Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Exceptionally low mortality despite widespread COVID-19 infection among Indigenous Tsimane and Moseten of Bolivia.

Social science & medicine (1982)·2026
Same author

Air pollution is linked to divergent cortical thickness patterns in brain regions vulnerable to Alzheimer's disease.

Neurotoxicology·2026
Same author

In memoriam: Thomas Eugene Johnson.

GeroScience·2026
Same author

Socio-economic influences from egg to exit: Emerging biology.

Ageing research reviews·2026
Same author

Segmentation and morphometry of intracranial internal carotid artery calcification in relation to brain atrophy.

Neuroradiology·2026
Same author

Single cell profiling reveals GSM-15606 attenuates air pollution-induced inflammation and preserves hippocampal neurogenesis.

bioRxiv : the preprint server for biology·2026

Related Experiment Video

Updated: Jul 2, 2026

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

Progesterone influence on neurite outgrowth involves microglia.

Angela M Wong1, Irina Rozovsky, Jason M Arimoto

  • 1Biogerontology Division, Davis School of Gerontology, University of Southern California, Los Angeles, California 90089, USA.

Endocrinology
|September 6, 2008
PubMed
Summary

Progesterone (P4) antagonizes estradiol (E2) effects on brain plasticity, with microglia playing a key role. This P4-E2 interaction, mediated by progesterone receptors, impacts neuronal function and has implications for hormone therapy.

More Related Videos

Culturing Microglia from the Neonatal and Adult Central Nervous System
11:28

Culturing Microglia from the Neonatal and Adult Central Nervous System

Published on: August 9, 2013

Related Experiment Videos

Last Updated: Jul 2, 2026

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

Culturing Microglia from the Neonatal and Adult Central Nervous System
11:28

Culturing Microglia from the Neonatal and Adult Central Nervous System

Published on: August 9, 2013

Area of Science:

  • Neuroscience
  • Endocrinology
  • Cell Biology

Background:

  • Estradiol (E2) promotes synaptic remodeling in the hippocampus.
  • Progesterone (P4) has been shown to antagonize E2's effects during the estrous cycle.
  • The precise mechanisms underlying P4's modulation of E2-dependent synaptic plasticity remain unclear.

Purpose of the Study:

  • To investigate the role of P4 in E2-modulated synaptic plasticity, particularly in response to neuronal injury.
  • To elucidate the cellular mechanisms, focusing on glial involvement, mediating P4's antagonism of E2.
  • To determine the involvement of progesterone receptors in this antagonistic interaction.

Main Methods:

  • Utilized entorhinal cortex lesions in ovariectomized rats to induce E2-dependent neurite sprouting.
  • Administered concurrent P4 and E2 treatments to assess effects on sprouting and microglial activation.
  • Employed a wounding-in-a-dish model with rat cortical neuron-glia cocultures to analyze glial contributions.
  • Used P4 receptor antagonists (ORG-31710, RU-486) to block P4's effects.

Main Results:

  • Concurrent P4 and E2 treatment attenuated E2-dependent neurite sprouting and microglial activation in vivo.
  • In neuron-astrocyte-microglia cocultures, P4 antagonized E2-induced neurite outgrowth and neuron viability.
  • Removal of microglia abolished P4's antagonistic effect on E2-dependent sprouting.
  • P4 receptor antagonists blocked P4's antagonism of E2-dependent sprouting.

Conclusions:

  • Microglia play a critical role in mediating P4's antagonism of E2-dependent neuronal plasticity.
  • This P4-E2 antagonism is dependent on progesterone receptors.
  • Findings suggest a novel mechanism for P4 in regulating neuronal plasticity, with relevance to hormone therapy and neurodegenerative diseases.