GABA Metabotropic Receptor

Cross references:    GABA    GABA Gate    GABAA Receptor Evolution    

This page is about the GABA GPCR.  For information on GABA as a ligand for ion channels, please see: 
GABA GateThe introductory paragraphs and diagram, given below, are repeated there. 

gamma-Aminobutyric acid (Wiki) 

GABAB receptor (Wiki) 
"GABAB receptors (GABABR) are metabotropictransmembrane receptors for
gamma-aminobutyric acid (GABA) that are linked via G-proteins to potassium channels.[1] These receptors are found in the central and peripheral autonomic nervous system.[2]

They can stimulate the opening of K+ channels which brings the neuron closer to the equilibrium potential of K+, hyperpolarising the neuron. This prevents sodium channels from opening, action potentials from firing, and VDCCs from opening, and so stops neurotransmitter release. Thus GABAB receptors are considered inhibitory receptors."  

GABA(B) receptor inhibition causes locomotor stimulation in mice  
The present study investigated the effect of the administration of the GABA(B) receptor antagonists, SCH 50911 [(2S)(+)-5,5-dimethyl-2-morpholineacetic acid], CGP 46381 [(3-aminopropyl)(cyclohexylmethyl)phosphinic acid] and CGP 52432 (3-[[(3,4-dichlorophenyl)methyl]amino]propyl]diethoxymethyl)phosphinic acid), on spontaneous locomotor activity in mice. All drugs were acutely administered at the doses of 10 and 30 mg/kg (i.p.). The dose of 30 mg/kg of all drugs resulted in a significant stimulation of locomotor activity. The locomotor stimulation elicited by SCH 50911 was completely blocked by haloperidol (0.1 mg/kg, i.p.), suggesting that hyperactivity induced by blockade of the GABA(B) receptor is mediated by enhanced dopamine release. These results suggest the existence of a GABA(B) receptor-mediated tonic inhibition of dopamine neurons."     

2013    178<2013 
GABAB Receptors Regulate Extrasynaptic GABAA Receptors.  
Tonic inhibitory GABA(A) receptor-mediated currents are observed in numerous cell types in the CNS, including thalamocortical neurons of the ventrobasal thalamus, dentate gyrus granule cells, and cerebellar granule cells. Here we show that in rat brain slices, activation of postsynaptic GABA(B) receptors enhances the magnitude of the tonic GABA(A) current recorded in these cell types via a pathway involving G G proteins, adenylate cyclase, and cAMP-dependent protein kinase. Using a combination of pharmacology and knockout mice, we show that this pathway is independent of potassium channels or GABA transporters. Furthermore, the enhancement in tonic current is sufficient to significantly alter the excitability of thalamocortical neurons. These results demonstrate for the first time a postsynaptic crosstalk between GABA(B) and GABA(A) receptors."     
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