# Streptozotocin-Induced Diabetic Rats Showed a Differential Glycine Receptor Expression in the Spinal Cord: A GlyR Role in Diabetic Neuropathy

**Authors:** Miguel Ángel Velázquez-Flores, Gustavo Sánchez-Chávez, Sara L. Morales-Lázaro, Ruth Ruiz Esparza-Garrido, Alejandro Canizales-Ontiveros, Rocío Salceda

PMC · DOI: 10.1007/s11064-023-04058-9 · Neurochemical Research · 2023-11-29

## TL;DR

This study shows that glycine receptor expression in the spinal cord changes in diabetic rats, suggesting a role in diabetic neuropathy.

## Contribution

The study is the first to report altered glycine receptor subunit expression in diabetic neuropathy using a rat model.

## Key findings

- The α2 subunit mRNA was overexpressed in diabetic rats 45 days after induction.
- Synaptic expression of α1 and α2 subunits decreased during diabetes, while α3 increased on day 45.
- Diabetic rats showed increased pain responses to capsaicin compared to controls.

## Abstract

In the spinal cord, attenuation of the inhibitory action of glycine is related to an increase in both inflammatory and diabetic neuropathic pain; however, the glycine receptor involvement in diabetic neuropathy has not been reported. We determined the expression of the glycine receptor subunits (α1–α3 and β) in streptozotocin-induced diabetic Long–Evans rats by qPCR and Western blot. The total mRNA and protein expression (whole spinal cord homogenate) of the α1, α3, and β subunits did not change during diabetes; however, the α2 subunit mRNA, but not the protein, was overexpressed 45 days after diabetes induction. By contrast, the synaptic expression of the α1 and α2 subunits decreased in all the studied stages of diabetes, but that of the α3 subunit increased on day 45 after diabetes induction. Intradermal capsaicin produced higher paw-licking behavior in the streptozotocin-induced diabetic rats than in the control animals. In addition, the nocifensive response was higher at 45 days than at 20 days. During diabetes, the expression of the glycine receptor was altered in the spinal cord, which strongly suggests its involvement in diabetic neuropathy.

The online version contains supplementary material available at 10.1007/s11064-023-04058-9.

## Linked entities

- **Proteins:** ATP6V0A1 (ATPase H+ transporting V0 subunit a1), ATP6V0A2 (ATPase H+ transporting V0 subunit a2), TCIRG1 (T cell immune regulator 1, ATPase H+ transporting V0 subunit a3), b (black)
- **Chemicals:** streptozotocin (PubChem CID 29327), capsaicin (PubChem CID 1548943)
- **Diseases:** diabetic neuropathy (MONDO:0006626)

## Full-text entities

- **Genes:** Ugt1a6a (UDP glucuronosyltransferase family 1 member A6a) [NCBI Gene 113992] {aka UDPGT 1-6, UGT1-06, UGT1.6, Udpgt, Ugt1, Ugt1a6}, Ugt1a7c (UDP glucuronosyltransferase 1 family, polypeptide A7C) [NCBI Gene 154516] {aka UDPGT 1-7, Ugt1, Ugt1a7, Ugt1a8}
- **Diseases:** Diabetic Neuropathy (MESH:D003929), inflammatory (MESH:D007249), Diabetic (MESH:D003920), diabetic neuropathic pain (MESH:D009437)
- **Chemicals:** glycine (MESH:D005998), capsaicin (MESH:D002211), Streptozotocin (MESH:D013311)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10884118/full.md

## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC10884118/full.md

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Source: https://tomesphere.com/paper/PMC10884118