| Temporal lobe epilepsy (TLE), one of the most common partial epileptic syndromes, is considered as intractable epilepsy (EP). Some patients have the most severe form of epilepsy with poor outcome even treated with drugs with different mechanisms. Therefore, it is necessary to further understand the mechanisms of its epileptogensis and its interference with drugs. Epileptic seizures can be considered as paroxysmal hypeysynchronous transient electrical discharges in the brain that is resulted from too much excitation or too little inhibition in the area in which the abnormal discharge starts. γ -Aminobutyric acid (GABA) is now recognized as the principal inhibitory neurotransmitter in the cerebral cortex,and serves to maintain inhibitory tone that counterbalances neuronal excitation. When this balance is perturbed, seizures may ensue. Recently, a strong correlation between GABA receptors and intrinsic epileptogenesis has been paid a lot attention by researchers. GABA exerts its effects through the activation of GABAa, GABAb and GABAc receptors. The GABAA/C receptors are ionotropic, i.e. ligand-gated ion channels, which induce rapid synaptic inhibition upon activation. In contrast, the metabotropic GABAb receptor couples to G proteins to produce longer lasting inhibitory signals. Functionally, GABAb receptors are suggested to play a key role in several neurological functions and disorders and hence they are attractive targets to treatment. In this study, in order to understand the role of GABAbR and possible adaptive changes of GABABR in TLE, we investigated the expression of GABAb receptor (GABAbR) subunit (GBRla and GBR2) in hippocampus of kainic-acid (KA) induced epileptic rats using in situ hybridization and immunocytochemistry. We further examined the effects of GABABR agonist, such as baclofen, on the expression GABAB receptor. This study could provide us a possible mechanism of EP at the molecular level.
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