Mechanisms of GABA-A and GABA-B receptor gene expression

DAVID FARB,; JANINE STEIGER,; MARIA CLARA GRAVIELLE; STELLA MARTIN,; TERRELL GIBBS,; SHELLEY RUSSEK,

The GABA receptor

The Humana Press

Lugar: New York; Año: 2007; p. 1 - 1

g-Aminobutyric acid (GABA) is the primary inhibitory transmitter in the adult nervous system and can activate three classes of receptors: metabotropic type A GABA (GABAA), metabotropic type B GABA (GABAB), and metabotropic type C GABA (GABAC) (for review see refs. 1–3). The ligandgated GABAA receptor (GABAA R) is a pentameric complex assembled from eight subunit families defined by amino acid (aa) sequence homology: á1–6, adult nervous system and can activate three classes of receptors: metabotropic type A GABA (GABAA), metabotropic type B GABA (GABAB), and metabotropic type C GABA (GABAC) (for review see refs. 1–3). The ligandgated GABAA receptor (GABAA R) is a pentameric complex assembled from eight subunit families defined by amino acid (aa) sequence homology: á1–6, metabotropic type C GABA (GABAC) (for review see refs. 1–3). The ligandgated GABAA receptor (GABAA R) is a pentameric complex assembled from eight subunit families defined by amino acid (aa) sequence homology: á1–6, GABAA receptor (GABAA R) is a pentameric complex assembled from eight subunit families defined by amino acid (aa) sequence homology: á1–6, eight subunit families defined by amino acid (aa) sequence homology: á1–6, â1–3, ã1–3, ä, å, ð, è, and ñ1–3. With the availability of powerful molecular tools, the cloning of GABAA Rs led to the discovery that each subunit is encoded by a distinct gene and most genes are organized in â-á-á-ã and â-á-1–3, ã1–3, ä, å, ð, è, and ñ1–3. With the availability of powerful molecular tools, the cloning of GABAA Rs led to the discovery that each subunit is encoded by a distinct gene and most genes are organized in â-á-á-ã and â-á-A Rs led to the discovery that each subunit is encoded by a distinct gene and most genes are organized in â-á-á-ã and â-á-â-á-á-ã and â-á- ã gene clusters on different chromosomes (4,5). Alternative splicing and alternative promoters generate additional heterogeneity in GABAA-R subunit variants that may allow for the assembly of thousands of possible pentameric combinations. In contrast, the metabotropic GABAB R is made up of two distinct subunits GABABR1 and GABABR2. It is now clear that the most abundant GABABR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).gene clusters on different chromosomes (4,5). Alternative splicing and alternative promoters generate additional heterogeneity in GABAA-R subunit variants that may allow for the assembly of thousands of possible pentameric combinations. In contrast, the metabotropic GABAB R is made up of two distinct subunits GABABR1 and GABABR2. It is now clear that the most abundant GABABR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).A-R subunit variants that may allow for the assembly of thousands of possible pentameric combinations. In contrast, the metabotropic GABAB R is made up of two distinct subunits GABABR1 and GABABR2. It is now clear that the most abundant GABABR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).B R is made up of two distinct subunits GABABR1 and GABABR2. It is now clear that the most abundant GABABR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).BR1 and GABABR2. It is now clear that the most abundant GABABR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).BR1 isoforms (GABABR1a and GABABR1b) are produced by alternative promoters in the GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).GABABR1 gene (6), and there is no evidence for GABAB2 variants (7).B2 variants (7).