UCLA Neuroscience Program Ph.D. Admissions Neuroscience Faculty UCLA and Beyond  



Jim Boulter
Molecular Neurobiology

Email Address:  jboulter@ucla.edu

Work Address:
MRL Building, Room 2557
MRL Building, Room 2774


Phone Numbers:
(310) 825-7067 (310) 825-7067 Phone Numbers:
(310) 206-6665 Office
(310) 206-9080 Laboratory


Selected Publications:

Nakauchi, S. Brennan, R. J. Boulter, J. Sumikawa, K. Nicotine gates long-term potentiation in the hippocampal CA1 region via the activation of alpha2* nicotinic ACh receptors. Eur J Neurosci. 2007; 25(9): 2666-81.
Lioudyno, M. I. Verbitsky, M. Glowatzki, E. Holt, J. C. Boulter, J. Zadina, J. E. Elgoyhen, A. B. Guth, P. S. The alpha9/alpha10-containing nicotinic ACh receptor is directly modulated by opioid peptides, endomorphin-1, and dynorphin B, proposed efferent cotransmitters in the inner ear. Mol Cell Neurosci. 2002; 20(4): 695-711.
Elgoyhen, A. B., Katz, E., Vetter, D. E., Rothlin, C. V., Heinemann, S., and Boulter, J Alpha 10: A determinant of nicotinic cholinergic receptor function in mammalian vestibular and cochlear mechanosensory hair cells. PNAS 2001; 98: 3501-3506.
Salas Ramiro, Sturm Renea, Boulter Jim, De Biasi Mariella Nicotinic receptors in the habenulo-interpeduncular system are necessary for nicotine withdrawal in mice. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2009; 29(10): 3014-8.
Taranda Julian, Maison Stéphane F, Ballestero Jimena A, Katz Eleonora, Savino Jessica, Vetter Douglas E, Boulter Jim, Liberman M Charles, Fuchs Paul A, Elgoyhen A Belén A point mutation in the hair cell nicotinic cholinergic receptor prolongs cochlear inhibition and enhances noise protection. PLoS biology. 2009; 7(1): e18.
Lipovsek Marcela, Plazas Paola, Savino Jessica, Klaassen Alwin, Boulter Jim, Elgoyhen Ana Belén, Katz Eleonora Properties of mutated murine alpha4beta2 nicotinic receptors linked to partial epilepsy. Neuroscience letters. 2008; 434(2): 165-9.
Vetter, D. E. Katz, E. Maison, S. F. Taranda, J. Turcan, S. Ballestero, J. Liberman, M. C. Elgoyhen, A. B. Boulter, J. The alpha10 nicotinic acetylcholine receptor subunit is required for normal synaptic function and integrity of the olivocochlear system. Proc Natl Acad Sci U S A. 2007; 104(51): 20594-9.
Vetter Douglas E, Katz Eleonora, Maison Stéphane F, Taranda Julián, Turcan Sevin, Ballestero Jimena, Liberman M Charles, Elgoyhen A Belén, Boulter Jim The alpha10 nicotinic acetylcholine receptor subunit is required for normal synaptic function and integrity of the olivocochlear system. Proceedings of the National Academy of Sciences of the United States of America. 2007; 104(51): 20594-9.
Nakauchi Sakura, Brennan Robert J, Boulter Jim, Sumikawa Katumi Nicotine gates long-term potentiation in the hippocampal CA1 region via the activation of alpha2* nicotinic ACh receptors. The European journal of neuroscience. 2007; 25(9): 2666-81.
Klaassen, A. Glykys, J. Maguire, J. Labarca, C. Mody, I. Boulter, J. Seizures and enhanced cortical GABAergic inhibition in two mouse models of human autosomal dominant nocturnal frontal lobe epilepsy. Proc Natl Acad Sci U S A. 2006; 103(50): 19152-7.
Klaassen Alwin, Glykys Joseph, Maguire Jamie, Labarca Cesar, Mody Istvan, Boulter Jim Seizures and enhanced cortical GABAergic inhibition in two mouse models of human autosomal dominant nocturnal frontal lobe epilepsy. Proceedings of the National Academy of Sciences of the United States of America. 2006; 103(50): 19152-7.
Ladi, E. Nichols, J. T. Ge, W. Miyamoto, A. Yao, C. Yang, L. T. Boulter, J. Sun, Y. E. Kintner, C. Weinmaster, G. The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands. J Cell Biol. 2005; 170(6): 983-92.
Ladi Ena, Nichols James T, Ge Weihong, Miyamoto Alison, Yao Christine, Yang Liang-Tung, Boulter Jim, Sun Yi E, Kintner Chris, Weinmaster Gerry The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands. The Journal of cell biology. 2005; 170(6): 983-92.
London, S. E. Boulter, J. Schlinger, B. A. Cloning of the zebra finch androgen synthetic enzyme CYP17: a study of its neural expression throughout posthatch development. J Comp Neurol. 2003; 467(4): 496-508.
Cui, C. Booker, T. K. Allen, R. S. Grady, S. R. Whiteaker, P. Marks, M. J. Salminen, O. Tritto, T. Butt, C. M. Allen, W. R. Stitzel, J. A. McIntosh, J. M. Boulter, J. Collins, A. C. Heinemann, S. F. The beta3 nicotinic receptor subunit: a component of alpha-conotoxin MII-binding nicotinic acetylcholine receptors that modulate dopamine release and related behaviors. J Neurosci. 2003; 23(35): 11045-53.
London Sarah E, Boulter Jim, Schlinger Barney A Cloning of the zebra finch androgen synthetic enzyme CYP17: a study of its neural expression throughout posthatch development. The Journal of comparative neurology. 2003; 467(4): 496-508.
Cui Changhai, Booker T K, Allen Roberta S, Grady Sharon R, Whiteaker Paul, Marks Michael J, Salminen Outi, Tritto Theresa, Butt Christopher M, Allen W R, Stitzel Jerry A, McIntosh J Michael, Boulter Jim, Collins Allan C, Heinemann Stephen F The beta3 nicotinic receptor subunit: a component of alpha-conotoxin MII-binding nicotinic acetylcholine receptors that modulate dopamine release and related behaviors. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2003; 23(35): 11045-53.
Haritunians Talin, Boulter Jim, Hicks Carol, Buhrman Jonathon, DiSibio Guy, Shawber Carrie, Weinmaster Gerry, Nofziger Donna, Schanen Carolyn CADASIL Notch3 mutant proteins localize to the cell surface and bind ligand. Circulation research. 2002; 90(5): 506-8.
Labarca, C Schwarz, J Deshpande, P Schwarz, S Nowak, MW Fonck, C Nashmi, R Kofuji, P Dang, H Shi, W Fidan, M Khakh, BS Chen, Z Bowers, BJ Boulter, J Wehner, JM Lester, HA Point mutant mice with hypersensitive alpha 4 nicotinic receptors show dopaminergic deficits and increased anxiety. Proceedings of the National Academy of Sciences of the United States of America. . 2001; 98(5): 2786-91.
Research Interest:

