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Experiment #00000015

Given that schizophrenia is characterized by a deficit in the attenuation of sensory input via corollary discharge, how might pathologically elevated RGC signaling—potentially caused by synaptic glutamate overflow without zinc modulation—interfere with the thalamic integration of extra-retinal CD signals to effectively reverse the predictive timing of visual stability?

SLC39A8 Protein _gates_from_slc39a8_protein Zinc Deficiency _gates_to_zinc_deficiency _gates_from_zinc_deficiency Glutamic Acid _gates_to_glutamic_acid _gates_from_glutamic_acid Thalamus _gates_to_thalamus

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