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Progesterone modulates neuronal excitability bidirectionally.

Jaideep Kapur1, Suchitra Joshi2

  • 1Department of Neurology, University of Virginia-HSC, Charlottesville, VA, 22908, United States; Department of Neuroscience, University of Virginia-HSC, Charlottesville, VA, 22908, United States; UVA Brain Institute, University of Virginia-HSC, Charlottesville, VA, 22908, United States.

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|January 9, 2021
PubMed
Summary
This summary is machine-generated.

Progesterone influences brain activity via its receptors and neurosteroids. It can excite neurons through progesterone receptors (PRs) or calm them via allopregnanolone (THP), impacting epilepsy.

Keywords:
AMPA receptorsAllopregnanoloneCatamenial epilepsyGABA-A receptorsProgesteroneProgesterone receptors

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Progesterone modulates neuronal activity through direct receptor binding and conversion to neurosteroids.
  • Progesterone receptors (PRs) mediate excitatory effects via enhanced alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor (AMPAR) expression.
  • The progesterone metabolite 5α,3α-tetrahydro-progesterone (allopregnanolone, THP) exerts anxiolytic and sedative effects by potentiating gamma-aminobutyric acid type-A receptors (GABAARs).

Purpose of the Study:

  • To review the neuromodulatory actions of progesterone through PRs and THP.
  • To elucidate the opposing roles of progesterone pathways in seizure regulation.
  • To examine the link between progesterone withdrawal and seizure exacerbation.

Main Methods:

  • Literature review of studies on progesterone, neurosteroids, and neuronal excitability.
  • Analysis of research on progesterone receptors (PRs) and their downstream effects.
  • Examination of the mechanisms of allopregnanolone (THP) on GABAARs.

Main Results:

  • Progesterone signaling via PRs enhances neuronal excitation through AMPARs.
  • Progesterone metabolite THP potentiates GABAARs, leading to inhibitory effects.
  • These opposing actions influence seizure activity, including catamenial epilepsy and withdrawal-induced seizures.

Conclusions:

  • Progesterone exerts dual neuromodulatory effects, excitation via PRs and inhibition via THP.
  • Understanding these pathways is crucial for managing epilepsy, particularly catamenial epilepsy.
  • Progesterone withdrawal represents a critical factor in seizure exacerbation.