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Role of GABA Receptors in the Postganglionic Regulation of Salivation
Author(s) -
Lee Joseph,
Giovannucci David
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb795
Subject(s) - gabaergic , saliva , gabaa receptor , neurotransmitter , receptor , gamma aminobutyric acid , endocrinology , muscarinic acetylcholine receptor , medicine , cholinergic , biology , neuroscience , gabab receptor , microbiology and biotechnology
The salivary gland secretes saliva components critical for oral health. Autonomic neural activity controls the secretory output of acini, the basic units of saliva production. This process can be disrupted in patients by benzodiazepine treament, leading to the severe oral condition of xerostomia, or dry mouth. Neural inputs to the acini are primarily cholinergic and noradrenergic, but the discovery of gamma‐aminobutyric acid (GABA) and its receptors in the salivary glands hints at an unexplored mechanism for benzodiazepine‐induced xerostomia. In the current study, biochemical, live‐cell imaging, immunofluorescence and electrophysiological methods were used to elucidate the GABAergic system in the mouse parotid gland and define its effect on acinar regulation. RT‐PCR identified mRNA transcripts for multiple GABA receptor subunits in enzymatically dispersed acinar cells and immunofluorescence microscopy indicated the expression of GABA receptors in mouse parotid tissue. However, both live cell calcium imaging and whole‐cell recordings of acinar cells revealed no acute impact of GABA or benzodiazepine treatment on cellular physiology. In contrast, immunohistochemical analysis of the autonomic autonomic ganglia and postganglionic innervations to the parotid gland aligned with the identification and characterization of GABA‐evoked chloride currents in a subset of neurons recorded from primary ganglionic cultures. Our data suggest GABA has no direct effect on the parotid acini but may downregulate acinar function by inhibiting neurotransmitter release from autonomic neural inputs. Support or Funding Information This work was funded by National Institutes of Health National Institute of Dental and Craniofacial Research Grant DE‐023418 and bridge funds from the University of Toledo College of Medicine.