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Amisulpride alleviates chronic mild stress-induced cognitive deficits: Role of prefrontal cortex microglia and

Ahmed M Mohamed1, Mohamed Z Habib1, Mai A Ebeid1

  • 1Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

European Journal of Pharmacology
|August 18, 2020
PubMed

Insights

Amisulpride treatment improved depressive-like behaviors and cognitive deficits in rats by modulating the Wnt/β-catenin pathway and reducing neuroinflammation via microglial activation.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Psychiatry

Background:

  • Neuroinflammation and microglial activation are implicated in cognitive dysfunction and depression.
  • The Wnt/β-catenin pathway plays a role in regulating microglia-mediated neuroinflammation.
  • Amisulpride has demonstrated antidepressant and pro-cognitive effects, but its direct impact on Wnt/β-catenin signaling and microglial activity requires further investigation.

Purpose of the Study:

  • To investigate the effects of chronic amisulpride treatment on Wnt/β-catenin signaling and pro-inflammatory microglial activation.
  • To determine if amisulpride alleviates depressive-like behavior and cognitive deficits induced by unpredictable chronic mild stress (UCMS).

Main Methods:

  • Male Wistar rats were subjected to unpredictable chronic mild stress (UCMS) to induce depressive-like behavior and cognitive deficits.
  • The effects of chronic amisulpride treatment (3 mg/kg/day) were assessed on behavioral and cognitive performance.
  • Wnt/β-catenin pathway expression and microglial activation in the prefrontal cortex (PFC) were analyzed.

Main Results:

  • UCMS induced depressive-like behavior and cognitive impairments, characterized by decreased total β-catenin and increased pro-inflammatory microglial activation in the PFC.
  • Amisulpride treatment significantly improved behavioral and cognitive deficits in UCMS-exposed rats.
  • Amisulpride ameliorated the dysregulation of Wnt/β-catenin signaling and reduced pro-inflammatory microglial activation.

Conclusions:

  • Amisulpride exhibits antidepressant and pro-cognitive effects in a rat model of depression.
  • These effects are potentially mediated through the modulation of the Wnt/β-catenin pathway and the reduction of pro-inflammatory microglial activation in the prefrontal cortex.
Keywords:
AmisulprideCognitive dysfunctionDepressionMicrogliaNeuroinflammationWnt/β catenin pathway

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