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Noradrenergic transmission in depression: under- or overfunction?
Pharmacopsychiatria
|January 1, 1981
Summary
The noradrenaline hypothesis of depression is reviewed, questioning if antidepressants cause receptor subsensitivity or if it
Area of Science:
- Neuroscience
- Pharmacology
- Psychiatry
Background:
- The noradrenaline hypothesis of depression suggests imbalances in noradrenergic systems.
- Recent theories propose antidepressants reduce postsynaptic beta-adrenergic receptor sensitivity, implying noradrenergic overfunction in depression.
Purpose of the Study:
- To critically assess the noradrenaline hypothesis of depression.
- To evaluate the role of postsynaptic receptor sensitivity changes in antidepressant action.
Main Methods:
- Review and critical analysis of existing evidence on the noradrenaline hypothesis.
- Examination of theories regarding antidepressant mechanisms and receptor sensitivity.
Main Results:
- Evidence supporting the involvement of noradrenergic systems in depression is convincing, though other neurotransmitters are likely involved.
- Postsynaptic receptor subsensitivity after antidepressant treatment is interpreted as a counterregulatory response to increased synaptic noradrenaline, not the primary cause of effect.
Conclusions:
- The overall functional activity of the noradrenergic system, not just pre- or postsynaptic components, is crucial.
- A model is proposed to explain the delayed therapeutic response and non-response to uptake inhibitors in depression treatment.