Ellen Hess - Recent Papers

Hess, E.J. Migraines in Mice? Cell, 87:1149-1151, 1996.

Campbell, D.B. and Hess, E.J. Cerebellar circuitry is activated during convulsive episodes in the tottering (tg/tg) mutant mouse. Neuroscience, 85:773-783, 1998.

Campbell, D.B. and Hess, E.J. L-type calcium channels contribute to the tottering mouse dystonic episodes. Molecular Pharmacology, 55:23-31, 1999.

Campbell, D.B., North, J.B. and Hess, E.J. Tottering mouse motor dysfunction is abolished on the Purkinje cell degeneration (pcd) mutant background. Experimental Neurology, 160:268-278, 1999.

Jinnah, H.A., Sepkuty, J.P., Ho, T., Drew, T., Rothstein, J.D. and Hess, E.J. Calcium channel activation and dystonia in the mouse. Movement Disorders, 15:542-551, 2000.  [PDF]

Fureman, B.E., Jinnah, H.A. and Hess, E.J. Paroxysmal dyskinesia in the calcium channel mouse mutant tottering, Pharmacology Biochemistry & Behavior, 73:631-637, 2002.   [PDF]

Pizoli, C.E. Jinnah, H.A., Billingsley, M.L. and Hess, E.J. Abnormal cerebellar signaling induces dystonia in mice, Journal of Neuroscience, 22:7825-7833, 2002.   [PDF]

Jones, M.D. and Hess, E.J. Norepinephrine regulates locomotor hyperactivity in the mouse mutant coloboma. Pharmacology Biochemistry & Behavior, 75:209-216, 2003.   [PDF]

Weisz, C.J.C., Raike, R.S., Soria-Jasso, L.E. and Hess, E.J. Potassium channel blockers inhibit the triggers of attacks in the calcium channel mouse mutant tottering. Journal of Neuroscience, 25:4141-4145, 2005.   [PDF]

Fureman, B.E. and Hess, E.J. Noradrenergic blockade prevents attacks in a model of episodic dysfunction caused by a channelopathy. Neurobiology of Disease, 20:227-232, 2005.   [PDF]

Bruno, K.J. and Hess, E.J. The (2C-adrenergic receptor mediates hyperactivity of coloboma mice, a model of attention deficit hyperactivity disorder. Neurobiology of Disease, 23:679-688, 2006.

von Coelln,  R., Thomas, B., Lim, K.L., Savitt, J.M., Saffary, R., Stirling, W., Bruno, K., Hess, E.J., Lee, M.K., Dawson, V.L. and Dawson, T.M.  Inclusion body formation and neurodegeneration are parkin-independent in a mouse model of (-synucleinopathy. Journal of Neuroscience, 26:3685-3696, 2006.

Bruno, K.J., Freet, C.S., Twining, R.C., Grigson, P.S., and Hess, E.J.  Abnormal latent inhibition and impulsivity in coloboma mice, a model of ADHD. Neurobiology of Disease, 25:206-216, 2007.

Fan, X. and Hess, E.J. D2-like dopamine receptors mediate the response to amphetamine in a mouse model of ADHD. Neurobiology of Disease, 26:201-211, 2007.

Devanagondi, R., Egami, K., Hess, E.J. and Jinnah, H.A. Neuroanatomical substrates for paroxysmal dyskinesia in lethargic mice. Neurobiology of Disease, 27:249-257, 2007.

Jen, J.C., Graves, T.D., Hess, E.J., Hanna, M.G., Griggs, R.C., Baloh, R.W. and the CINCH investigators. The primary episodic ataxias: diagnosis, pathogenesis and treatment. Brain, 130:2484-2493, 2007.

Shirley, T.L., Rao, L.M., Hess, E.J. and Jinnah, H.A.  Paroxysmal dyskinesias in mice. Movement Disorders, 23:259-264, 2008.

Jinnah, H.A., Richter, A., Mink, J.W., Caldwell, G.A., Caldwell, K., Gonzales-Allegre, P., Cookson, M.R., Breakefield, X.O., Delong, M.R. and Hess, E.J.  Animal models for drug discovery in dystonia. Expert Opinion on Drug Discovery, 3:83-97, 2008.

Jinnah, H.A. and Hess, E.J. Experimental therapeutics in dystonia. Neurotherapeutics, 5:198-209, 2008.