David McKemyThe cold sensing circuit forms in the utero but does not develop for sometime after birth. Newborn mice’s cold sensing neural circuits take about two weeks to become fully active according new analysis by experts from the University of Southern California. The findings may help to understand the cold sensing protein TRPM8 in a class of proteins known as ion channel. The purpose of the latter is to turn on the cell when they receive stimulus. It senses painful cold and soothing cold of menthol-based creams.

Researchers reveal that mice are born with a keen sense of smell that is essential to breast feed successfully by contrast. In humans direct research of the cold sensing protein TRPM8 is not yet possible. Sensory developments in mice and humans are different; for example mice are born blind. Research reveals a possible biological basis for conclusions of changed cold sensitivity among premature infants.

“About three or four days before the animal is born, the protein is expressed. However, the axons of these nerves going into the spinal cord are not fully formed until probably two weeks after birth”, shares USC College professor David McKemy, an assistant professor of neurobiology.

Previous studies of temperature sensation conducted by the Institute of Child Health at University College London revealed that 11 year old premature children were less sensitive to temperature as compared to children who were born at term. Mice genetically engineered to convey a green fluorescent protein whenever TRPM8 was produced helped researchers identify the progression of cold sensing.

McKemy quotes, “This is consistent with our observations that the circuitry is not fully developed until after birth, thus anything that disrupts this formation at this important stage could have long-term effects. There are other reports that injury and inflammation in rodent models that occur during the [prenatal] period lead to altered temperature sensitivity as well as altered neural circuits.”

McKemy suspected that internal architecture of the neuron differs, with each adapted to painful or pleasant cold signals from TRPM8. Analysis of this protein may help researchers know the molecular mechanism of sensation. This may enable them to develop better drugs for relief of chronic pain states that include extreme sensitivity to cold faced by some diabetes patients.

McKemy shares that in order to comprehend conditions like cold allodynia it is necessary to find out what is their main cause. Understanding the basic nuts and bolts of molecules and neurons and how they detect pain generally may help identify pain when we shouldn’t.

This research was published online by Neuroscience.