Cell Signaling Technology

Product Pathways - Neuroscience

GABA(B)R2 Antibody #3839

Applications Reactivity Sensitivity MW (kDa) Source
W IP H M R Endogenous 105 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

GABA(B)R2 Antibody detects endogenous levels of total GABA(B)R2 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to human GABA(B)R2. Antibodies are purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse and rat brain using GABA(B)R2 Antibody.

Background

GABA (γ-aminobutyric acid) is the primary inhibitory neurotransmitter in the central nervous system and interacts with three different receptors: GABA(A), GABA(B) and GABA(C) receptor. The ionotropic GABA(A) and GABA(C) receptors are ligand-gated ion channels that produce fast inhibitory synaptic transmission. In contrast, the metabotropic GABA(B) receptor is coupled to G proteins that modulate slow inhibitory synaptic transmission (1). Functional GABA(B) receptors form heterodimers of GABA(B)R1 and GABA(B)R2 where GABA(B)R1 binds the ligand and GABA(B)R2 is the primary G protein contact site (2). Two isoforms of GABA(B)R1 have been cloned: GABA(B)R1a is a 130 kD protein and GABA(B)R1b is a 95 kD protein (3). G proteins subsequently inhibit adenyl cylase activity and modulate inositol phospholipid hydrolysis. GABA(B) receptors have both pre- and postsynaptic inhibitions: presynaptic GABA(B) receptors inhibit neurotransmitter release through suppression of high threshold calcium channels, while postsynaptic GABA(B) receptors inhibit through coupled activation of inwardly rectifying potassium channels. In addition to synaptic inhibition, GABA(B) receptors may also be involved in hippocampal long-term potentiation, slow wave sleep and muscle relaxation (1).

  1. Jones, K.A. et al. (2000) Neuropsychopharmacology 23, S41-9.
  2. Duthey, B. et al. (2002) J Biol Chem 277, 3236-41.
  3. Kaupmann, K. et al. (1997) Nature 386, 239-46.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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