Abstract
Gamma amino butyric acid (GABA), the principal inhibitory neurotransmitter in the cerebral cortex, maintains the inhibitory tones that counter balances neuronal excitation. When this balance is perturbed, seizures may ensue. In the present study, alterations of the general GABA, GABAA and GABAB receptors in the cerebral cortex of the epileptic rat and the therapeutic application of Bacopa monnieri were investigated. Scatchard analysis of [3H]GABA, [3H]bicuculline and [3H]baclofen in the cerebral cortex of the epileptic rat showed significant decrease in Bmax (P < 0.001) compared to control. Real Time PCR amplification of GABA receptor subunits such as GABAAά1, GABAAγ, GABAAδ, GABAB and GAD where down regulated (P < 0.001) in epileptic rats. GABAAά5 subunit and Cyclic AMP responsible element binding protein were up regulated. Confocal imaging study confirmed the decreased GABA receptors in epileptic rats. Epileptic rats have deficit in radial arm and Y maze performance. Bacopa monnieri and Bacoside-A treatment reverses epilepsy associated changes to near control suggesting that decreased GABA receptors in the cerebral cortex have an important role in epileptic occurrence; Bacopa monnieri and Bacoside-A have therapeutic application in epilepsy management.
Highlights
Gamma amino butyric acid (GABA), the principal inhibitory neurotransmitter in the cerebral cortex, maintains the inhibitory tones that counter balances neuronal excitation
Bacopa monnieri and Bacoside-A treatment reverses epilepsy associated changes to near control suggesting that decreased GABA receptors in the cerebral cortex have an important role in epileptic occurrence; Bacopa monnieri and Bacoside-A have therapeutic application in epilepsy management
Glutamate decarboxylase (GAD) is the rate limiting enzyme of GABA synthesis and it is used as a marker for GABAergic activity [6]. cAMP response element-binding protein (CREB) is a transcription factor that has been implicated in the activation of protein synthesis required for long-term memory and seizure formation [7]
Summary
Gamma amino butyric acid (GABA), the principal inhibitory neurotransmitter in the cerebral cortex, maintains the inhibitory tones that counter balances neuronal excitation. When this balance is perturbed, seizures may ensue. CAMP response element-binding protein (CREB) is a transcription factor that has been implicated in the activation of protein synthesis required for long-term memory and seizure formation [7]. Findings shows that GABAB receptor subunit gene expression in hippocampal neurons is mediated through the CREB by binding to unique cAMP response elements in the alternative promoter regions [8]. Radial arm maze is a means to examine the neural systems that are involved in memory and the influence of pharmacological compounds on memory [9,10]. Y-maze used to evaluate the spatial learning by the different animal models of the rats [11]
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