GABAergic system is also critically involved in cognitive processes, especially memory. Many human and animal studies show that benzodiazepine receptor agonists impair memory formation. Conversely drugs that decrease GABA function can have memory-enhancing properties. Since anxiety conditioning involves both the experience of anxiety and the formation of an association (a form of memory) it can be postulated that inhibition of GABAergic transmission is a powerful mechanism in predisposing an organism to increased and sometimes inappropriate anxiety reactivity. Conversely, increased GABAergic stimulation would be powerfully anxiolytic by inhibiting both the experience of anxiety and the aversive reinforcement. There may be many clinical sequelae from this relationship. Traumatic memories, such as those which occur in post-traumatic stress disorder, are extremely deeply encoded, probably because of the high level of emotion and arousal at the time of the original insult as well as the negative reinforcement on re-experience of the events. Anxiety leads to rapid and profound learning of escape and avoidance behaviours, as in agoraphobia following a panic attack, or anxious avoidance after being bitten by a dog. Apart from animal studies, clinical evidence of reduced GABA in the genesis of anxiety comes from the use of pentylenetetrazol as a convulsant agent before electroconvulsive therapy was introduced in clinical practice. Pentylenetetrazol acts by blocking GABA A receptor function and has been reported to produce extreme anxiety, traumatic memories and extreme avoidance behaviour when used clinically (reviewed in Kalueff & Nutt, 1997 ). Recently, Goddard et al ( 2001 ) have reported decreased