![]() Pain was assessed using the Von Frey assay, where mice are placed on an elevated grate and their paws are poked with different sized filaments ( Decosterd and Woolf, 2000 Shields et al., 2003). To investigate the mechanisms underlying hypersensitivity to touch, the team (which includes some of the researchers involved in the 2016 study) damaged the sciatic nerves of male and female mice lacking the gene for the CSF1 protein in their sensory neurons. Now, in eLife, Allan Basbaum, Anna Molovsky and colleagues from the University of California, San Francisco – including Julia Kuhn and Ilia Vainchtein as co-first authors – report that microglia and another immune cell population respond differently to pain signals in male and female mice ( Kuhn et al., 2021). However, microglia have also been shown to be sexually dimorphic, playing different roles in disease and pain in males and females ( Mogil, 2020). In 2016, a group of scientists discovered that male mice became hypersensitive to touch when their microglia were activated by nerve injury or by injecting CSF1 in to the space around the spinal cord ( Guan et al., 2016). In this activated state, microglia proliferate, change their form and alter their behavior. Previous work showed that injured sensory neurons release a protein called CSF1 (short for colony stimulating factor 1), which activates microglia, the main immune cell type in the brain and spinal cord. One important player in controlling pain related to nerve damage is the immune system ( Calvo et al., 2012 Scholz and Woolf, 2007). ![]() Damaging these neurons can lead to persistent and chronic pain, but the mechanisms underlying this are not fully understood. ![]() ![]() These stimuli are detected by sensory neurons, which transmit signals to the spinal cord and brain. Pain cautions our bodies against harmful stimuli – such as a burning flame or the pointy end of a needle – and protects us when we are injured. ![]()
0 Comments
Leave a Reply. |