The Abnormal Neural Activites Of The Superior Colliculus And Dysfunction Of Innate Visual Defensive Response On DISC1 Transgenic Rodent Model

Mental disorder, brings intense suffering to the patients and huge burden to their family and society. Accumulating evidence indicated that patients with mental disorder had deficit in emotional face recognition, especially those of negative emotions like fear. Meanwhile, mental disorder patients showed dysfunction in the attention related eye movement, which is largely known as coordinating by the midbrain superior colliculus(SC). Recent report from our demonstrated, the SC medaiting the initialization of the innate visual threat evoked fear response. Thus in the current study, we investigated the possible abnormality of SC neural activites in the DISC1 transgenic mouse model.Using the DISC1 mice as an animal model of mental disorder, we conducted awake head-fixed multichannel electrophysiologic recording to the SC neurons during no stimulation and looming stimuli; the behaviors with optogenetic activation of SC neurons was also analyzed. Comparing with the control mice, the DISC1 mice with mental disorder symptoms induced by tamoxifen showed decreased bursts in the neurons with a frequency above 8Hz. During looming stimuli, the neural activity of DISC1 mice decreased in the upper layer of SC while increased in the deep layer of SC. Furthermore, the fear responses induced by optically activating the middle and deep SC neurons was weaker in DISC1 mice. The present results suggest that the abonormal neural activities in SC may lead to a disturbed output of SC neurons, and finally reduced visual threat induced innate fear response, in the DISC1 mice with mental disorder symptoms. Our data for the first time indicated that the dysfunction of fear related visual stimuli processing in mental disorder mouse. It might contribute to the understanding of the pathogenesis of mental disorder.