EN
INTRODUCTION: It is generally accepted that neuronal plasticity can be induced at the cortical level. In our previous study we observed that relatively strong visual stimulation enhanced responses both at the cortical and subcortical level. The backward projection from the visual cortex to superior colliculus (SC) may facilitate the reinforcement of response in this midbrain structure. AIM(S): In the current study we examined how inactivation of the visual cortex affects responses in the SC after visual training. METHOD(S): Visual evoked potentials (VEPs) were recorded in anesthetized rats (n=5) from the primary visual cortex (VCx) and the SC, contralateral to stimulated eye, in response to flashing white‑light‑emitting diodes (LEDs) placed 10 cm in front of the rat. Monocular visual stimulation consisted of series of 300 repetitions of light flashes with 2 s intervals, presented every 15 minutes through 3 hours. In order to temporary block the activity of the cortex after 3-hour visual stimulation, a well above the contralateral VCx was fulfilled with xylocaine solution (2.5%). During cortical inactivation a single series of visual stimulation (300 stimulus repetitions) was presented and the SC VEP amplitudes were analysed. RESULTS: Chemical inactivation resulted in strong attenuation of cortical VEP amplitudes. In the case of the SC, cortical deactivation did not cause any significant difference in VEP amplitudes as compared to responses after 3 h of visual training. Collicular VEPs were still at the high level and significantly differed from control recording at the beginning of training, which indicates a minor impact of the VCx on response enhancement in the SC. CONCLUSIONS: Temporary deactivation of the visual cortex didn’t result in decline of VEP amplitudes in the SC, which indicates that increase of responses in SC after visual training is most likely due to enhancement of the retinal input to the SC. FINANCIAL SUPPORT: Supported by the Polish National Science Center grant Symfonia 1 (2013/08/W/NZ4/00691).