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Methylmercury (MeHg) exposure causes prefrontal cortex (PFC) hyperexcitability by disrupting the excitatory-inhibitory balance. This neurotoxicant

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Area of Science:

  • Neuroscience
  • Toxicology
  • Neurodegenerative Diseases

Background:

  • Prefrontal cortex (PFC) dysfunction is linked to cognitive deficits and frontotemporal disorders (FTDs).
  • PFC neurons are vulnerable to excitotoxicity and environmental toxicants, potential FTD contributors.
  • The impact of environmental neurotoxicants on PFC function remains understudied.

Purpose of the Study:

  • To investigate methylmercury's (MeHg) ability to induce hyperexcitability in medial prefrontal cortex (mPFC) neurons.
  • To elucidate the mechanisms underlying MeHg-induced mPFC dysfunction.
  • To assess MeHg's potential contribution to FTD pathogenesis.

Main Methods:

  • Whole-cell patch-clamp recordings were used to assess mPFC pyramidal neuron activity.
  • Acute exposure to methylmercury (MeHg) was administered.
  • Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were analyzed.

Main Results:

  • MeHg exposure (20 μM) significantly increased mPFC excitability by shifting the excitatory-inhibitory (E-I) balance.
  • Both EPSC and IPSC charges increased, with enhanced EPSC frequency and reduced paired-pulse depression.
  • MeHg induced temporal synchrony in spontaneous IPSCs and increased intrinsic neuronal excitability and firing rate.

Conclusions:

  • Methylmercury induces hyperexcitability in mPFC neurons, disrupting E-I balance and inhibitory network function.
  • These findings suggest a mechanism by which environmental neurotoxicants like MeHg may contribute to cognitive and emotional deficits seen in FTD.
  • MeHg's effects on mPFC circuits highlight its potential role in the etiology of neurodegenerative diseases.