GABA B receptor

GABAB receptors (GABABR) are metabotropic transmembrane receptors that are linked via G-proteins to potassium channels (Chen et al., 2005). These receptors are found in the central and peripheral autonomic nervous system (Martin and Dunn, 2002). 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 VOCCs from opening, and so stops neurotransmitter release. Thus GABAB receptors are considered inhibitory receptors.

GABAB receptors can also reduce the activity of adenylyl cyclase and  decrease the cell’s conductance to Ca2+ (Siegel et al., 1999; Martin and Dunn, 2002).

GABAB receptors are involved in behavioral actions of ethanol, gamma-hydroxy butyric acid (GHB; "rape drug"), and possibly in pain. Recent research suggests that these receptors may play an important developmental role.

GABABRs are similar in structure to and in the same receptor family with metabotropic glutamate receptors (MRC, 2003). There are two subtypes of the receptor, GABAB1 and GABAB2 (Purves et al., 2001; Martin and Dunn, 2002), and these appear to assemble as heterodimers in neuronal membranes by linking up by their intracellular C termini (Martin and Dunn, 2002; MRC, 2003). It is speculated that binding of GABA causes the subunits to swing shut around the agonist like a venus fly trap (Martin and Dunn, 2002).

Baclofen is a GABA analogue selective for GABAB receptors used as a muscle relaxant. However, it can aggravate absence seizures, and so is not used in epilepsy. Saclofen and phaclofen are selective antagonists.