The new antibody found by Duke University researchers works by targeting the voltage-sensitive sodium channels in the cell membrane of neurons.
Voltage-sensitive sodium channels control the flow of sodium ions through the neuron's membrane. One particular type of sodium channel, called the Nav1.7 subtype, is responsible for sensing pain.
Mutations in the human gene encoding the Nav1.7 sodium channel can lead to either the inability to sense pain or pain hypersensitivity.
These mutations do not affect other sensations such as touch or temperature. Hence, the Nav1.7 sodium channel might be a very specific target for treating pain disorders without perturbing the patients' ability to feel other sensations.
He designed antibodies that would capture the sodium channels so that he could study them.
"The channel is off when it is closed. Since the antibody stabilises the closed state, the channel becomes less sensitive to pain," said Lee.
If this held true in live animals, then the animals would also be less sensitive to pain.
To test this idea, Lee sought the help of Ru-Rong Ji, an expert in the study of pain and itch sensation.
More importantly, mice receiving the treatment did not show signs of physical dependence or enhanced tolerance towards the antibody.
"Pain and itch are distinct sensations, and pain is often known to suppress itch," said Ji.
The team found that the antibody can also relieve acute and chronic itch in mouse models, making them the first to discover the role of Nav1.7 in transmitting the itch sensation.
"Now we have a compound that can potentially treat both pain and itch at the same time," said Lee. Both of these symptoms are common in allergic contact dermatitis.
"We hope our discovery will garner interest from pharmaceutical companies that can help us expand our studies into clinical trials," Lee said.
The finding appears in the journal Cell.
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