Neurons communicate with each other via gateways known as synapses, with the help of special proteins known as neurotransmitters. The major excitatory neurotransmitter in the brain is known as glutamate, whilst the main inhibitory neurotransmitter is called GABA.

There are two known receptors for GABA within the nervous system; GABAa and GABAb, and these regulate chloride and potassium
ion channels respectively. When GABA acts on either receptor, the effect is essentially the same, but it is achieved slightly differently.

Nerve networks in the brain spontaneously change between persistently active 'up' states and quiet 'down' states. The 'up' states are maintained by recurrent excitation within groups of neurons, and these can be turned on and off, depending on the activity at the synapses within them.

Scientists believe that GABA inhibition is important for stabilising persistent activity, by balancing excitation, and that it might even have a role in stopping 'up' states altogether.

Researchers at the University of Oxford have recently explored these ideas. They developed an experimental model of epilepsy, in which 'up' and 'down' states could be expressed. Interestingly, when the GABAa receptor blocker, gazapine, was applied in the 'up' state, the duration of this state was decreased. The greater the concentration of gazapine (within a set range), the shorter the 'up' state, and this eventually led to epileptic activity. The same experiment was then performed with a GABAb receptor blocker called CGP55845, and this both increased the duration of the 'up' state and prevented any transition to a 'down' state.

These results suggest that GABAa and GABAb receptors have very distinct roles. Rather than suppressing persistent excitation, activation of GABAa receptors appears to stabilise the 'up' state. It seems that activation of GABAb, however, acts to physically end the 'up' state.

This knowledge could be useful in developing more effective GABA-enhancing epilepsy treatments in the future.

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