Chlorpromazine induces hyposalivation by inhibiting muscarinic Ca signaling in salivary glands.

Chlorpromazine (CPZ), a dopamine D2 receptor antagonist, is an antipsychotic drug widely used in the treatment of schizophrenia. While CPZ is known to induce hyposalivation, the exact mechanism by which it inhibits secretory function in the salivary glands remains unclear. In this study, we investigated the molecular mechanism underlying CPZ-induced hyposalivation.

Major depression-related factor NEGR1 controls salivary secretion in mouse submandibular glands.

Salivary gland cells, which secrete water in response to neuronal stimulation, are closely connected to other neurons. Transcriptomic studies show that salivary glands also express some proteins responsible for neuronal function. However, the physiological functions of these common neuro-exocrine factors in salivary glands are largely unknown.

PRMT7 deficiency causes dysregulation of the HCN channels in the CA1 pyramidal cells and impairment of social behaviors.

HCN channels regulate excitability and rhythmicity in the hippocampal CA1 pyramidal cells. Perturbation in the HCN channel current (I) is associated with neuropsychiatric disorders, such as autism spectrum disorders. Recently, protein arginine methyltransferase 7 (PRMT7) was shown to be highly expressed in the hippocampus, including the CA1 region.