Bruce Bean

Bruce Palmer Bean, PhD

Robert Winthrop Professor of Neurobiology

Neuronal Excitability and Ion Channel Pharmacology

Neurons communicate with each other using electrical impulses. Information is encoded as patterns of “action potentials”, millisecond-long reversals of the voltage across the cell membrane. Different neurons in the brain fire action potentials with a variety of distinct patterns. The Bean lab seeks to understand these different patterns of firing in terms of the underlying molecular devices – tiny pores in the membrane known as ion channels.

In mammalian brains, each neuron possesses several dozen different types of ion channels. Most of these are closed when the neuron is at rest (electrically silent). It is the coordinated, transient opening, or “gating” of particular types of ion channels that underlies electrical signaling. To understand how different combinations of ion channels work together to generate the distinct patterns of action potential firing in different neurons, we make electrical recordings of these cells using patch clamp, voltage clamp and other electrophysiological approaches.

Our goal is to use knowledge of the particular ion channels in different kinds of neurons to find new drugs that can selectively inhibit or enhance electrical activity of specific type of neurons by targeting specific ion channels. In collaboration with Dr. Clifford Woolf’s laboratory, we are currently focused on finding new drugs to treat pain, itch, and cough. We are also seeking to identify new drugs to disrupt epileptic activity.

Publications View
Bidirectional flow of the funny current (If) during the pacemaking cycle in murine sinoatrial node myocytes.
Authors: Authors: Peters CH, Liu PW, Morotti S, Gantz SC, Grandi E, Bean BP, Proenza C.
Proc Natl Acad Sci U S A
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Cannabidiol inhibition of murine primary nociceptors: Tight binding to slow inactivated states of Nav1.8 channels.
Authors: Authors: Zhang HB, Bean BP.
J Neurosci
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Inhibition of inflammatory pain and cough by a novel charged sodium channel blocker.
Authors: Authors: Tochitsky I, Jo S, Andrews N, Kotoda M, Doyle B, Shim J, Talbot S, Roberson D, Lee J, Haste L, Jordan SM, Levy BD, Bean BP, Woolf CJ.
Br J Pharmacol
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BK channel regulation of after-potentials and burst firing in cerebellar Purkinje neurons.
Authors: Authors: Niday Z, Bean BP.
J Neurosci
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Lidocaine binding enhances inhibition of Nav1.7 channels by the sulfonamide PF-05089771.
Authors: Authors: Jo S, Bean BP.
Mol Pharmacol
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Vagal sensory neurons drive mucous cell metaplasia.
Authors: Authors: Talbot S, Doyle B, Huang J, Wang JC, Ahmadi M, Roberson DP, Yekkirala A, Foster SL, Browne LE, Bean BP, Levy BD, Woolf CJ.
J Allergy Clin Immunol
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Novel charged sodium and calcium channel inhibitor active against neurogenic inflammation.
Authors: Authors: Lee S, Jo S, Talbot S, Zhang HB, Kotoda M, Andrews NA, Puopolo M, Liu PW, Jacquemont T, Pascal M, Heckman LM, Jain A, Lee J, Woolf CJ, Bean BP.
Elife
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Publisher Correction: Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug.
Authors: Authors: Barak B, Zhang Z, Liu Y, Nir A, Trangle SS, Ennis M, Levandowski KM, Wang D, Quast K, Boulting GL, Li Y, Bayarsaihan D, He Z, Feng G.
Nat Neurosci
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Deep Sequencing of Somatosensory Neurons Reveals Molecular Determinants of Intrinsic Physiological Properties.
Authors: Authors: Zheng Y, Liu P, Bai L, Trimmer JS, Bean BP, Ginty DD.
Neuron
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Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug.
Authors: Authors: Barak B, Zhang Z, Liu Y, Nir A, Trangle SS, Ennis M, Levandowski KM, Wang D, Quast K, Boulting GL, Li Y, Bayarsaihan D, He Z, Feng G.
Nat Neurosci
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