Is nitric oxide (NO) involved in the transmission of acoustic input to the rat auditory cortex?

NO has been proposed to act as an intercellular messenger, possibly involved in neuronal plasticity and in the transmission of somatosensory information. Aim of the present study is to check whether, at the infedor colliculus (IC) level, NO may participate in the processing and transmission of acoustic signals to the auditory cortex of the rat. Animals were anaesthetised with ketamine and xylazine (66 and 13 mg/kg, respectively, i.p.) and implanted with a stainless steel guide cannula to allow drug injection into the IC (0.5-1.0 rtl at 1.0 lal/min rate). Auditory middle latency (MLR) and brain stem (ABR) responses were evoked by click stimuli of supramaximaI intensity at 4/s and recorded from the auditory cortex by Ag/AgCt electrodes. IC injection of N%nitro- L-arginine methyl ester (L-NAME, 1.0 mM), an inhibitor of NO synthase (NOS), reduced by 51.7--~.6% (n=5) the amplitude of Pla-N1 com- ponent of MLRs without significantly affecting the latency of MLRs as well as ABRs. This inhibitory effect was concentration-dependent and it ranged from 5.5_+3.2% for the concentration of 0.5 mM (n=3) to 69.0_+ 3.3% for 5.0 mM (n=5). L-NAME injection performed 10 min after pre- treatment with the endogenous precursor of NO, L-arginine (5.0 raM), produced 24.2_+3.6% reduction of P1,-N~ amplitude and this was significantly lower (P<0.01) than that elicited by L-NAME given alone. IC injection of D-NAME (1.0 mM; n=5), the less active isomer of NAME, yielded no significant decrease in Pla-N1 amplitude. IC infusion of dizo- cilpine (MK801; 1.0 pM, n=5) or LY274614 (1.0 mM; n=3), two selective NMDA receptor antagonists, reduced P~,-N~ amplitude by 48.2_+7.4% and 83.7_+5.0%, respectively. The stereospecific and concentration- dependent effects of L-NAME suggest that IC NO is involved in the transmission of acoustic input to the auditory cortex. Stimulation of NOS activity under our experimental conditions might be due to a rise in intracellular Ca2÷levels induced by NMDA-receptor activation.