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Sigma-1 Receptor Promotes Glycolysis in Neuronal Systems by Suppressing GRIM19.

Simon Couly¹, Yuko Yasui¹, Ioannis Grammatikakis²

¹Cellular Pathobiology Section, Integrative Neuroscience Research Branch, Intramural Research Program, National Institute on Drug Abuse, NIH/DHHS, Suite 3512, 333 Cassell Drive, Baltimore, MD, 21224, USA.

Biorxiv : the Preprint Server for Biology

|August 6, 2025

Summary

Sigma-1 receptor (S1R) regulates cellular energy by modulating glycolysis and NAD+ metabolism in neurons. Loss of S1R reduces glycolysis and alters NAD+/NADH ratios, impacting brain glucose uptake.

Keywords:

Sigma-1 receptor energy metabolism glycolysis mitochondria neurons nicotinamide adenine dinucleotide (NAD)

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Area of Science:

Neuroscience
Cellular Metabolism
Biochemistry

Background:

Sigma-1 receptor (S1R) is an endoplasmic reticulum chaperone influencing calcium signaling.
Mitochondrial metabolism is closely linked to cellular glycolysis.
The role of S1R in glycolysis and overall cellular energy metabolism remains unclear.

Purpose of the Study:

To investigate the function of S1R in glycolysis, mitochondrial activity, and NAD+/NADH metabolism.
To determine the impact of S1R on cellular energy metabolism in neuronal systems.

Main Methods:

Utilized wild-type and S1R knockout Neuro2a cells and mice.
Performed primary cortical neuron cultures and in-vivo imaging.
Analyzed glycolysis, mitochondrial respiration, NAD+/NADH ratios, and [18F]fluorodeoxyglucose uptake.

Main Results:

S1R knockout (KO) cells and neurons exhibited reduced glycolytic activity.
S1R KO conditions showed an increased NAD+/NADH ratio and elevated mitochondrial complex I protein GRIM19.
S1R KO mice displayed decreased brain glucose uptake via positron emission tomography.
Knocking down GRIM19 rescued the glycolytic deficit in S1R KO conditions.

Conclusions:

S1R plays a crucial role in modulating glycolysis and NAD+ metabolism in neuronal systems.
These findings reveal a novel function of S1R in cellular energy regulation.
Understanding S1R's role in glycolysis may offer therapeutic strategies for aging and neurodegenerative diseases.