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. 2010 May 6;44(2):222–229. doi: 10.1165/rcmb.2010-0109OC

Figure 1.

Figure 1.

Detection and expression of GABAA receptors in monkey in cultured bronchial epithelial cells (BECs) in vivo and in vitro. (A) RT-PCR indicated the presence of glutamate decarboxylase (GAD)67, GABAA receptors α2, α5, β1, β3, ρ, and γ2, GAT1, GAT3, and GABAA receptor-associated protein (GABARAP). Monkey cortex was included as a positive control. No bands were evident in negative control (water), which lacked input RNA. (B) Real-time PCR analysis of the effect of nicotine exposure (1 μM for 48 hours) on GAD, GABAA receptors γ2, β2, β1, and α5, GAT1, and GAT3 mRNA levels in BECs. The nicotinic acetylcholine receptor (nAChR) antagonists mecamylamine (Mec; 25 μM) and methyllycaconitine (MLA; 30 nM) inhibited the nicotine-induced increases in GAD, GABAA receptors γ2, β2, β1, and α5, GAT1, and GAT3 mRNA concentrations in BECs. *P < 0.05, **P < 0.01, and ***P < 0.005 for nicotine exposure compared with controls. (C) Immunohistochemical detection of GABAA receptor α5 expression in control cultured BECs and in cultured BECs incubated with 1 μM nicotine for 48 hours. GABRA, GABA receptor A.