Laurence Trussell, Ph.D.
Laurence Trussell received his Ph.D. in Biology from the University of California, Los Angeles in 1983. After initial postdoctoral work at UCLA, he obtained further training at Washington University, St. Louis. In 1990, he received a faculty appointment at the University of Wisconsin, Madison. In 1999, he was appointed as professor in the Oregon Hearing Research Center with an appointment as scientist at the Vollum Institute.
Summary of Current Research
Using chemical and electrical signals, neurons preserve, process, and integrate information about sensory stimuli in the environment. Each sensory modality presents the brain with special challenges. These challenges are met by unique neuronal circuitry and by unique cellular characteristics in the neurons themselves. Laurence Trussell and his associates are interested in the fine tuning of membrane properties and synapses requisite to the incredible feats of computation performed in the auditory system, where even microsecond differences in signals have behavioral consequences.
The Trussell lab works on neurons in the cochlear nuclei and trapezoid body because their synapses offer the opportunity to study synaptic transmission at high resolution and because the investigators can relate findings about cellular mechanisms to activity measured in vivo. Patch-clamp analyses reveal that these neurons express a complement of glutamate receptors and potassium channels that enable the cells to fire reliably in response to incoming stimuli, thus passaging signals with little temporal jitter. The lab is finding that mechanisms of neurotransmitter release and clearance are also fine-tuned to the tasks of preserving timing information. Moreover, these neurons express presynaptic receptors that regulate electrical activity in unusual ways. Trussell and colleagues employ electrophysiological and optical approaches to reveal how single synapses participate in this process. Other studies in the lab are directed toward understanding the mechanisms and functions of long-term synaptic plasticities within auditory circuits.
Kuo SP and Trussell LO. (2011) Spontaneous spiking and synaptic depression underlie noradrenergic control of feed-forward inhibition. Neuron 71:306-318.
Huang H and Trussell LO. (2011) KCNQ5 channels control resting properties and release probability of a synapse. Nature Neurosci. 14:840-847.
Bender KJ, Ford CP, and Trussell LO. (2010) Dopaminergic modulation of axon initial segment calcium channels regulates action potential initiation. Neuron 68:500-511.
Roberts MT and Trussell LO. (2010) Molecular layer inhibitory interneurons provide feedforward and lateral inhibition in the dorsal cochlear nucleus. J. Neurophysiol. 104:2462-2473.
Kim Y and Trussell LO. (2009) Negative shift in the glycine reversal potential mediated by a Ca2+- and pH-dependent mechanism in interneurons. J. Neurosci. 29:11495-11510.
Balakrishnan V, Kuo SP, Roberts PD, and Trussell LO. (2009) Slow glycinergic transmission mediated by transmitter pooling. Nature Neurosci. 12:286-294.
Bender KJ and Trussell LO. (2009) Axon initial segment Ca2+ channels influence action potential generation and timing. Neuron 61:259-271.
Huang H and Trussell LO. (2008) Control of presynaptic function by a persistent Na+ current. Neuron 60:975-979.
Roberts MT, Bender KJ, and Trussell LO. (2008) Fidelity of complex spike-mediated synaptic transmission between inhibitory interneurons. J. Neurosci. 28:9440-9450.
Lu T, Rubio ME, and Trussell LO. (2008) Glycinergic transmission shaped by the co-release of GABA in a mammalian auditory synapse. Neuron 57:524-535.
Tzounopoulos T, Rubio ME, Keene JE, and Trussell LO. (2007) Coactivation of pre- and postsynaptic signaling mechanisms determines cell-specific spike-timing-dependent plasticity. Neuron 54:291-301.