POSSIBLE MODULATION OF AUDITORY MIDDLE LATENCY RESPONSES BY NITRIC-OXIDE IN THE INFERIOR COLLICULUS OF ANESTHETIZED RATS

Nitric oxide (NO) is a short-lived radical species endowed with interc ellular signalling functions in the mammalian brain. In the present st udy we have investigated the effects of focal injection into one infer ior colliculus of N-omega-nitro-L-arginine methyl ester (L-NAME), a ni tric oxide synthase inhibitor, on the acoustic middle latency response s (MLRs) evoked by click stimuli and recorded from the auditory cortex in anaesthetized rats. Microinfusion of L-NAME (1.0 mM) did not alter the latency of MLRs nor did it affect the evoked brain stem responses (ABRs), By contrast, L-NAME reduced P-1a-N-1 amplitude of MLRs by 51. 7 +/- 6.6% (mean +/- SEM; n = 5) and almost complete recovery to backg round amplitude was obtained 15-25 min after treatment. The less activ e isomer, D-NAME (1.0 mM; n = 5), failed to produce consistent effects on the evoked MLRs. A higher concentration of L-NAME (5.0 mM; n = 5) yielded a 69.0 +/- 13.3% inhibition whereas maximum inhibition produce d by 0.5 mM (n = 3) L-NAME was congruent to 10% of control value. The inhibitory effect typically evoked by 1.0 mM L-NAME was prevented by t reating rats with L-arginine (5.0 mM; n = 5), the endogenous precursor of NO synthesis. Reduction of MLR amplitude was also obtained in rats receiving intracollicular injection of dizocilpine (MK801; 1.0 mu M) and LY274614 (1.0 mM), two selective N-methyl-D-aspartate (NMDA) recep tor antagonists. In conclusion, the present data support a role for in tracollicular NO in the processing and transmission of the acoustic in put to the auditory cortex in the rat.