Yu-Qing Cao, Ph.D.
ion channel, migraine, headache, chronic pain, synaptic transmission, neuronal excitability, electrophysiology
genetic and epigenetic mechanisms underlying episodic and chronic migraine
Migraine is one of the most common neurovascular disorders and an enormous burden to the healthcare system. One of the major symptoms of migraine, the recurring headache, is highly debilitating, poorly understood and difficult to treat. A significant proportion of patients have headaches that are not responsive to current therapies and increase in frequency over time, eventually becoming chronic migraine.
Research in our lab focuses on understanding the mechanisms of episodic and chronic migraine from both cellular and systems neuroscience perspectives. We employ a multidisciplinary approach including state-of-the-art technologies in electrophysiology, time-lapse imaging, anatomical tracing, single neuron profiling as well as mouse genetics and behavioral assays. Current research projects include:
1) To understand how migraine-associated ion channel mutations affect channel biophysics, neuronal excitability, synaptic transmission and ultimately the encoding of headache.
2) To study the genetic and epigenetic mechanisms underlying the transition from episodic to chronic migraine in mouse models.
3) To investigate how the innate and adaptive immune systems modulate the neuronal circuits underlying migraine headache.
Through theses mechanistic studies, we hope to identify novel molecular and cellular targets for the development of new abortive and prophylactic therapeutics for migraine and other primary headache disorders.
Ren L., Dhaka, A., and Cao, Y. Q. (2015). Function and postnatal changes of dural afferent fibers expressing TRPM8 channels. Molecular Pain [electronic resource] 11(1), 37. PMID 26111800
Guo, Z. H., Liu, P., Ren, F., and Cao, Y. Q. (2014). Non-migraine associated TRESK K+ channel variant C110R does not increase the excitability of trigeminal ganglion neurons. J Neurophysiol 112, 568-579. PMID_24805079
Guo, Z. H., and Cao, Y. Q. (2014). Over-expression of TRESK K+ channels reduces the excitability of trigeminal ganglion nociceptors. PLoS One [electronic resource] 9(1), e87029. PMCID_3900698
Liu, P., Xiao, Z. M., Ren, F., Guo, Z. H., Chen, Z. W., Zhao, H. C., and Cao, Y. Q. (2013). Functional analysis of a migraine-associated TRESK K+ channel mutation. J Neurosci 33, 12810-12824. PMCID_3728689
Huang, D. Y., Li, S. Y., Dhaka, A., Story, G. M., and Cao, Y. Q. (2012). Expression of the transient receptor potential channels TRPV1, TRPA1 and TRPM8 in mouse trigeminal primary afferent neurons innervating the dura. Molecular Pain [electronic resource] 8, 66. PMID 22971321
Tao, J., Liu, P., Xiao, Z., Zhao, H., Gerber, B. R., and Cao, Y. Q. (2012). Effects of familial hemiplegic migraine type 1 mutation T666M on voltage-gated calcium channel activities in trigeminal ganglion neurons. J Neurophysiol 107, 1666-1680. PMID 22190617
Cao, Y. Q., and Tsien, R. W. (2010). Different relationship of N- and P/Q-type Ca2+ channels to channel-interacting slots in controlling neurotransmission at cultured hippocampal synapses. J Neurosci 30(13): 4536-4546.
Cao, Y. Q., and Tsien, R. W. Effects of Familial Hemiplegic Migraine type 1 mutations on neuronal P/Q-type Ca2+ channel activity and inhibitory synaptic transmission. (2005) Proc Natl Acad Sci USA 102, 2590-2595.
Cao, Y. Q., Piedras-Renteria, E. S., Smith, G. B., Chen, G., Harata, N. C., and Tsien, R. W. (2004). Presynaptic Ca2+ channels compete for channel type-preferring slots in altered neurotransmission arising from Ca2+ channelopathy. Neuron 43, 387-400.
Cao, Y. Q., Mantyh, P. W., Carlson, E. J., Gillespie, A. M., Epstein, C. J., and Basbaum, A. I. (1998). Primary afferent tachykinins are required to experience moderate to intense pain. Nature 392, 390-394.
Last Updated: 8/11/2015 4:53:13 PM