Killing the agony

日期:2019-03-07 05:03:05 作者:胶崇 阅读:

By Philip Cohen A “LETTER BOMB” molecule that destroys renegade nerve cells in rats could provide relief for people suffering from chronic pain. Chronic pain occurs when nerve cells in the spinal cord amplify pain responses by mistake, making a pinprick feel like a knife stab. Cancer, arthritic swelling or nerve damage can all trigger the condition. Powerful analgesics such as morphine ease the suffering but can have serious side effects. Pain-amplifying neurons use a neurotransmitter called substance P to communicate with each other. So Patrick Mantyh of the University of Minnesota in Minneapolis and his colleagues decided to transform this innocuous messenger to carry a deadly payload into the renegade neurons. To make the new chemical, dubbed SP-SAP, they linked substance P to saporin, a toxic plant protein. Mistaking the molecule for the genuine neurotransmitter, the cells take it in and are then poisoned. To test the effectiveness of the treatment, Mantyh’s team damaged the spinal nerves of rats, then measured the weight that an animal could tolerate on a paw before it withdrew it in pain. Animals that had been given a spinal infusion of SP-SAP could tolerate more than twice the weight compared with controls given placebos. The pain relief was still active 200 days after the treatment. The rats remained sensitive to mildly painful stimuli, for which morphine was still an effective analgesic, showing that other mechanisms for pain sensing and control were unaffected. “It is important, imaginative work,” says Stephen Hunt, a molecular neuroscientist at University College London. “It’s as if they’ve taken away pain’s volume control.” Mantyh says that since the drug destroys neurons, it might only ever be appropriate for extreme cases, such as relieving the pain of people who are terminally ill. But he thinks it should also be possible to make the “letter bomb” carry a less destructive payload. “We can try to slow down the neurons, or maybe even change their behaviour,