Do anxiety and depression have a
common pathophysiological mechanism?
by
Boyer P
Paris 7 University,
Hopital de La Pitie-Salpetriere, France.
Acta Psychiatr Scand Suppl 2000;(406):24-9

ABSTRACT

OBJECTIVE: To review, examine and propose a common mechanism for anxiety and depression based on modifications observed in neurotransmitter systems (mainly noradrenergic and serotonergic) and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. METHOD: The relevant papers were identified by searches in Medline, Excerpta Medica, PsychLIT and other databases. The primary reports were reviewed and classified into animal and human data concerning: modifications of the monoamine receptors in anxiety and depression, pathophysiology of endocrine factors in anxiety and depression, pathophysiology of the hypothalamic-pituitary-adrenal (HPA) axis and the pathophysiology of the HPA dysregulation in anxiety and in depression. In addition, a proposed model of a neuroendocrine continuum for anxiety and depression, in which anxiety occurs first during the life course and major depressive episodes occur later, was examined. RESULTS: Based on the available literature, increased concentrations of corticotropin-releasing factor (CRF) in the cerebrospinal fluid has been reported in both anxiety and depression. However, release of other peptides or hormones of the HPA axis is regulated differently in the two disorders. Anxiety is characterized by hypocortisolemia, supersuppression after dexamethasone and increased numbers of glucocorticoid receptors, whereas depression is characterized by hypercortisolemia, nonsuppression after dexamethasone and decreased numbers of glucocorticoid receptors. A 'neuroendocrine continuum' model is proposed to explain these differences. A general desensitization of CRF receptors at pituitary, limbic (amygdala) and cortical as well as hippocampal levels could be secondary to the loss of hippocampal inhibition resulting from hippocampal damage linked to repeated stressing events. CONCLUSION: The proposed hypothesis remains to be tested by examination of either the changes in receptors and neurotransmission or the mechanisms underlying the dysregulation of endocrine factors.

GAD
SSRIs
Stress
Anxiety
Gepirone
Buspirone
Alprazolam
Adinazolam
Barbiturates
Benzodiazepines
Future anxiolytics
Sedative hypnotics
Subthreshold syndromes
Anxious golden hamsters
Buspirone plus venlafaxine
Anxiolytics/antidepressants
Anxiolytics and antidepressants
Neurobiology and genetics of anxiety
Types of depression and mood-disorder
Anxioselective compounds and GABA(A)
GABAergic dysfunction in mood disorders
Stress, dynorphin, dysphoria and the kappa opioid system

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