Scientists decrease pain in rats by blocking signals in the brain

The expanded understanding of the brain's role in determining pain may lead to new therapies for chronic pain patients.

By Stephen Feller

MONTREAL, Oct. 9 (UPI) -- Doctors have long searched for an effective treatment for chronic pain, which is caused by disease or trauma to the nervous system. Researchers found that blocking specific channels in the brain that control pain signals sent to the anterior cingular cortex, or ACC, "dramatically" reduced feelings of pain.

The finding will likely have an effect on the way chronic pain is treated, and may lead to the development of new methods, said researchers in a study conducted at McGill University.


"The ACC has been shown to be a key center to cognitive functions linked to memory and affective functions involved in feelings and emotions," said Dr. Philippe Séguéla, a professor at McGill, in a press release. "We know that patients who suffer from chronic pain experience impairment of their working memory, difficulties focusing on certain tasks and may suffer from depression and anxiety. Our findings open new doors to research possible treatment of these debilitating symptoms that are linked to chronic pain."

Using rats with spared nerve injury, researchers confirmed previous knowledge that hyperpolarization-activated cyclic nucleotide-gated, or HCN, channels in the brain control the transmission of pain signals to the ACC. When these channels were blocked, however, the rats experienced vastly reduced levels of pain.


The researchers wrote in the study that increasing how much is understood about the brain's role in pain perception may lead to potential therapies for pain that focus on what patients feel, in addition doctors pursuit of solving the causes of pain.

"We were able to show that reducing hyperexcitability of the ACC by blocking the HCN channels had analgesic effects -- basically the feelings of pain were dramatically decreased," Séguéla said. "Our study has revealed one important mechanism linking chronic pain to abnormal activity of the ACC and it provides a cellular and molecular explanation for the overstimulation of neurons in the prefrontal cortex. This gives us new perspectives on therapeutic strategies that could target the HCN channels to help relieve chronic pain."

The study is published in the Journal of Neuroscience.

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