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Effect of liposome entrapped‐GABA on the expression of nNOS and GABAA receptors in neurons (1130.11)
Author(s) -
Vaz Gisele,
Sharma Neeru,
Zheng Hong,
Bahia Ana Paula,
Zimmerman Matthew,
Frezard Frederic,
Fontes Marco,
Patel Kaushik
Publication year - 2014
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.28.1_supplement.1130.11
Subject(s) - gabaa receptor , neurotransmitter , receptor , chemistry , liposome , inhibitory postsynaptic potential , immunostaining , pharmacology , medicine , endocrinology , biology , biochemistry , immunohistochemistry
Liposomes are concentric lipid vesicles that allow a sustained release of entrapped substances. GABA is the most prevalent inhibitory neurotransmitter in the central nervous system. Here we determined the effect of sustained release of GABA on the expression of neuronal nitric oxide synthase (nNOS) and GABAA receptor (GABAAR) in a neuronal culture (NG108‐15 cells). GABA entrapped‐liposomes particles (GEL) were prepared by the freeze‐thawing method. In vitro studies using NG108‐15 neurons treated with different doses of GEL for 12 hr showed an increase in nNOS (138, 157 and 165% at doses of 20, 50 and 100 ng respectively) and GABAAR (54 and 50% at the doses of 10 and 20 ng respectively) compared with control. Moreover, we found a decreased expression of protein inhibitor of nNOS (PIN) with GEL treatment (26, 66 and 57% at doses of 20, 50 and 100 ng, respectively). Time course experiments in cells treated with 50 ng of GEL, showed an increase in GABAAR (23%) after 1 hr followed by an increase in nNOS (55, 46 and 55%) and decrease in PIN (22, 28 and 53%) at 8, 12, 24 hr, respectively. Immunostaining also showed an increase in nNOS expression (134%) in cells after 12 hr of GEL treatment. These results suggest that the slow release of GABA can change the expression of nNOS in neuronal cultures, potentially by altering the expression of PIN. Supported by NIH grants HL62222 & DK82956 & CNPq fellowship to GCV. Grant Funding Source : NIH grants HL62222 & DK82956 & CNPq fellowship to GCV