Hippocampus anxiety disorders

Many patients with anxiety disorders experience an increased susceptibihty to psychosocial stress. Behavioral sensitization may account for these cHnical phenomena, hi the laboratory model of sensitization, single or repeated exposure to physical stimuU or pharmacological agents sensitizes an animal to subsequent stressors (reviewed in Charney et al. 1993). For example, in animals with a history of prior stress, there is a potentiated release of NE in the hippocampus with subsequent exposure to stressors (Nisenbaum et al. 1991). Similar findings were observed in medial prefrontal cortex (Finlay and Abercrombie 1991). The hypothesis that sensitization is underlying neural mechanism contributing to the course of anxiety disorders is supported by clinical studies demonstrating that repeated exposure to traumatic stress is an important risk factor for the development of anxiety disorders, particularly PTSD (Table 1). 

All these data involved the hippocampus, a structure traditionally involved in learning and memory, and adult neurogenesis in depression and anxiety disorders (Thomas and Peterson, 2003). Antidepressant treatments may increase neural plasticity and adult neurogenesis, especially in the hippocampus. However, the neurogenic theory of depression remains the source of debate and controversy, and requires further study (Feldmann et al.,... 

A deficit in GABAa receptors has been identified in the hippocampus and parahippocampus of patients with panic disorder and generalized anxiety disorders (96-98). Also, GABAa receptor antagonists elicit anxiety in patients with panic disorder, which suggests an underlying deficit in receptor function in these individuals (99). 

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