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Related Concept Videos

Secondary Messengers in Hormone Action01:26

Secondary Messengers in Hormone Action

Water-soluble hormones cannot cross the plasma membrane, so they rely on protein receptors that span the membrane to trigger intracellular signaling pathways. These pathways then activate second messengers inside the cell, including cAMP or calcium ions.
Many hormones bind to transmembrane G protein-coupled receptors that connect to regulatory G proteins. These G proteins can then activate enzymes such as adenylyl cyclase or phospholipase C. Adenylyl cyclase converts ATP to cAMP, activating...
Amplifying Signals via Second Messengers01:15

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Many receptor binding ligands are hydrophilic; they do not cross the cell membrane but bind to cell-surface receptors. Thus, their message must be relayed by second messengers present in the cell cytoplasm. There are several second messenger pathways, each with its own way of relaying information. For example, the G protein-coupled receptors can activate both phosphoinositol and cyclic AMP (cAMP) second messenger pathways. The phosphoinositol pathway is active when the receptor induces...
Interactions Between Signaling Pathways01:19

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Mechanism of Angiogenesis01:10

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Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
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Collateral Ganglia
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Related Experiment Video

Updated: May 14, 2026

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
07:32

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina

Published on: June 23, 2014

Modeling secondary messenger pathways in neurovascular coupling.

James Hadfield1, Michael J Plank, Tim David

  • 1Department of Mathematics and Statistics, University of Canterbury, Christchurch, New Zealand.

Bulletin of Mathematical Biology
|January 30, 2013
PubMed
Summary

This study models how glial cells regulate blood flow via calcium signaling. It reveals how different production speeds of epoxyeicosatrienoic acids and 20-hydroxyeicosatetraenoic acids explain rapid vasodilation followed by slower return to baseline.

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A Microbiomechanical System for Studying Varicosity Formation and Recovery in Central Neuron Axons
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Last Updated: May 14, 2026

Assessment of Vascular Regeneration in the CNS Using the Mouse Retina
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Neurovascular Network Explorer 2.0: A Simple Tool for Exploring and Sharing a Database of Optogenetically-evoked Vasomotion in Mouse Cortex In Vivo
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A Microbiomechanical System for Studying Varicosity Formation and Recovery in Central Neuron Axons
09:58

A Microbiomechanical System for Studying Varicosity Formation and Recovery in Central Neuron Axons

Published on: April 30, 2018

Area of Science:

  • Neuroscience
  • Computational Biology
  • Physiology

Background:

  • Neurovascular coupling links neural activity to blood flow changes.
  • Glial cells, particularly astrocytes, are key mediators connecting neurons and blood vessels.
  • Calcium signaling within glial cells is hypothesized to drive vascular responses through secondary messengers.

Purpose of the Study:

  • To model astrocyte intracellular calcium dynamics and its role in neurovascular coupling.
  • To investigate the relationship between calcium concentration and the production of vasoactive secondary messengers.
  • To explain the temporal dynamics of vascular response to neural stimulation.

Main Methods:

  • Developed a computational model for intracellular calcium dynamics in astrocytes.
  • Coupled the calcium model with a novel model of vasoactive secondary messenger production.
  • Modeled the production of epoxyeicosatrienoic acids (EET) and 20-hydroxyeicosatetraenoic acid (20-HETE).

Main Results:

  • Demonstrated that stable oscillatory behavior of intracellular calcium is possible in astrocytes under specific conditions.
  • Showed that different production time scales for EET and 20-HETE influence vascular response dynamics.
  • The model supports the observed rapid vasodilation followed by a slower return to baseline.

Conclusions:

  • Astrocyte calcium dynamics play a crucial role in neurovascular coupling.
  • The differential production rates of EET and 20-HETE explain the biphasic vascular response.
  • This modeling approach provides insights into the cellular mechanisms underlying blood flow regulation.