An overview of our Research
Because animals live in a constantly changing environment (think about the fluctuations in temperature that take place seasonally or during a single day), their survival depends critically on their ability to detect and react to these alterations. To this end, the entire surface of the body, including the eyes and the mouth, and many viscera (gut, lungs, etc) are equipped with tiny nerve endings that express specialized receptors that act as miniature signal amplifiers, detecting changes in temperature, mechanical forces and a variety of chemical irritants. The general objective of our research group is to try to understand how the nervous system senses the environment, focusing on the role played by ion channels in mechanosensation, temperature sensing and pain. Detecting these signals is obviously useful and can protect our body from harm. However, in many pathological conditions (arthritis, diabetes, etc), activity in these receptors is altered, leading to exaggerated pain and other unpleasant sensations like itch. In our studies, we combine different experimental approaches. Using genetic labeling strategies, we can identify subpopulations of sensory neurons that are involved in the transduction of specific stimuli. These neurons are further characterized using electrophysiological recordings or purified for biochemical analysis or genomic profiling. We also perform behavioral characterization of animals lacking specific ion channels in different models of chronic pain. The ultimate goal of our research program is to establish the contribution of particular ion channels to somatic and viscera sensations and their role in pathological conditions like chronic pain and inflammation. Finally, we also explore the potential to develop novel analgesic drugs targeting these receptors.
To study the expression and function of ion channels, sensory ion channels, and thermoreceptors in particular, in different pathological conditions that lead to abnormal pain sensations. This knowledge is fundamental to eventually use these molecular receptors as analgesic targets.
We are also interested in understanding the cellular and molecular bases of low and high-threshold mechanotransduction by mammalian primary sensory neurons under conditions of inflammation and the effects of specific components of the extracellular matrix on articular pain.