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Queen's University

Richard J. Beninger


Lab Alumni

Tyson W. Baker | Tomek J. Banasikowski | Cynthia Di Prospero | Emily Hawken | Josh Lister | Susan Quarterone | Sarah Simpson




Tyson W. Baker, Ph.D.

Area of research: My focus is on food-reinforced behaviours and how they are affected by dopaminergic drugs.  My recent research investigated the effects of antipsychotics and other dopaminergic drugs on lever press acquisition: an area that has been relatively unresearched, possibly due to high variance in the rates of acquisition.  I have modified a shaping-free lever press acquisition protocol to rapidly elicit robust lever pressing.  At present, I am using touch screen operant chambers to administer "human" computer-based tasks to rats.  I then plan on using the touch screen tasks to expand the known behavioural profile of the drugs used in my lever press acquisition studies.  My previous research has investigated the role of dopamine D3 receptors and amphetamine in operant responding for food-conditioned reward.  My master’s research in this lab improved upon a two-link heterogeneous chain schedule devaluation procedure and found minor changes in food restriction allowed or disallowed devaluation to occur.



Peer-reviewed Publications  


Baker TW, Weisman RG, Beninger RJ. (2012) Reinforcer devaluation by extinction depends on the food restriction protocol. Behavioural Processes, accepted February 15, 2012


Beninger RJ, Baker TW, Florczynski MM, Banasikowski T. (2010) Regional differences in the action of antipsychotic drugs: implications for cognitive effects in schizophrenic patients. Neurotoxicity Research18: 229-243



Tomek J. Banasikowski, Ph.D. 

Postdoctoral Scholar
University of Pittsburgh
Department of Neuroscience

Area of research: My work at the Neurotransmitters and Behaviour Laboratory at Queen’s has focused primarily on dissociating the effects of dopamine (DA) receptor-subtypes in a number of conditioned behaviors in rats. My current interests examine the mechanisms of catalepsy sensitization and conditioned catalepsy where rats are treated with a sub-threshold dose of antipsychotic drug, specifically haloperidol, in a particular environment. Initially the rats do not exhibit catalepsy, however with time, day-to-day catalepsy sensitization is observed but only in the drug paired environment. More interestingly, when rats are given saline instead of haloperidol they continue to exhibit catalepsy, now conditioned. Meanwhile, if the same dose of haloperidol is injected and catalepsy tested in another environment, animals fail to express catalepsy (see figure below). Thus, this effect is strongly conditioned to the test environment and the expected behaviour associated with daily administration of the drug (haloperidol) can be mitigated by placing the animal in a new environment. Conversely, administration of placebo (saline) without changing the environment produces the expected behaviour indicating a conditioning effect of environment. This model allows us to study the role of dopamine in the control of behavior by environmental stimuli.



Peer-reviewed Publications


Banasikowski TJ, Beninger RJ. (2012) Reduced expression of haloperidol conditioned catalepsy in rats by the dopamine D3 recetor antagonists nafadotride and NGB 2904. European Neuropsychopharmacology, accepted February 16, 2012 


Banasikowski TJ, Beninger RJ. (2012) Dopamine D1-like receptors are critical for haloperidol conditioned catalepsy in rats. International Journal of Neuropsychopharmacology, DOI:10.1017/S1461145711001696 


Banasikowski TJ, McLeod LS, Beninger RJ. (2012) Comparison of the effects of nafadotride, CNQX and. haloperidol on acquisition vs. expression of amphetamine conditioned place preference in rats. Behavioural Pharmacology 23: 89-97


T.J. Banasikowski, A. Bespalov, K. Drescher, B. Behl, L. Unger, A. Haupt, H. Schoemaker, J.P. Sullivan, G. Gross, R.J. Beninger. (2010) Double dissociation of the effects of haloperidol and the dopamine d3 receptor antagonist ABT-127 on acquisition vs. expression of cocaine-conditioned activity in rats. Journal of Pharmacology and Experimental Therapeutics 335(2), 506-15.  

T.J. Banasikowski, R.J. Beninger. (2010) Conditioned drug effects. In: Stolerman IP (ed.) Encyclopedia of Psychopharmacology. Springer, Heidelberg, Germany, pp. 325-331.

R.J. Beninger, T.W. Baker, M.M. Florczynski, T.J. Banasikowski. (2010) Regional differences in the action of antipsychotic drugs: implications for cognitive effects in schizophrenic patients. Neurotoxicity Research 18(3-4), 229-43.


