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Nathaniel Himmel

Grad Student    

Nate obtained his B.S. from the University of Florida in 2013. His major field was biology, and his studies also included philosophy. Subsequently, Nate completed two years of post-baccalaureate research at Emory University, in the lab of Mitsi Blount, PhD, where he studied cAMP-dependent signaling, polycystic kidney disease (PKD), and the renal effects of lithium.

Nate’s research in the Cox Lab concerns multidendritic sensory neurons in Drosophila melanogaster, and primarily focuses on a class of neurons recently implicated in cold nociception.  These neurons are multimodal—responding to mechanical stimuli in addition to noxious cold—and drive a number of stimulus-specific behaviors.  Additionally, at least some of the ion channels implicated in noxious cold detection (such as nompC and Pkd2) are themselves multimodal.  Nate’s research, in conjunction with that of his colleagues, seeks to understand how this sensory system detects, and processes, multimodal sensory information, and subsequently produces stimulus-specific behaviors.

More broadly, Nate is interested in the molecular, cellular, and network mechanisms underlying sensory transduction, multimodal sensory processing, and behavior selection/generation.  He is also interested in how the focus of his research relates to—or can be understood in light of—topics of philosophical interest (including decision making and mental representation, among others).


Himmel NJ, Patel AA, Cox DN. Invertebrate Nociception. 2016. The Oxford Encyclopedia of Neuroscience. (in press).

Turner HN, Armengol K, Patel AA, Himmel NJ, Sullivan L, Iyer SC, Battacharya S, Iyer EPR, Landry C, Galko MJ, Cox DN. The TRP channels Pkd2, NompC, and Trpm mediate unique aversive behaviors to noxious cold in Drosophila. 2016. Curr. Biol. (in press).

Sim JH, Himmel NJ, Redd SK, Pulous FE, Rogers RT, Black LN, Hong SM, von Bergen TN, Blount MA. Absence of PKC-Alpha Attenuates Lithium-Induced Nephrogenic Diabetes Insipidus. PloS one, 9(7): e101753, July 2014.