5HT1A receptors) desensitize, allowing the increased neurotransmitter levels to have their effect. Recent attempts to visualize this mechanism have demonstrated that using PET techniques, there can be a 30-40% decrease in the surface dendritic expression of 5HT1A receptors following fluoxetine treatment.90 Thus, use of specific PET probes may provide a viable and rapid means of assessing the potential of antidepressant therapy in any given individual and may serve as a surrogate marker for efficacy. Recent work has provided evidence that the delayed onset of action of antidepressants is dependent on hippocampal neurogenesis.91 Treatment of mice with SSRIs or SNRIs increased the differentiation of hippocampal progenitor cells into neurons over a time course consistent with the onset of anxiolytic activity; focal hippocampal irradiation to deplete dividing cells prevented the anxiolytic-like effects. Evidence suggests that 5HT1A receptors may mediate these effects along with brain-derived growth factor.

Amongst the SNRIs that have also been developed for depression and other disorders, venlafaxine and nefazedone are used in anxiety disorders, and an extended release formulation of venlafaxine was recently approved for use in GAD (see Figure 7).

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