Theanne Griffith, Ph.D.
4135 Tupper Hall,
For more information, visit the Griffith Laboratory website.
Our ability to accurately encode thermal signals is critical for survival and allows us to avoid potentially harmful ambient conditions. Additionally, aberrant temperature encoding is a hallmark of various pathologies, including certain forms of chemotherapy-induced peripheral neuropathy and sickle-cell anemia. Despite the essential nature of thermosensation to human survival, our understanding of thermal processing in the peripheral nervous system is limited. The identification of temperature-sensing ion channels, such as TRPV1 and TRPM8, has advanced our knowledge of how thermosensory transduction is initiated; however, a major outstanding question in sensory physiology is how thermal information is transmitted to the central nervous system. The long-term goal of the Griffith lab is to investigate the cellular and molecular mechanisms underlying the transmission of thermal sensations in both health and disease. We aim to identify the ion channels and receptors that constitute the transmission machinery in thermosensitive sensory neurons, as well as understand how their function is regulated under physiological and pathological conditions. To accomplish this, we use innovation combination of mouse genetics, patch-clamp electrophysiology, behavior, molecular profiling, and imaging.
Griffith TN, Docter, TA, Lumpkin EA (2019) Tetrodotoxin-sensitive sodium channels mediate action potential firing and excitability in menthol-sensitive Vglut3-lineage sensory neurons. J Neurosci. 9(36):7086-7101.
Hoffman BU, Baba Y, Griffith TN, Mosharov EV, Woo SH, Roybal DD, Karsenty G, Patapoutian A, Sulzer D, and Lumpkin EA (2018) Merkel cells activate sensory neural pathways through adrenergic synapses. Neuron. 100(6):1401-1413.
Griffith TN & Swanson GT (2015) Identification of critical functional determinants of kainate receptor modulation by auxiliary protein Neto2. J Physiol. 593(22):4815-33. Comment in: Howe JR (2015) Auxiliary subunits highlight a role for the LBD–TMD linkers in glutamate receptor desensitization. J Physiol. 593(22):4813-4.
VanLeeuwen JE, Rafalovich I, Sellers K, Jones KA, Griffith TN, Huda R, Miller RJ, Srivastava DP, Penzes P (2014) Coordinated nuclear and synaptic shuttling of afadin promotes spine plasticity and histone modifications. J Biol. Chem. 289(15):10831-42.
Inestrosa NC, Tapia-Rojas C, Griffith TN, Carvajal FJ, Benito MJ, Rivera-Dictter A, Alvarez AR, Serrano FG, Hancke JL, Burgos PV, Parodi J, Valera-Nallar L (2011) Tetrahydrohyperforin prevents cognitive deficit, Ab deposition, tau phosphorylation and synaptotoxicity in the APPswe/PSEN1"E9 model of Alzheimer’s disease: A possible effect on APP processing. Transl Psychiatry 1: e20;doi:10.1038/tp.2011.19.
Griffith TN, Varela-Nallar L, Dinamarca MC, Inestrosa NC (2009) Neurobiological effects of hyperforin and its potential in Alzheimer's Disease Therapy. Curr Med Chem 17(5):391-406.
Hall AC, Griffith TN, Tsikolia M, Kotey FO, Gill N, Humbert DJ, Watt EE, Yermolina YA, Goel S, El-Ghendy B, Hall CD (2011) Cyclohexanol analogues are positive modulators of GABA(A) receptor currents and act as general anesthetics in vivo. Eur J Pharmacol 667(1-3):175-81.
Watt EE, Betts BA, Kotey FO, Humbert DJ, Griffith TN, Kelly EW, Veneskey KC, Gill N, Rowan KC, Jenkins A, Hall AC (2008) Menthol shares general anesthetic activity and sites of action on the GABAA receptor with the intravenous agent, propofol. Eur J Pharmacol 590(1-3):120-6.