Serotonin 1B Receptors Regulate Prefrontal Function by Gating Callosal and Hippocampal Inputs.
Celia Kjaerby1, Jegath Athilingam1, Sarah E Robinson1
1Department of Psychiatry, University of California, San Francisco, San Francisco, CA 94143-0444, USA; Weil Institute for Neurosciences, University of California, San Francisco, San Francisco, CA 94143-0444, USA; Kavli Institute for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94143-0444, USA; Sloan-Swartz Center for Theoretical Neurobiology, University of California, San Francisco, San Francisco, CA 94143-0444, USA.
Serotonin suppresses specific brain inputs to the medial prefrontal cortex (mPFC) via 5-HT1B receptors, reducing anxiety-like behaviors in mice by altering neural activity patterns.
Area of Science:
- Neuroscience
- Behavioral Neuroscience
- Molecular Psychiatry
Background:
- The medial prefrontal cortex (mPFC) and serotonin are crucial in regulating anxiety.
- The precise mechanisms by which serotonin influences mPFC function to control anxiety remain unclear.
Purpose of the Study:
- To investigate how serotonin modulates mPFC activity and anxiety-related behaviors.
- To identify the specific serotonin receptors and neural pathways involved.
Main Methods:
- Utilized optogenetics and synaptic physiology in mice.
- Infused a 5-HT1B receptor agonist into the mPFC.
- Measured neural activity and anxiety-like behaviors using the elevated plus maze.
Main Results:
- Serotonin selectively suppresses inputs to the mPFC from the contralateral mPFC and ventral hippocampus (vHPC) via presynaptic 5-HT1B receptors.
- Activating mPFC 5-HT1B receptors reduced theta-frequency mPFC activity.
- This activation also decreased avoidance of anxiogenic areas in the elevated plus maze.
Conclusions:
- Serotonin regulates prefrontal circuit function and anxiety-related behaviors through 5-HT1B receptor-mediated suppression of specific inputs.
- Findings link specific receptors, synaptic actions, neural activity patterns, and behavior.
- This provides a potential mechanism for serotonin's role in anxiety modulation.
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