Scientists at the University of Michigan have identified the protein that is responsible for sensing cold temperatures.
In a groundbreaking study conducted by researchers at the University of Michigan, a critical protein responsible for cold sensation in mammals has been identified, finally shedding light on a longstanding mystery in the realm of sensory biology. Published in the prestigious journal Nature Neuroscience, this discovery has the potential to revolutionize our understanding of how we perceive and react to cold temperatures, particularly in the context of various disease conditions that can alter our sensitivity to cold stimuli.
The quest to unravel the mechanisms underlying temperature perception commenced over two decades ago with the identification of TRPV1, a protein linked to sensing heat. Despite subsequent discoveries of proteins associated with detecting hot and warm temperatures, the elusive cold sensor remained unidentified until now. The research team, led by neuroscientist Shawn Xu at the U-M Life Sciences Institute, made a significant breakthrough by pinpointing the cold-sensing protein in mammals, known as GluK2 (Glutamate ionotropic receptor kainate type subunit 2).
The foundation for this groundbreaking finding was laid in a previous study from 2019, where researchers in Xu's lab identified a cold-sensing receptor protein in a species of worms called Caenorhabditis elegans. This discovery paved the way for investigating the cold sensor in mammals, as the gene responsible for producing the C. elegans protein is evolutionarily conserved across diverse species, including mice and humans.
To validate their hypothesis, the research team conducted experiments using mice lacking the GluK2 gene, rendering them incapable of producing GluK2 proteins. Through a series of tests measuring the mice's responses to different temperatures and mechanical stimuli, the researchers observed that while the mice reacted normally to hot, warm, and cool temperatures, they exhibited no response to extreme cold stimuli, confirming the crucial role of GluK2 in cold sensation.
Although GluK2 is predominantly found in neurons in the brain, where it facilitates inter-neuronal communication, it is also expressed in sensory neurons in the peripheral nervous system. This dual functionality indicates that GluK2 plays a distinct role in processing temperature cues in the peripheral nervous system, contrary to its more recognized role in the brain.
Professor Bo Duan, co-senior author of the study, highlighted the potential evolutionary origins of GluK2's temperature-sensing function, suggesting that this ancient capability may have been repurposed as organisms evolved more complex nervous systems. This intriguing insight into the protein's evolutionary history offers valuable context for understanding its diverse roles in different organisms.
Beyond its fundamental implications for sensory biology, the discovery of GluK2 as a cold sensor holds significant promise for potential applications in human health. For instance, cancer patients undergoing chemotherapy often experience heightened sensitivity to cold, leading to painful reactions. By uncovering the role of GluK2 in cold sensation, researchers hope to explore new avenues for alleviating cold-induced pain and developing targeted therapies for patients with heightened cold sensitivity.
Supported by the National Institutes of Health, the study adhered to rigorous ethical standards for animal research, with all procedures performed on mice approved by the Institutional Animal Care and Use Committee. The collaborative efforts of researchers from the University of Michigan and Johns Hopkins University School of Medicine culminated in this groundbreaking discovery, underscoring the importance of interdisciplinary cooperation in advancing scientific knowledge.
In conclusion, the identification of GluK2 as the protein responsible for cold sensation represents a significant milestone in the field of sensory biology, offering novel insights into the mechanisms underlying temperature perception in mammals. This discovery not only fills a longstanding gap in our understanding of cold sensing but also opens up exciting possibilities for further research into pain management and therapeutic interventions for conditions involving altered sensitivity to cold stimuli.
Source: https://www.eurekalert.org/news-releases/1036648
The quest to unravel the mechanisms underlying temperature perception commenced over two decades ago with the identification of TRPV1, a protein linked to sensing heat. Despite subsequent discoveries of proteins associated with detecting hot and warm temperatures, the elusive cold sensor remained unidentified until now. The research team, led by neuroscientist Shawn Xu at the U-M Life Sciences Institute, made a significant breakthrough by pinpointing the cold-sensing protein in mammals, known as GluK2 (Glutamate ionotropic receptor kainate type subunit 2).
The foundation for this groundbreaking finding was laid in a previous study from 2019, where researchers in Xu's lab identified a cold-sensing receptor protein in a species of worms called Caenorhabditis elegans. This discovery paved the way for investigating the cold sensor in mammals, as the gene responsible for producing the C. elegans protein is evolutionarily conserved across diverse species, including mice and humans.
To validate their hypothesis, the research team conducted experiments using mice lacking the GluK2 gene, rendering them incapable of producing GluK2 proteins. Through a series of tests measuring the mice's responses to different temperatures and mechanical stimuli, the researchers observed that while the mice reacted normally to hot, warm, and cool temperatures, they exhibited no response to extreme cold stimuli, confirming the crucial role of GluK2 in cold sensation.
Although GluK2 is predominantly found in neurons in the brain, where it facilitates inter-neuronal communication, it is also expressed in sensory neurons in the peripheral nervous system. This dual functionality indicates that GluK2 plays a distinct role in processing temperature cues in the peripheral nervous system, contrary to its more recognized role in the brain.
Professor Bo Duan, co-senior author of the study, highlighted the potential evolutionary origins of GluK2's temperature-sensing function, suggesting that this ancient capability may have been repurposed as organisms evolved more complex nervous systems. This intriguing insight into the protein's evolutionary history offers valuable context for understanding its diverse roles in different organisms.
Beyond its fundamental implications for sensory biology, the discovery of GluK2 as a cold sensor holds significant promise for potential applications in human health. For instance, cancer patients undergoing chemotherapy often experience heightened sensitivity to cold, leading to painful reactions. By uncovering the role of GluK2 in cold sensation, researchers hope to explore new avenues for alleviating cold-induced pain and developing targeted therapies for patients with heightened cold sensitivity.
Supported by the National Institutes of Health, the study adhered to rigorous ethical standards for animal research, with all procedures performed on mice approved by the Institutional Animal Care and Use Committee. The collaborative efforts of researchers from the University of Michigan and Johns Hopkins University School of Medicine culminated in this groundbreaking discovery, underscoring the importance of interdisciplinary cooperation in advancing scientific knowledge.
In conclusion, the identification of GluK2 as the protein responsible for cold sensation represents a significant milestone in the field of sensory biology, offering novel insights into the mechanisms underlying temperature perception in mammals. This discovery not only fills a longstanding gap in our understanding of cold sensing but also opens up exciting possibilities for further research into pain management and therapeutic interventions for conditions involving altered sensitivity to cold stimuli.
Source: https://www.eurekalert.org/news-releases/1036648
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