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Somatostatin receptor subtype 4 modulation of L‐type Ca 2+ channels in rat retinal ganglion cells
Author(s) -
Farrell Spring,
Brecha Nicholas,
Barnes Steven
Publication year - 2011
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.25.1_supplement.1081.6
Subject(s) - somatostatin receptor , somatostatin , chemistry , somatostatin receptor 1 , receptor , retinal , endocrinology , neuroscience , microbiology and biotechnology , somatostatin receptor 2 , medicine , biology , biochemistry
Preventing retinal ganglion cell (RGC) loss could improve outcomes in retinal disease or injury. Studies suggest that somatostatin may be beneficial in some retinal diseases. As RGCs are the only cell type in the retina that express sst 4 , a better understanding of the sst 4 signaling pathway may provide a selective therapeutic target in retinal disease. The aim of the present study was to examine the signaling pathways involved in sst 4 stimulation in RGCs. Experiments used whole‐cell patch clamp techniques to isolate I Ca in isolated rat RGCs. L‐803,087 (selective sst 4 agonist, L‐803) suppressed I Ca by 39% compared to control. Pretreatment with pertussis toxin (G i/o inhibitor, PTX) had no effect on basal I Ca amplitudes or the ability of L‐803 to suppress I Ca . Administration of L‐803 in GF109203X (GFX, a PKC antagonist) pretreated cells showed similar suppression of I Ca compared to cells not pretreated with GFX. These results suggest that suppression of I Ca by L‐803 is not mediated by a G i/o signaling pathway, nor is it mediated by the actions of PKC (G q signaling pathway). Ongoing studies are examining a potential role of βγ subunits in the modulation of Ca 2+ channels by sst 4 . Support from CIHR‐NSHRF RPP, NIH.