Moreover, depletion of glutamatergic stores leading to enhanced synaptic depression has also been directly suggested in relation to schizophrenia: Several studies have shown that specific proteins known to be impaired in schizophrenics, such as the phosphoprotein Synapsin II, are involved in glutamatergic synaptic plasticity and that disabling these proteins in knockout mice leads to enhanced synaptic depression due to a decrease in the vesiclar reserve pool in these synapses [47]–[48]. The gene discussed is SYN2; the disease is schizophrenia.