Fig. 6.

Proposed role of the interaction between hDAAO and pLG72 on the d-serine bioavailability at glutamatergic synapses under normal and pathological (schizophrenia susceptibility) conditions [69]. Up to now, pLG72 was identified only in glial cells, therefore we focused on the modulation of hDAAO activity in astrocytes. According to our hypothesis, pLG72 modulates the amount of active hDAAO acting on the stability of the flavoenzyme (left panel). An abnormal, low expression of pLG72 under pathological conditions could result in hyperactivation of hDAAO and decrease d-serine concentration (right panel). Importantly, the decrease in d-serine concentration results in a lower amount of activated NMDAR and, thus, in a hypofunction of the glutamatergic neurotransmission (see also Fig. 1 for details about the overall mechanisms of d-serine regulation at synapsis)