
concentration of 1 mM or higher. In contrast, this concentration of MCPG
did not affect the reduction of forskolin- stimulated cAMP formation by
ACPD. These results corroborate recent findings that mGluRs are required
for the induction of LTP in CA1 and CA3 in vitro (Bashir et al., 1993;
Sergueeva et al., 1993) and in vivo (Riedel and Reymann, 1993). The process
of STP is found to be independent of mGluR activation.(ABSTRACT TRUNCATED
AT 400 WORDS)
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