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Mice with compromised 5-HTT function lack phosphotyrosine-mediated inhibitory control over prefrontal 5-HT responses. | LitMetric

Mice with compromised 5-HTT function lack phosphotyrosine-mediated inhibitory control over prefrontal 5-HT responses.

J Neurosci

Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada, Department of Psychiatry, Columbia University, New York, New York 10032, and Department of Obstetrics and Gynaecology, University of Toronto, Toronto, Ontario M5S 1A8, Canada.

Published: April 2014

AI Article Synopsis

  • The prefrontal cortex's activity is crucial for processing emotions and is influenced by serotonin (5-HT), but the specific mechanisms affecting 5-HT receptor function are not well understood.
  • Research on mouse models with disrupted serotonin transporter (5-HTT) function revealed changes in how 5-HT receptors signal electrically in the prefrontal cortex.
  • A new mechanism involving tyrosine kinase was discovered that impacts 5-HT1A receptor activity, suggesting a link between these receptors and emotional disorders like anxiety and depression.

Article Abstract

The activity of the prefrontal cortex is essential for normal emotional processing and is strongly modulated by serotonin (5-HT). Yet, little is known about the regulatory mechanisms that control the activity of the prefrontal 5-HT receptors. Here, we found and characterized a deregulation of prefrontal 5-HT receptor electrophysiological signaling in mouse models of disrupted serotonin transporter (5-HTT) function, a risk factor for emotional and cognitive disturbances. We identified a novel tyrosine kinase-dependent mechanism that regulates 5-HT-mediated inhibition of prefrontal pyramidal neurons. We report that mice with compromised 5-HTT, resulting from either genetic deletion or brief treatment with selective serotonin reuptake inhibitors during development, have amplified 5-HT1A receptor-mediated currents in adulthood. These greater inhibitory effects of 5-HT are accompanied by enhanced downstream coupling to Kir3 channels. Notably, in normal wild-type mice, we found that these larger 5-HT1A responses can be mimicked through inhibition of Src family tyrosine kinases. By comparison, in our 5-HTT mouse models, the larger 5-HT1A responses were rapidly reduced through inhibition of tyrosine phosphatases. Our findings implicate tyrosine phosphorylation in regulating the electrophysiological effects of prefrontal 5-HT1A receptors with implications for neuropsychiatric diseases associated with emotional dysfunction, such as anxiety and depressive disorders.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3996227PMC
http://dx.doi.org/10.1523/JNEUROSCI.3762-13.2014DOI Listing

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