The long-term research objective of our laboratory is to use a molecular genetic approach to understand the role of nicotinic acetylcholine receptors (nAChRs) in vertebrate central and peripheral nervous system function. Although considerable molecular data regarding the structure and function of the ten known nAChR subunit genes is available, far less is known about neural circuitry or roles subserved by the individual receptors assembled from the various subunits. Moreover, little is known about the physiological consequences of mutations within these genes, the precise roles of receptor subtypes in the normal ontogeny and modulation of central nervous system synapses, or in the establishment of nicotine-induced dependence, tolerance, and withdrawal among habitual tobacco users. As a first step towards addressing some of these issues, our lab is conducting experiments which use homologous recombination in mice to introduce null or altered-function mutations in selected nAChR subunit genes. The rationale for such studies rests on the assumption that deficits or alterations in targeted genes can, upon analysis of subject animals, reveal or clarify the function of the mutated gene. Ongoing projects include construction of a transgenic mouse containing a deletion of the nAChR alpha 6 subunit gene. Since alpha 6 is actively transcribed in catecholaminergic nuclei (ventral tegmental area, substantia nigra, and locus coeruleus), it is anticipated that null mutants will help to define central cholinergic circuits which modulate locomotion. Likewise, an alpha 6 null mutation is anticipated to have profound effects on behaviors which originate in the mesolimbic dopamine system and are relevant to the reinforcing properties of nicotine, or to the basic motivational processes which underlie learning and cognitive behavior. A second genetically engineered mouse will harbor a specific mutation (Ser248Phe) in the nAChR alpha 4 subunit gene. In vitro this mutation potentiates onset and slows recovery from receptor desensitization, while in vivo this mutation is responsible for a human disorder known as autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). The purpose of this set of experiments is to provide an animal model to analyze the molecular pathology of partial epilepsy, and to offer a paradigm for the development and evaluation of cholinergic therapeutic strategies. Finally, we are beginning a new project in the lab to determine the possible role of central and peripheral nAChR in the perception of pain. Recent experiments from a number of laboratories have demonstrated that synthetic derivatives of epibatadine (a high affinity, naturally occurring, nicotinic cholinergic agonist) are potent, non-opioid analgesics which show considerable promise for the treatment of chronic, neurodegenerative and inflammatory pain. As a first step towards defining the nAChRs involved in peripheral nociception we are examining the repertoire of nAChRs expressed in spinal cord and dorsal root ganglion neurons (primary sensory afferents) using a combination of in situ hybridization, immunocytochemistry, and reverse-transcription PCR.