Scientists reported that active neurons release an enzyme called vertebrate lonesome kinase (VLK) into the space between cells. VLK can phosphorylate — that is, add a phosphate group to — proteins on the outside of other cells. This extracellular modification can control interactions between cell-surface proteins and alter how pain signals are sent.
In mouse experiments, VLK increased the function of a receptor involved in pain, learning and memory. Removing VLK from pain-sensing neurons prevented the normal pain response after surgery, while movement and basic sensation remained intact. Conversely, adding extra VLK increased pain responses. The study was published in Science.
Researchers suggest that targeting extracellular enzymes such as VLK could be a safer way to influence pain pathways, avoiding direct blockade of NMDA receptors and reducing potential side effects.
Difficult words
- enzyme — a protein that speeds up chemical reactions
- phosphorylate — to add a phosphate group to a molecule
- extracellular — located outside cells, in the space between them
- receptor — a protein on a cell that receives signalsreceptors
- neuron — a nerve cell that sends and receives signalsneurons
- blockade — an action that stops or blocks a process
Tip: hover, focus or tap highlighted words in the article to see quick definitions while you read or listen.
Discussion questions
- Do you think targeting extracellular enzymes could make pain medicines safer? Why or why not?
- How might preventing the normal pain response after surgery affect a patient’s recovery?
- The article says a receptor is involved in pain, learning and memory. Would you worry about side effects that change learning or memory? Explain.
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Connie Nshemereirwe is an educational measurement specialist and former engineer who promotes Africa-led research, better science communication and stronger ties among scientists in the global South. She also directs the Africa Science Leadership Program.
