Animal models of: drug addiction Parkinson's disease schizophrenia

Contact Information Phone: 207-786-6184 Email: jkelsey@bates.edu Office: Pettengill 359

• B.A. Psychology - Grinnell College, 1966
• Ph.D. Biopsychology - University of Chicago, 1971

Drug addiction: Although drug addiction, by definition, requires a drug, the process is also dependent on a variety of environmental factors, especially those related to conditioning. Professor Kelsey's main interests are in the neural pathways, e.g., the mesolimbic dopamine pathway projecting to the n. accumbens, that mediate the rewarding effects of drugs, especially nicotine, and the aversive effects of withdrawal from those drugs. He is also interested in the role of conditioning factors and context in maintaining drug addiction and the potential for using conditioning procedures, e.g., extinction, to reduce addiction.

Parkinson's disease (PD): It is well established that PD is due to degeneration of the nigrostriatal bundle that projects dopamine (DA) neurons from the midbrain to the corpus striatum in the forebrain. It is also well established that replacement of the lost DA with L-DOPA remains the most effective symptomatic therapy, although it does not reduce the ongoing degeneration and it produces debilitating side effects, e.g., dyskinesia. Professor Kelsey is interested in exploring the ability of non-DA drugs, such as those that modulate glutamate, adenosine, and cannabinoids, to reduce PD by themselves or reduce the side effects produced by L-DOPA.

Schizophrenia: Schizophrenia is a debilitating disorder consisting of three sets of symptoms: positive, e.g., hallucinations; negative, e.g., social withdrawal; and cognitive, e.g., poor attention and memory. Recent evidence suggests that all three of these symptoms can be produced in normal humans and rats by phencyclidine (PCP), a drug that blocks a particular kind of receptor for glutamate, called the NMDA receptor. Although traditional antipsychotic medications typically block DA transmission, Professor Kelsey is interested in examining drugs, especially those that more directly affect glutamate, that may be effective in reducing the effects of PCP in rats without producing the side effects associated with traditional antipsychotics, and, therefore, drugs that may be useful in treating this disorder in humans.

• PSYC 250 Motivation and Emotion
  
• PSYC 305 Animal Learning
  
• PSYC 362 Psychopharmacology: How Drugs Affect Behavior
  
• NS/PY 363 Physiological Psychology
  
• PSYC 399 Junior-Senior Seminar in Biological Psychology
  

^* indicates Bates student

Kelsey, J. E., *Beer, T., *Lee, E., & *Wagner, A. (2002). Low doses of dizocilpine block the development and subsequent expression of locomotor sensitization to nicotine in rats. Psychopharmacology, 161, 370-378.

Kelsey, J. E., *Mague, S. D., *Pijanowski, R. S., *Harris, R. C., Kleckner, N. W., & *Matthews, R. T. (2004). NMDA receptor antagonists ameliorate the stepping deficits produced by unilateral medial forebrain bundle injections of 6-OHDA in rats. Psychopharmacology, 175, 179-188.

Kelsey, J. E., & *Calabro, S. (2008) Rimonabant blocks the expression but not the development of locomotor sensitization to nicotine in rats. Psychopharmacology, 198, 461-466.

Kelsey, J. E., *Langelier, N.A., *Oriel, B. S., & *Reedy, C. (2009). The effects of systemic, intrastriatal, and intrapallidal injections of caffeine and systemic injections of A_2A and A₁ antagonists on forepaw stepping in the unilateral 6-OHDA-lesioned rat. Psychopharmacology, 201, 529-539.

Kelsey, J. E., *Gerety, L. P., & *Guerriero, R. M. (2009). Electrolytic lesions of the nucleus accumbens core (but not the medial shell) and the basolateral amygdala enhance context specific locomotor sensitization to nicotine in rats. Behavioral Neuroscience, 123, 577-588.

Kelsey, J. E., *Harris, O., & *Cassin, J. J. (2009). The CB₁ antagonist rimonabant is adjunctively therapeutic as well as monotherapeutic in an animal model of Parkinson's disease. Behavioural Brain Research, 203, 304-307.