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Triggering Reactive Gliosis In Vivo by a Forebrain Stab Injury

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Hedgehog Pathway-Mediated Vascular Alterations Following Trigeminal Nerve Injury.

N Moreau^1,2, W Dieb^1,3, A Mauborgne¹

¹1 Centre de Psychiatrie et Neurosciences, Inserm U894, Paris, France.

Journal of Dental Research

|November 19, 2016

Summary

The Hedgehog pathway is inhibited after trigeminal nerve injury, causing blood-nerve barrier disruption and inflammation, leading to orofacial neuropathic pain.

Keywords:

blood vessels endoneurium inflammation neuropathic pain tight junctions vascular permeability

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Area of Science:

Neuroscience
Vascular Biology
Pain Research

Background:

Neurovascular interactions are crucial in spinal neuropathic pain.
Limited research exists on neurovascular aspects of orofacial neuropathic pain.

Purpose of the Study:

Investigate vascular changes in the infraorbital nerve (IoN) after chronic constriction injury (CCI) in rats.
Explore the role of the Hedgehog pathway in orofacial neuropathic pain.

Main Methods:

Induced IoN-CCI in male Sprague-Dawley rats.
Assessed tight junction proteins, vascular permeability (sodium fluorescein), immunocyte markers (CD3, CD11b), and innate immunity markers (TLR2, TLR4).
Examined Hedgehog pathway components (Patched-1, Gli-1) and used cyclopamine to inhibit the pathway.

Main Results:

IoN-CCI led to downregulated Claudin-1 and Claudin-5, increased vascular permeability, and elevated immunocyte and innate immunity markers.
Hedgehog pathway readouts were downregulated post-CCI.
Cyclopamine administration replicated CCI-induced changes.

Conclusions:

Hedgehog pathway inhibition plays a key role in trigeminal nerve injury-induced vascular permeability.
This facilitates immune cell infiltration, neuroinflammation, and neuropathic pain-like behaviors.