Few cell lines with GABAA mRNAs have functional receptors

Abstract

In the preceding companion article (Tyndale et al., 1994) we used the PCR to investigate the occurrence of 13 GABAA receptor subunit mRNAs in several cell lines, including those derived from brain (B65, B104, and NB41A3), cerebellum (C17), glia (C6), pituitary (AtT-20), adrenal medulla (PC12), and the endocrine pancreas (RINm5F and beta TC3). In the present study we used the whole-cell configuration of the patch- clamp technique to determine which of these cell lines express functional GABAA receptors. All of the cell lines contain detectable levels of at least one GABAA receptor subunit mRNA (Tyndale et al., 1994); however, only RINm5F and beta TC3 cells exhibited GABA-evoked currents. GABA activated currents in all RINm5F cells, but currents were only barely detectable in 50% of beta TC3 cells tested. Many of the cell lines that failed to respond to GABA were derived from cell types with functional GABAA receptors. For example, the failure of PC12 cells to respond to GABA contrasts with the observation of GABA responses recorded from all primary cultured adrenomedullary chromaffin cells tested. GABA-evoked currents recorded from beta TC3 cells were too small (< 10 pA) to characterize pharmacologically. However, GABA activated robust currents recorded from RINm5F cells. These currents reversed at a holding potential similar to the equilibrium potential for Cl-, were blocked by the antagonist bicuculline methiodide (10 microM), and were potentiated by pentobarbital (100 microM). RINm5F cell GABAA receptors were insensitive to diazepam (10 microM) and were inhibited by Zn2+ (10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Etifoxine improves peripheral nerve regeneration and functional recovery

“…That etifoxine exerts neurotrophic effects by acting directly on neurons was shown in cultures of PC12 cells, where the drug caused a striking outgrowth of neurites. PC12 cells contain functional TSPO binding sites but do not express functional GABA A receptors (24)(25)(26)(27). In agreement, neurite extension in PC12 cells was sensitive to selective TSPO ligands but not to an agonist or an antagonist of GABA A receptors.…”

Glial cells have heart: rH1 Na+ channel mRNA and protein in spinal cord astrocytes

“…Regulation of receptor gene expression occurs at the post-transcriptional or post-translational levels in certain neurons, including neurons which express GABA A (Hales and Tyndale, 1994) and NMDAR1 (Sucher et al, 1993) mRNAs but do not express functional receptors on their surface membranes. The apparent cytoplasmic distribution of rH1 protein in spinal cord astrocytes, in some cases limited to the perinuclear portion of the cytoplasm, is consistent with sequestration of rH1 protein, or of partially processed protein, within a cytoplasmic compartment such as the Golgi apparatus.…”

Glucose-Dependent Regulation of γ-Aminobutyric Acid (GABAA) Receptor Expression in Mouse Pancreatic Islet α-Cells

“…The presence of several GABA A R subunits has been described in guinea pig (21), human (␣2, ␤3, ␥1) (31), and rat (␣1, 4; ␤1, 2, 3 [22], ␣1, 2, 3; ␤1, 2, 3; ␥1, 2; ␦ [32], and ␣1, 2; ␤1; ␥2 [33]) pancreatic tissue as well as in insulinoma cell lines (33)(34)(35), though in only a few instances has cell surface expression of GABA A R subunit protein been demonstrated. However, it is not known whether pancreatic GABA A Rs are subject to the same plasticity of expression seen in neuronal GABA A Rs.…”