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Background <p>Major depressive disorder is a prevalent and debilitating psychiatric condition. Understanding its molecular mechanisms can aid in the development of more effective treatments. Gap junctions (GJs), composed of connexin (CX) proteins, facilitate direct intercellular communication and have been implicated in the pathophysiology of depression. In particular, connexin 36 (CX36) and connexin 43 (CX43) play key roles in neuronal and glial interactions, respectively. This study aimed to investigate whether fluoxetine modulates the expression of <i>CX36</i> and <i>CX43</i> in specific limbic regions, including the ventral hippocampus (v Hip), medial prefrontal cortex (m PC), and basolateral amygdala (BLA) of rats subjected to chronic unpredictable stress (CUS).</p> Methods and results <p>Adult male <i>Wistar</i> rats (<i>n</i> = 7 per group) were assigned to control, CUS, and CUS + fluoxetine groups. Our results revealed that <i>CX36</i> expression was significantly reduced in the v Hip and m PC of CUS rats (<i>P</i> &lt; 0.05), while <i>CX43</i> expression was significantly lower in all examined brain regions compared to controls (<i>P</i> &lt; 0.05, <i>P</i> &lt; 0.001). Fluoxetine administration significantly upregulated both <i>CX36</i> and <i>CX43</i> expression across all regions compared to the CUS group (<i>P</i> &lt; 0.05).</p> Conclusions <p>These findings suggest that fluoxetine may exert part of its antidepressant effects by modulating gap junction communication, highlighting a potential novel mechanism for fluoxetine action in depression.</p>

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Antidepressant effects of fluoxetine: upregulation of connexin 36 and 43 in the hippocampus, prefrontal cortex, and amygdala

  • 期刊论文

  • 发表日期：

    2025年6月11日

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  • Saeidreza Hosseinirezaabad,
  • Sahel Motaghi,
  • Manijeh Dogani,
  • Masoud Teimouri

摘要

Background

Major depressive disorder is a prevalent and debilitating psychiatric condition. Understanding its molecular mechanisms can aid in the development of more effective treatments. Gap junctions (GJs), composed of connexin (CX) proteins, facilitate direct intercellular communication and have been implicated in the pathophysiology of depression. In particular, connexin 36 (CX36) and connexin 43 (CX43) play key roles in neuronal and glial interactions, respectively. This study aimed to investigate whether fluoxetine modulates the expression of CX36 and CX43 in specific limbic regions, including the ventral hippocampus (v Hip), medial prefrontal cortex (m PC), and basolateral amygdala (BLA) of rats subjected to chronic unpredictable stress (CUS).

Methods and results

Adult male Wistar rats (n = 7 per group) were assigned to control, CUS, and CUS + fluoxetine groups. Our results revealed that CX36 expression was significantly reduced in the v Hip and m PC of CUS rats (P < 0.05), while CX43 expression was significantly lower in all examined brain regions compared to controls (P < 0.05, P < 0.001). Fluoxetine administration significantly upregulated both CX36 and CX43 expression across all regions compared to the CUS group (P < 0.05).

Conclusions

These findings suggest that fluoxetine may exert part of its antidepressant effects by modulating gap junction communication, highlighting a potential novel mechanism for fluoxetine action in depression.