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Anticholinesterase Agents: Poisoning and Treatment01:26

Anticholinesterase Agents: Poisoning and Treatment

Anticholinesterases, also known as cholinesterase inhibitors, work by blocking the breakdown of acetylcholine, leading to its accumulation in the synaptic cleft. This accumulation indirectly enhances both muscarinic and nicotinic actions. These agents are classified as reversible or irreversible based on their mechanism of action.     
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Bisphenol-A Neurotoxic Effects on Basal Forebrain Cholinergic Neurons In Vitro and In Vivo.

Andrea Flores1, Paula Moyano1, Emma Sola1

  • 1Departamento de Farmacología y Toxicología, Facultad de Veterinaria, Universidad Complutense de Madrid, 28040 Madrid, Spain.

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|June 28, 2023
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Summary

The plasticizer bisphenol-A (BPA) causes neurodegeneration and cognitive decline by damaging basal forebrain cholinergic neurons. BPA exposure downregulates synaptic proteins and alters neurotransmitter pathways, mediated by histone deacetylase 2 (HDAC2) overexpression.

Keywords:
WNT/β-Catenin pathwaybasal forebrainbisphenol-Acholinergic neuronshistone deacetylase 2neurodegenerationsynaptic plasticity

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Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Bisphenol-A (BPA) is a widely used plasticizer linked to neurodegeneration and cognitive disorders.
  • Basal forebrain cholinergic neurons (BFCN) are crucial for memory and learning; their loss is implicated in Alzheimer's disease.
  • Mechanisms underlying BPA's neurotoxicity, particularly on BFCN, remain incompletely understood.

Purpose of the Study:

  • To investigate the neurotoxic effects of BPA on BFCN.
  • To elucidate the molecular mechanisms driving BPA-induced neurotoxicity in BFCN.

Main Methods:

  • Utilized Wistar rats and the SN56 cholinergic cell line as models for BFCN.
  • Administered acute and sub-chronic BPA exposure to assess neuronal loss and molecular changes.
  • Analyzed synaptic protein expression, glutamate levels, vesicular transport, WNT/β-Catenin pathway, and histone deacetylase 2 (HDAC2) activity.

Main Results:

  • Acute BPA exposure led to significant loss of BFCN in rats.
  • BPA exposure downregulated key synaptic proteins (PSD95, synaptophysin, spinophilin, NMDAR1) and vesicular glutamate transporter 2 (VGLUT2).
  • BPA increased glutamate content via enhanced glutaminase activity, suppressed the WNT/β-Catenin pathway, induced cell death in SN56 cells, and these effects were mediated by HDAC2 overexpression.

Conclusions:

  • BPA induces neurodegeneration and cognitive dysfunction by targeting BFCN.
  • The neurotoxic effects of BPA involve synaptic protein downregulation, altered neurotransmitter metabolism, and pathway dysregulation.
  • HDAC2 overexpression is a key mediator of BPA's toxicity in cholinergic neurons, offering potential targets for prevention.