FIG. 7.
Endogenous GABA and glutamate suppress the GABAergic transmission in NL neurons. A: averaged IPSCs elicited by a train of synaptic stimulation (100 Hz, 20 pulses) under conditions of control, GABABR antagonist 3-[[(3,4-dichlorophenyl)methyl]amino]propyl] diethoxymethyl)phosphinic acid (CGP 52432; 10 μM), and washout. B: CGP 52432 significantly increases the IPSC amplitude (P < 0.01, n = 6) measured at 20 ms after the last stimulus pulse. C: to study endogenous activity of presynaptic mGluRs in modulating GABA release in the NL, the stimulation electrode was placed in an area dorsal and lateral to the NL to activate both the GABAergic and the glutamatergic pathways. Under control conditions, both excitatory postsynaptic currents (EPSCs) and IPSCs were elicited in response to the same electrical stimulus. Antagonists for ionotropic glutamate receptor (50 μM DNQX plus 100 μM APV) eliminated the EPSCs. D: averaged IPSCs under conditions of control, mGluR antagonists (2S)-2-amino-2-[(1S,2S)-2-carboxycycloprop-1-yl]-3-(xanth-9-yl) propanoic acid (LY341495; 4 μM) plus (RS)-α-cyclopropyl-4-phosphonophenylglycine (CPPG; 10 μM), and washout. E: LY341495 and CPPG significantly increase the IPSC amplitude (P < 0.001, n = 6). Stimulus artifacts in A and D are blanked for clarity.