in synaptic neurotransmission and associated with the glutamatergic synapse (Fig. 2). Together, these data further support the involvement of cortical and striatal glutamatergic synaptic dysfunction in OCD pathogenesis. Using our global DEG data, we also estimated broad cell type representation from our tissue samples, finding significantly different fractions of astrocytes, vascular cells, and medium spiny neurons between OCD and unaffected comparison subjects (Fig. 3).
