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Sympathetic Signaling

Sympathetic Signaling

Sympathetic signaling, a vital part of the autonomic nervous system, plays a crucial role in mobilizing the body's resources in response to stress or emergencies. It involves the transmission of nerve impulses from sympathetic preganglionic fibers to postganglionic fibers. This results in the release of specific neurotransmitters and activation of adrenergic receptors.
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Related Experiment Video

Updated: Oct 3, 2025

Author Spotlight: Innovative Use of nsPEF to Boost Peripheral Nerve Regeneration

Author Spotlight: Innovative Use of nsPEF to Boost Peripheral Nerve Regeneration

Published on: May 3, 2024

Small Molecules Targeting PTPσ-Trk Interactions Promote Sympathetic Nerve Regeneration.

Matthew R Blake^1,2, Ryan T Gardner¹, Haihong Jin¹

¹Department of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon 97239, United States.

ACS Chemical Neuroscience

|February 14, 2022

Summary

This summary is machine-generated.

New small molecules, HJ-01 and HJ-02, promote nerve regeneration by disrupting chondroitin sulfate proteoglycans (CSPGs) interactions with receptor protein tyrosine phosphatase sigma (PTPσ) and enhancing tropomyosin receptor kinases (Trks) signaling.

Keywords:

acrylamide chondroitin sulfate proteoglycan nerve regeneration protein tyrosine phosphatase receptor sigma

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Area of Science:

Neuroscience
Biochemistry
Pharmacology

Background:

Chondroitin sulfate proteoglycans (CSPGs) form scars that inhibit nerve regeneration after injuries like myocardial infarction, traumatic brain injury, and spinal cord injury.
Current therapeutics cannot effectively promote nerve regrowth through CSPG-rich scar tissue.

Purpose of the Study:

To develop small-molecule therapeutics that promote nerve regeneration by targeting the interaction between CSPGs and neuronal receptors.
To identify compounds that can overcome the inhibitory effects of CSPGs on axon outgrowth.

Main Methods:

Synthesis and characterization of novel small molecules, HJ-01 and HJ-02.
Investigation of the molecules' ability to disrupt the interaction between receptor protein tyrosine phosphatase sigma (PTPσ) and tropomyosin receptor kinases (Trks).
Assessment of the molecules' effects on Trk signaling and sympathetic nerve regeneration in the presence of CSPGs.

Main Results:

The developed small molecules, HJ-01 and HJ-02, successfully disrupt the PTPσ-Trk interaction.
These molecules enhance Trk signaling pathways, which are crucial for axon growth.
HJ-01 and HJ-02 promote sympathetic nerve regeneration across CSPG-containing inhibitory environments.

Conclusions:

Small molecules HJ-01 and HJ-02 represent a promising therapeutic strategy for promoting nerve regeneration.
Targeting the PTPσ-Trk pathway offers a novel approach to overcoming scar-mediated inhibition of nerve regrowth.