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Published on: October 28, 2019
Antidepressants encounter autophagy in neural cells
1Max Planck Institute of Psychiatry, Chaperone Research Group, Munich, Germany. zschocke@mpipsykl.mpg.de
Autophagy
|June 7, 2011
Summary
Certain antidepressants, like amitriptyline and citalopram, enhance autophagy, a cellular cleaning process, suggesting a new mechanism of action beyond neurotransmitter effects.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Current understanding of antidepressant (AD) mechanisms centers on neurotransmitter systems.
- Emerging evidence suggests ADs may interact with other cellular targets, influencing efficacy and side effects.
- Autophagy, a crucial cellular degradation process, has been implicated but not fully explored as an AD target.
Purpose of the Study:
- To investigate the impact of different classes of antidepressants on autophagy in primary neurons and astrocytes.
- To determine if observed changes in autophagy markers correlate with functional autophagic flux.
- To elucidate the specific pathways, such as phosphoinositide 3-kinase and reactive oxygen species (ROS), involved in AD-induced autophagy.
Main Methods:
- Primary astrocyte and neuron cultures were treated with amitriptyline (AMI), citalopram (CIT), and venlafaxine.
- Autophagy markers, including LC3B-II and Beclin 1, were quantified using Western blotting or similar techniques.
- Autophagic flux was assessed to confirm functional autophagy.
- Involvement of class III PtdIns 3-kinase and ROS pathways was investigated through specific inhibitors or activators.
Main Results:
- Amitriptyline (AMI) and citalopram (CIT) significantly upregulated autophagic markers LC3B-II and Beclin 1 in astrocytes and neurons.
- Venlafaxine did not induce changes in these autophagy markers.
- The autophagy initiated by AMI and CIT was confirmed to be functional, indicating enhanced autophagic flux.
- This functional autophagy was partially dependent on class III PtdIns 3-kinase activity and ROS signaling.
Conclusions:
- Certain antidepressants, specifically amitriptyline and citalopram, modulate cellular autophagy.
- This modulation involves functional autophagic flux and is partially mediated by class III PtdIns 3-kinase and ROS pathways.
- These findings reveal a novel mechanism of antidepressant action independent of traditional monoaminergic neurotransmission.
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