Eric Senning

Eric Senning completed his B.A. in Biochemistry at the Colorado College in Colorado Springs, CO. He then joined the lab of Dr. Andrew Marcus at the University of Oregon to investigate the microscopic fluctuations of mitochondria in cells and energy transfer in fluorescent proteins with Fourier Imaging Correlation Spectroscopy (FICS), a specialized fluorescence technique. After finishing his Ph.D. in Chemistry at the University of Oregon, Eric pursued his interest in dynamics of physiological processes by joining the lab of Dr. Sharona Gordon at the University of Washington as a post-doctoral fellow. His post-doctoral research on the ion channel TRPV1 encompassed single molecule fluorescence, energy transfer, and electrophysiological techniques. In 2017 Eric joined the Department of Neuroscience at the University of Texas at Austin.

The Senning lab focuses on the mechanisms of ion channel regulation in a class of sensory neurons known as nociceptors. The brain receives signals from the peripheral nervous system through the spinal cord. Some of these signals come in through the dorsal horn from DRG nociceptors, which extend processes out to the peripheral tissues, where molecular receptors act to change the excitability of the neuron. Because of its role in pain sensation, our research effort is directed at the function of TRPV1, which is a non-selective ion channel expressed in nociceptors. We consider three aspects of TRPV1 regulation and consequences to nociceptor excitability:

Nociceptors are modulated by a wide variety of sensory inputs. In the case of TRPV1 positive neurons, capsaicinoids, heat, acid and oxidation directly activate gating of TRPV1 to affect the excitability of the nociceptor. The poly-modal activation of TRPV1 beckons the question as to how such a broad set of inputs at near physiological levels can be integrated by the channel to modulate opening and closing.

Tissue inflammation results in the presences of an inflammatory soup that bathes the nociceptor in signaling molecules that influence the function of TRPV1 both directly (for example through acidity) or indirectly through signaling cascades. Both calcium and phosphatidylinositol 4,5-bisphosphate (PIP2) act as second messengers to influence the function of TRPV1, but the contentious issue is to what degree these act directly on the channel versus through indirect mechanisms such as channel phosphorylation.

The pseudo-unipolar character of the DRG nociceptor is evident given its branched axon and absence of any post-synaptic structures. This presents an interesting problem since an organizational polarity is lacking that would place TRPV1 at the periphery of the nociceptor. Our research is directed at identifying a mechanism that recruits TRPV1 to physiologically relevant sites.