A new study has opened up the possibility of new drug targets for memory loss and epileptic seizures with the finding that pain receptors in the brain may be linked to memory and learning.
Washington, Mar 14 : A new study has opened up the possibility of new drug targets for memory loss and epileptic seizures with the finding that pain receptors in the brain may be linked to memory and learning.
The research, by Julie Kauer has found that the activation of the nervous system receptor known as TRPV1 can trigger long-term depression, a phenomenon that creates lasting changes in the connections between neurons.
These changes in the brain - and the related process of neural reorganization known as long-term potentiation - are believed to be the cellular basis for memory making.
"We've known that TRPV1 receptors are in the brain, but this is some of the first evidence of what they actually do there. And the functional role we uncovered is unexpected. No one has previously linked these pain receptors to a cellular mechanism underlying memory. So we may have found a whole new player in brain plasticity," Kauer said.
TRPV1, short for transient receptor potential vanilloid subtype, can be found all over the nervous system, including the skin, spinal cord and brain. These receptors can sense heat, trigger inflammation and transmit pain.
As a part of the study, Kauer, professor of medical science in the Department of Molecular Pharmacology, Physiology and Biotechnology at Brown, treated rat brain tissue from the hippocampus, the brain's seat of learning and memory, with capsaicin, the compound that creates the spicy kick in chili peppers and to which the receptors also respond.
The team found that this compound activated TRPV1 channels - which alone triggered long-term depression in the brain tissue.
They also found that the weight-loss pill rimonabant, which is sold in Europe under the name Acomplia - that can block TRPV1 receptors, entirely blocked long-term depression by blocking TRPV1 channels.
After testing brain tissue from mice that lacked TRPV1 receptors, the researchers then found that long-term depression was absent.
The implications, say the researchers, are many.
While on one hand the find opens up the possibilities of new targets for drugs that could prevent memory loss or could possibly treat neural disorders such as epilepsy, it also warns that drugs that block TRPV1 receptors are likely to influence more than just pain-related functions.
Funded by the National Institutes of Health, the study is published in the journal Neuron.
ANI