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Intracellular recording from CA3 pyramidal neurons in a slice culture from rat found a slow excitatory response to Glu application in the presence of blocking agents for the ionotropic GluRs. Further experimentation revealed that ACPD could evoke the same response, which was due to the depression of I(K, Ca) and voltage-gated I(K) Show
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A subsequent study in rat slice cultures has shown that bath application of MCPG (a mGluR antagonist) blocks the inward Ca-dependent K-current associated with ACPD application or mossy fiber stimulation in the presence on ionotropic GluR antagonists Show
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Another study using bath application of 1S,3R-ACPD in rat slice cultures during single electrode voltage clamp recording showed that depolarizing current steps revealed a suppression of K currents leading to a negative slope conductance at potential between -55mV and -40 mV Show
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mGluR2 knockout mice show normal LTP and synaptic transmission but not LTD Show
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It has also been shown (using whole and perforated patch recording from acutely isolated CA3 pyramidal neurons) that application of Glu and quisqualatic acid (in the presence of D-AP5, an NMDAR-antagonist, and CNQX, an AMPAR antagonist) results in responses that consist of an inward current that may be preceded by an outward current. Both of these currents are affected by bath [K] and they had different pharmacological properties (Harata et al, 1996). Show
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