Summary of Research:
Movement is an ancient and basic function that is integral to the survival of the individual and species. As such, disorders of movement have a profound impact upon all facets of life. One of the most common movement disorders is Parkinson's disease, a neurodegenerative disorder that compromises dopaminergic areas of the brain rendering the individual unable to initiate, coordinate and execute movement. By employing animal models of Parkinson's disease and a combination of gene therapy, chemogenetic and neurochemical techniques, we examine the role of various neurocircuits and neurotransmitters responsible for this debilitating disorder. As importantly, we explore pharmacological targets within the brain that may aid in the development of more efficacious treatment for the Parkinsonian patient. Our projects, funded by the National Institutes of Health and various foundations investigate neuroplasticity in the movement systems that may provide a novel target for the reduction of Parkinsonian symptoms and side effects that occur as a result of chronic drug therapy.
I am both a mentor and scientist and I would have it no other way. It is not an exaggeration to say that my students are the secret to my success. Regardless of level, the mentor-mentee relationship is an active collaboration. Graduate students in my laboratory, through study and experience, will learn to expertly apply the scientific method to timely research questions accelerating their trajectory to confident, thoughtful and independent scientists. Under this mentorship model trainees will develop a multi-faceted investigational approach and master cutting-edge neuroscience techniques that will lead to the design, execution and communication of sound and innovative research. As part of this process, they are strongly encouraged to cross-train with other faculty, here and at other institutions, to foster collaborative acumen and diversify their technical skill set. I also encourage grant development and writing, so students can experience this process so critical to success in our field.
Representative Publications (+graduate student author, *undergraduate student author):
+Lovejoy, P.C, *Foley, K., +Conti, M.M., *Meadows, S.M, Bishop, C. and Fiumera, A.C. (2020). The genetic basis of susceptibility to low dose paraquat and variation between the sexes in D. melanogaster. (Submitted).
Steece-Collier, K., Collier, T.J., Lipton, J.W., Stancati, J.A., Winn, M.E., Cole-Strauss, A., Sellnow, R., +Conti, M.M., Mercad, N.M., Nillni, E.A., Sortwell, C.E., Manfredsson, F.P. and Bishop, C. (2020). Striatal nurr1, but not FosB expression links a levodopa-induced dyskinesia phenotype to genotype in Fisher 344 vs. Lewis hemiparkinsonian rats Experimental Neurology, Aug.; 330 (In press). (PMID:32387389)
+Kiessling, C.Y., +Lanza, K., *Feinberg, E., Bishop. C. (2020). Dopamine receptor cooperativity synergistically drives dyskinesia, motor behavior, and striatal GABA neurotransmission in hemiparkinsonian rats. Neuropharmacology May 31; 174, (In press). (PMID:32492451)
+Chambers, N.E., +Lanza, K. and Bishop C. (2020). Pedunculopontine nucleus degeneration contributes to both motor and non-motor symptoms of Parkinson’s disease. Frontiers in Pharmacology Jan. 15; 10:1494. (PMID: 32009944)
+Lanza, K., Chemakin, K., Lefkowitz, S., Saito, C., Chambers, N. and Bishop, C. (2020). Reciprocal cross-sensitization of D1 and D3 receptors following pharmacological stimulation in the hemiparkinsonian rat. Psychopharmacology 237(1):155-165. (PMID: 31435690)
Bishop, C. (2019). Neuroinflammation; fanning the flames of L-DOPA-induced dyskinesia. Movement Disorders 34(12):1758-1760. (PMID: 31845761)
+Lanza, K., Perkins, A., Deak T. and Bishop, C. (2019). Late aging-associated increases in L-DOPA-induced dyskinesia is associated with heightened neuroinflammation in the hemi-Parkinsonian rat. Neurobiology of Aging 81:190-199. (PMID: 31306813)
+Chambers, N.C., *Meadows, S.M., *Taylor, A., *Sheena, E., +Lanza, K., +Conti, M.M. and Bishop, C. (2019). Effects of muscarinic acetylecholine m1 and m4 receptor blockade on dyskinesia in the hemi-parkinsonian rat. Neuroscience Jun. 15; 409:180-194. (PMID:31029732)
Guitart, X., Moreno, E., Rea, W., Sanchez-Soto, M., Cai, N-S., Bourque, L., Bishop, C., Newman, A.H., Casado, V. and Ferre, S. (2019). Heteromerization with dopamine D3 receptor biases D1 receptor to G protein-independent signaling. Implications for L-DOPA-induced dyskinesia. Mol Neurobiol 56(10):6756-6769. (PMID:30919214)
Sellnow, R.C., West, A.R., Steece-Collier, K., Sandoval, I.M., +Chambers, N., Benskey, M.J., Bishop, C. and Manfredsson, F.P. (2019). Regulation of dopamine neurotransmission from serotonergic neurons by ectopic expression of dopamine D2 autoreceptors blocks levodopa-induced dyskinesia. Acta Neuropathologica Communications Jan. 15; 7(1):8. (PMID: 30646956).
*Meadows, S.M., +Conti, M.M., *Gross, L., +Chambers, N., *Avnor, Y., +Ostock, C.Y., +Lanza, K. and Bishop, C. (2018). Combined serotonin transporter inhibition and 5-HT1A receptor stimulation with Vilazodone reduces L-DOPA-induced dyskinesia in hemi-parkinsonian rats. Movement Disorders 33(11):1740-1749. (PMID: 30485908)
- PhD, MA, Wayne State University
- BA, Hope College
- Parkinson's Disease
- Drug Development
- The Diseased Brain
- Experimental Psychology-Learning
- Movement Disorders Laboratory
- Clinical Neuroscience
- Faculty Recognition Award from Service for Students with Disabilities
- Dean’s Research Semester Award for Junior Faculty
- Phi Eta Sigma Faculty Award
- Stagner Memorial Award for outstanding research
- State University of New York Chancellor’s Award for Excellence in Teaching
Bishop Laboratory Webpage Link: https://cbishoplab.wordpress.com/Bishop Laboratory Google Scholar Link: https://scholar.google.com/citations?user=Cgnm6uoAAAAJ&hl=en