Associate ProfessorEmail: email@example.com
After completing undergraduate work in Chemistry and Biology at Lincoln University, Darrell Jackson received a Ph.D. in Pharmacology/Toxicology from Washington State University in 1990 at Pullman. Following postdoctoral positions at Massachusetts Institute of Technology, Boston University, and University of Washington, and faculty positions at Washington State University and Morehouse School of Medicine in Atlanta, he moved to The University of Montana as an Associate Professor in 2004.
Field of Study
Our studies have significant implications for linking dysfunctions in G-protein-coupled receptor (GPCR) signaling with numerous neurological disorders that includes Alzheimer's disease, Parkinson's disease, and stroke. A major focus in the laboratory is identifying and characterizing the mechanisms that regulate the endosomal sorting of internalized cell surface GPCRs in neurons. Sequestration of cell surface neurotransmitter receptors, such as GPCRs, is one mechanism utilized by neurons to terminate receptor signaling. The mechanism regulating endosomal sorting of internalized GPCRs in neurons remains unclear. A second focus in the laboratory involves elucidating the underlying mechanisms that mediate the polarize sorting of selective GPCRs in neurons to either dendritic or axonal compartments.
Jones, K., Echeverry, M., Mosser, V., Gates, A., and Jackson, D.A. (2006) Agonist mediated internalization of M2 mAChR is beta-arrestin-dependent. Journal of Molecular Signaling. In Press.
Mou, L., Gates A., Mosser V., Tobin A., and Jackson D.A. (2006). Transient hypoxia induces sequestration of M1 and M2 muscarinic acetylcholine receptors. Journal of Neurochemistry 96:510-519.
Mou, L., and Jackson, D.A. (2001). Transient hypoxia differentially decreases GRK2 protein levels in CHO cells stably expressing the m1 mAChR. Biochemical and Biophysical Research Communications 286: 848-851.
Jan Krzysztof Blusztajn, Jennifer Marie Cermack, Thomas Holler, and Darrell A. Jackson (1998). Imprinting of hippocampal metabolism of choline by its availability during gestation: Implications for cholinergic neurotransmission. J Physiology 9:199-203.
Cermak, J.M., Holler, T., Jackson, D.A., and Blusztajn, J.K. (1998). Prenatal availability of choline modifies development of the hippocampal cholinergic system. FASEB 12: 349-357.
Jackson, D.A., and Nathanson, N.M. (1997). Transforming growth factor-b1 decreases expression and function of m2 and m4 muscarinic receptors in cultured embryonic chick heart cells. Biochemical Pharmacology 54:525-527.
White, S.R., S.J. Fung, D.A. Jackson, and K.M. Imel (1996). Serotonin, norepinephrine and associated neuropeptides: effects on somatic motoneuron excitability. In G. Holstege, R. Bandler, and C.B. Saper (eds.), The Emotional Motor System. Progress in Brain Research 107: 183-199.
Jackson, D.A., and Nathanson, N.M. (1995). Subtype-specific regulation of muscarinic receptor expression and function by heterologous receptor activation. Journal of Biological Chemistry 270: 22374-22377.
Hamilton, S.E., McKinnon, L.A., Jackson, D.A., Goldman, P.S., Migeon, J.C., Habecker, B.A., Thomas, S.L., and Nathanson, N.M. (1995). Molecular analysis of the regulation of muscarinic receptor function and expression. Life Sciences 56: 939-943.
Jackson, D.A., Kischka, U., and Wurtman, R.J.(1995) Choline enhances scopolamine-induced release of acetylcholine in the dorsal hippocampus of conscious freely moving rats. Life Sciences 56: 45-49.
Blusztajn, J.K., Venturini, A., Jackson, D.A., Schuler, U., Lee, H.J., and Wainer, B.H. (1993). Cholinergic cell lines as model for testing drug efficacy and toxicity. Alternative Methods in Toxicology 9:3-8.
Blusztajn, J.K., Venturini, A., Jackson, D.A., Lee, H.J., and Wainer, B.H. (1992). Acetylcholine synthesis and release is enhanced by dibutyryl cyclic AMP in a neuronal cell line derived from mouse septum. J Neuroscience 12:793-799.
Jackson, D.A., and White S.R. (1990). Receptor subtypes mediating facilitation by serotonin of excitability of spinal motoneurons. Neuropharmacology 29:787-797.
White, S.R., Crane, G.K., and Jackson, D.A. (1989). Thyrotropin releasing hormone (TRH) effects on spinal cord neuronal excitability. Ann NY Acad Sci 553:337-350.
Jackson, D.A., and White, S.R. (1988). Thyrotropin releasing hormone (TRH) modifies excitability of spinal cord dorsal horn cells. Neurosci Lett 92:171-176.
Esser, S.L., Jackson, D.A., Kirkpatrick, R., LaHann T.R. (1987). Microcomputerized data collection for the pharmacology lab. Proc West Pharmacol Soc 30:197-200.
Specialized Research Interests
Dysfunctional glutamatergic receptor trafficking and signaling in neurological disorders including stroke, and traumatic brain injury.
BIOH 380 - Cellular & Molecular Neuroscience
BMED 662 - Neuroscience 2
BMED 610 - Neuropharmacology
Phar Sci Research Interests
To identify and develop small molecule inhibitors that have neuroprotective affects against neurodegenerative diseases that includes traumatic brain injury and stroke.
Neuroscience Research Interests
To understand the intracellular mechanisms responsible for stroke-induced delayed neuronal death.