Metabotropic glutamate receptors (mGluR) are implicated in long-term memory storage. mGluR-I and mGluR-II antagonists impede various forms of learning and long-term potentiation (LTP) in animals. Despite the evidence linking mGluR to learning mechanisms, their role in mossy fiber-CA3 long-term potentiation (LTP) is not yet clear. To explain the involvement of mGluR-I in memory mechanisms, we examined the function of the mGluR-I antagonist AIDA on the induction of mossy fiber-CA3 LTP in vivo in male Sprague Dawley and Fischer 344 (F344) rats. Acute extracellular MF responses were evoked by stimulation of the MF bundle and recorded in the stratum lucidum of CA3. The EPSP magnitude was measured by using the initial slope of the field EPSP slope measured 2-3 ms after response onset. Following collection of baseline MF-CA3 responses at 0.05 Hz, animals received either CPP (NMDA-R antagonist, 10 mg/kg, i.p.), naloxone (opioid-R antagonist, 10 mg/kg), or AIDA (mGluR antagonist, 1 mg/kg, i.p., or 37.5 nmol, i.c.). LTP was induced by two 100-Hz trains at the intensity sufficient to evoke 50% of the maximal response. Responses were collected for an additional 1 hour. AIDA blocked induction of LTP in the mossy fiber pathway (p<0.05) in both strains of rats following systemic injection, and in Sprague Dawley rats following intrahippocampal injection.