Several studies of the pharmacology of behaviour conducted on rodents have revealed that mechanisms involved in anxiety were also found in epilepsy, body balance control and certain mnesic processes. This is probably due to the widespread presence of GABA, a cerebral transmitter which plays a role in all these phenomena. An analysis of the findings suggests the hypothesis that mild anxiety is part of normal brain function.
Anxiety is a vast physiological phenomenon which can be evidenced in both humans and a number of animal species. Normal anxiety is the response of the nervous system to a potentially dangerous stimulus, allowing subjects to fight or flee in such dangerous circumstances. Anxiety can be excessive or pathological when it appears with no direct relation to a potentially dangerous stimulus . But even when seen from this point of view, anxiety is far from being a single phenomenon. Normal anxiety is often divided into trait-anxiety and state-anxiety [2,3,4]. Trait-anxiety is a stable character trait in an individual, either human or animal, whereas state-anxiety is a temporary burst of anxiety induced by an anxiogenic event. The fourth edition of the Diagnostic and Statistical Manual (DSM-IV)  divided pathological anxiety in humans into seven types of anxiety disorders: obsessive compulsive disorders, post-traumatic stress, phobias, agoraphobia, panic disorders, social phobias and generalised anxiety.
When anxiety is viewed as a complex phenomenon , it is not surprising to see that it can be related to several brain processes. The present paper will show the pharmacological studies can highlight a relationship between anxiety processes and epileptic disorders, body balance control and memory processes. In fact, a number of classical arguments already support such hypotheses: limbic structures have been shown to be involved in anxiety , epileptic disorders [8,9], perception of space  and memory processes [11,12,13,14]. The argument to be presented here is that these processes are extensively related, as observed at the molecular level, in the transmitter systems which make the brain “work”, and specifically in the ubiquitous transmitter, GABA.
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