Background: Metabotropic glutamate could contribute to the development of neuropathic
pain-related behaviors. Previously, we have confirmed that the glutamic acid and dizocilpine maleate
in the hippocampal CA3 region are involved in the modulation of noxious stimulation. However,
whether the metabotropic glutamate receptor 7 (mGluR7) can modulate the pain-evoked electrical activities
of pain-excited neurons and pain-inhibited neurons in the hippocampal CA3 region is not clear.
Objective: The study aimed to examine the effects of mGluR7 allosteric agonist N,N'-dibenzhydrylethane-
1,2-diamine dihydrochloride (AMN082) and antagonist 6-(4-methoxyphenyl)-5-methyl-3-
pyridin-4-ylisoxazolo[4,5-c]pyridin-4(5H)-one (MMPIP) on the pain-evoked electrical activities of
pain-excited neurons and pain-inhibited neurons in the CA3 region of rats.
Method: A train of electric impulses applied to the sciatic nerve were used for noxious stimulation.
The bio-electrical activities of pain-excited neuron or pain-inhibited neuron in the CA3 region were recorded
by a glass microelectrode.
Results: Our results exhibited that intra-CA3 region administration of the glutamic acid or AMN082
increased the pain-evoked discharged frequency and shortened the latency of pain-excited neuron,
while decreased the pain-evoked discharged frequency and prolonged the inhibitory duration of paininhibited
neuron in the CA3 region. The intra-CA3 region microinjection of MMPIP produced the opposite
Conclusion: These findings demonstrated that the glutamic acid and mGluR7 in hippocampal CA3 region
are involved in the modulation of nociceptive information transmission by regulating pain-evoked
electric activities of pain-excited neurons and pain-inhibited neurons.