Nitric oxide (NO) modulates the release of some classical neurotransmitters and the onset of synaptic plasticity.[7,8] NO molecules cross the synaptic gap into presynaptic neurons, where soluble guanyl cyclase (sGC) is activated and produces cyclic GMP (cGMP), thereby affecting the neurotransmitter release mechanism and regulating the opening of ion channels, thus influencing the pathogenesis of depression and schizophrenia.[9] The facilitation of gas signaling molecules is mainly associated with the production of carbon monoxide (CO). Here, SGCB is linked to depressive symptom measurement.