(RS)-α-Methyl-4-carboxyphenylglycine (MCPG) does not block theta burst-induced long-term potentiation in area CA1 of rat hippocampal slices
1994; Elsevier BV; Volume: 170; Issue: 1 Linguagem: Inglês
10.1016/0304-3940(94)90228-3
ISSN1872-7972
AutoresRitchie E. Brown, Holger Rabe, Klaus G. Reymann,
Tópico(s)Neural dynamics and brain function
ResumoWe have used the selective metabotropic glutamate receptor antagonist (RS)-α-methyl-4-carboxyphenylglycine (MCPG) to investigate in the CA1 hippocampal subregion in vitro whether coactivation of N-methyl-d-aspartate (NMDA) and metabotropic glutamate receptors is necessary for the induction of long-term potentiation (LTP) when LTP is induced by theta burst stimulation (TBS). When MCPG (500 μM) was bath applied 14–30 min prior to a triple high-frequency tetanization (100 Hz, 1 s) and washed out immediately afterwards the potentiation of the extracellularly recorded field potentials decayed gradually to baseline (P < 0.05) over 2–3 h. However, when MCPG was applied in the same manner before a triple TBS (10 bursts at 5 Hz, 100 Hz within the bursts) the resulting potentiation remained stable for at least 4 h. MCPG had no effect on baseline synaptic transmission or post-tetanic potentiation. These results demonstrate a clear difference in the mechanisms underlying these two different forms of LTP.
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