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Related Experiment Video

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Desensitization and Recovery of Crayfish Photoreceptors Upon Delivery of a Light Stimulus

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Published on: November 9, 2019

Delayed Antidepressant Efficacy and the Desensitization Hypothesis.

Kathryn G Commons^1,2, Sofia E Linnros^1,2

¹Department of Anesthesiology, Perioperative and Pain Medicine , Boston Children's Hospital , Boston , Massachusetts 02115 , United States.

ACS Chemical Neuroscience

|February 27, 2019

Summary

Conventional antidepressants’ delayed mood effects may not stem from serotonin 5-HT1A receptor desensitization. Other slow-acting changes, possibly in glutamate systems, might explain the therapeutic onset.

Keywords:

Serotonin antidepressants depression feedback fluoxetine glutamate

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Area of Science:

Neuroscience
Pharmacology
Psychiatry

Background:

Conventional antidepressants rapidly increase extracellular serotonin.
Therapeutic mood effects of these drugs are delayed by weeks.
This delay presents a significant clinical challenge.

Purpose of the Study:

To investigate the mechanism behind the delayed efficacy of conventional antidepressants.
To re-evaluate the widely accepted "desensitization hypothesis" regarding 5-HT1A autoreceptors.
To explore alternative explanations for the delayed therapeutic onset.

Main Methods:

Review of existing neurobiological and pharmacological evidence.
Analysis of the role of serotonin 5-HT1A autoreceptors in feedback inhibition.
Examination of evidence for and against the 5-HT1A desensitization hypothesis.

Main Results:

Initial increases in extracellular serotonin engage feedback inhibition via 5-HT1A autoreceptors, reducing neuron firing.
While 5-HT1A receptors may desensitize with chronic treatment, feedback inhibition persists.
Baseline serotonin neuron firing rate returns to normal despite ongoing feedback inhibition.

Conclusions:

The desensitization of 5-HT1A autoreceptors is unlikely to be the primary cause of delayed antidepressant efficacy.
Persistent feedback inhibition suggests other mechanisms are at play.
Slow-adaptive changes, potentially involving glutamatergic synaptic plasticity, may mediate the therapeutic effects of antidepressants.