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benzodiazepine receptor complex

This subject is central to any discussion of anxiety and its treatment. Gamma aminobutyric acid (GABA) is probably the most important inhibitory transmitter in the central nervous system. GABAergic neurones are distributed widely in the CNS but are virtually absent outside the brain and the spinal cord. GABA controls the state of excitability in all brain areas and the balance between excitatory inputs (mostly glutamatergic) and the inhibitory GABAergic activity determines the prevailing level of neuronal activity. If the balance swings in favour of GABA, then sedation, amnesia, muscle relaxation and ataxia appear and nervousness and anxiety are reduced. The mildest reduction of GABAergic activity elicits arousal, anxiety, restlessness, insomnia and exaggerated reactivity.

When GABA binds with the GABAA-benzodia-zepine receptor complex, the permeability of the central pore of the receptor to chloride ions increases, allowing more ions into the neurone and decreasing excitability. Classical benzodiazepines (BDZs) in clinical use enhance the effectiveness of GABA by lowering the concentration of GABA required for opening the channel, so enabling the GABAergic circuits to produce a larger inhibitory effect (Fig. 19.4). These drugs are agonists at the receptor and there is an antagonist (flumazenil) which prevents agonists from binding at the receptor site and enhancing GABA function.

Drugs that act as agonists at this receptor are used mostly but not exclusively in sleep and anxiety disorders. Benzodiazepines (see later) have hypnotic, sedative, anxiolytic, anticonvulsant and (central) muscle relaxant actions. They form a significant but not the only part of available pharmacological treatments, as the following account will illustrate.

Ben zodiazepines, Zopiclone Zolpidem, Zaleplon

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