Jane Witten

Associate Professor
 (414) 229-4993
 Lapham Hall N409


  • Postdoc, Dev. Neuroscience, University of Arizona, Tucson, AZ, 1990-92
  • Postdoc, Dev. Neuroscience, University of Washington, Seattle, WA, 1986-90
  • Postdoct, Neuroscience, University of Geneva, Switzerland, 1984-86
  • PhD, Pharm. & Physiol. Sci., University of Chicago, Chicago, IL, 1984
  • BA, Bio-Psychology, Wesleyan University, Middletown, CT, 1974

Research Interests

Animals live in a constantly changing environment. Survival demands that nervous systems must be flexible to accommodate to these changes. My research interests are to elucidate the cellular and molecular mechanisms that produce this flexibility or plasticity. We are focusing on how steroid hormones, neuropeptides, and potassium ion channels interact to contribute to nervous system development, flexibility and function. We are taking a multidisciplinary approach using physiological, biochemical, immunochemical, and molecular techniques to address these questions. The model system that we use for our studies is metamorphosis of the tobacco hornworm, Manduca sexta.

The nervous system of this animal contains a relatively small number of neurons, most of which can be studied as identified individuals. Metamorphosis results in a dramatic reorganization of the moth’s nervous and muscular systems facilitating our search for mechanisms underlying neuronal and behavioral plasticity. We have shown that a family of neuropeptides, FLRFamides, are differentially expressed and developmentally regulated. Our biochemical studies suggest the neurosecretory cells release these neuropeptides at each molt and we propose that two modulate muscles to coordinate molting behavior. Our molecular studies suggest that multiple genes encode the Manduca FLRFamide peptide family; the expression of one gene is cell specific and developmentally modulated by steroid hormones. Our investigation of how modulation of ion channels may contribute to neuronal plasticity is focusing on voltage-gated potassium ion channels. Defects in their normal development or function can lead to disruption of neuronal signaling and then to neurological and neuromuscular diseases. We have cloned and molecularly characterized the Manduca eag and Manduca slowpoke homologs and immunochemically characterized Manduca Shakerlike proteins. Currently, we are studying their cellular distribution, developmental expression, steroid hormone regulation, and functions in the nervous system and muscles.

Courses Taught

BioSci 354 – Introduction to Neuroscience I
BioSci 370 – Animal Physiology
BioSci 372 – Animal Physiology and Neurobiology Laboratory
BioSci 596 – Neuropharmacology

Selected Publications

Keyser, Matthew, and Witten, Jane L. “Calcium-Activated Potassium Channel of the Tobacco Hornworm Manduca sexta: Molecular Characterization and Expression Analysis.” J. Exp. Biology 208. (2005): 4167-4179.
Keyser, Matthew, Titus, Steven A., Anson, Blake, Ganetzky, Barry B., and Witten, Jane L. “Molecular Characterization, Functional Expression and Developmental Profile of an Ether à-go-go K+ Channel in the Tobacco Hornworm Manduca sexta.” J. Neurobiol. 55. (2003): 73-85.
Lu, D., Lee, K.-Y., Horodyski, F. M., and Witten, Jane L. “Molecular characterization and cell-specific expression of a Manduca sexta FLRFamide gene.” J. Comp. Neurol. 446. (2002): 377-396.
Miao, Yongsheng, Waters, Elizabeth M., and Witten, Jane L. “Developmental and regional-specific expression of FLRFamide peptides in the tobacco hornworm, Manduca sexta, suggests functions in ecdysis behaviors.” J. Neurobiol. 37. (1998): 468-484.