Abstract

CALIXTO, Eduardo. The GABA withdrawal: 20 years of a hyperexcitability neuronal model. Salud Ment [online]. 2012, vol.35, n.5, pp.427-434. ISSN 0185-3325.

The sudden interruption of increase in the concentration of the synaptic cleft of the inhibitory neurotransmitter in the cerebral cortex, the γ-amino butyric acid (GABA), determines an increase in the neuronal activity. GABA withdrawal is a heuristic analogy with withdrawal symptoms developed by other GABA receptor-agonists such as benzodiazepines, barbiturates, neurosteroids and alcohol. GABA withdrawal is a model of neuronal hyperexcitability in complete animal validated by EEG, in which complex spikes-wide of high- frequency and amplitude appear. In brain slices, GABA withdrawal was identified by increased firing synchronization of pyramidal neurons and by changes in the active properties of the neuronal membrane. The increase in neuronal excitability of this model is the result of dynamic changes in consecutive pre- and post-synaptic components such as: a) the decrease in the synthesis/release of GABA; b) the decrease in the expression and composition of GABA_A receptors associated with increased calcium entry into the cell. This model is an excellent bioassay to study partial epilepsy, epilepsy refractory to drug treatment and a model to reverse or prevent the generation of abstinence from different drugs.

Keywords : GABA; hyperexcitability; withdrawal.

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