R. J. Beninger, J. Beuk, T. J. Banasikowski, M van Adel, G. A. Boivin, J. N. Reynolds. (2010) Subchronic phencyclidine in rats: Alterations in locomotor activity, maze performance, and GABAA receptor binding. Behavioural Pharmacology, 21(1), 1-10.


R.J. Beninger, T.J. Banasikowski. (2008) Dopaminergic mechanism of reward-related incentive learning: Focus on the dopamine d3 receptor. Neurotoxicity Research, 14(1), 57-70.   



Cynthia Di Prospero, B.A. (Hons.)

M. Sc. Candidate

Centre for Neuroscience Studies

Area of research: As a research technician in the lab I have had the opportunity to work on a variety of diverse projects involving conditioned activity, conditioned catalepsy, conditioned place preference, stereotaxic surgery, histologies and extractions for western blotting. Most of my work has focused on examining the role of GSK3-β in learning using systemic and central injections of GSK3-β inhibitor SB 216763 in the amphetamine-based conditioned activity paradigm. My focus for the coming year will be on signaling molecules involved in conditioned catalepsy.




Emily Hawken, Ph.D.

CIHR Postdoctoral Fellow
Queen's University
Department of Biomedical and Molecular Sciences

Area of research: During my time in the lab I used animal models of schizophrenia-like symptoms to examine excessive water drinking (polydipsia) commonly associated with schizophrenia. My short term goal was to learn about how our neurophysiology processes information from the environment. My long term goal is world domination.



Peer-reviewed Publications


Hawken ER, Lister J, Winterborn AN, Beninger RJ. (2013) Spontaneous polydipsia in animals treated subchronically with MK-801. Schizophrenia Research 143: 228-230. DOI: 10.1016/j.schres.2012.11.013


Hawken ER, Delva NJ, Reynolds JR, Beninger RJ. (2011) Increased schedule-induced polydipsia in the rat following subchronic treatment with MK-801. Schizophrenia Research 125: 93-98

Hawken ER, Owen JA, Hudson RW, Delva NJ (2009) Specific effects of escitalopram on neuroendocrine response. Psychopharmacology (in press)


Hawken ER, M. Crookall MJ, Reddick D, Millson RC, Milev R, Delva N (2009) Mortality over a 20-year period in patients with primary polydipsia associated with schizophrenia: a retrospective study. Schizophrenia Research 107: 128-133.


Hawken ER, Owen JA, Van Vugt D, Delva NJ (2006) Effects of oral racemic citalopram on neuroendocrine responses. Progress in Neuro-Psychopharmacology & Biological Psychiatry 30:694-700.


Hawken ER, Delva NJ, Lawson JS (2001) Successful use of propranolol in migraine associated with electroconvulsive therapy. Headache 41:92-96



Josh Lister, B.Sc. (Hons.) 

Area of research: Validated animal models of schizophrenia-like symptoms provide insight into the underlying mechanisms of the human disorder while concurrently facilitating the discovery of novel pharmacotherapeutics. I am currently examining the effects of early social isolation and sub-chronic exposure to dizocilpine (MK-801, a non-competitive NMDA receptor antagonist) on locomotor activity and performance in several memory-dependent tasks. Subsequently, I plan to evaluate the efficacy of a novel psychotropic agent in the amelioration of behavioural abnormalities observed in affected animals.



Peer-reviewed Publications


Hawken ER, Lister J, Winterborn AN, Beninger RJ. (2013) Spontaneous polydipsia in animals treated subchronically with MK-801. Schizophrenia Research 143: 228-230. DOI: 10.1016/j.schres.2012.11.013


CSBBCS Poster Presentation


Lister J, Reynolds JN, Beninger RJ. Post-weaning social isolation increases exploratory behaviour and elevates locomotor activity in response to novelty, stress, and amphetamine challenge.

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Susan E. Quartarone, B.A. (Hons.)

M.Sc. Candidate in Psychology 

Brain, Behaviour, and Cognitive Science

Area of research: I am interested in neurotransmitters in the brain and their involvement in learning, specifically incentive learning. Dopamine (DA) is of particular interest as it is paramount in reward-related learning. In fact, mice without DA signalling exhibit deficits in goal-directed behaviour due to decreased motivation to obtain rewards. An important signalling molecule in the DA question is glycogen-synthase-kinase-3-beta (GSK-3β), as it has been proposed as an essential component in DA-mediated behaviours. GSK-3β is part of the protein kinase B (Akt) protein phosphatase-2A (PP2A) beta arrestin 2 (βArr2) signalling complex. It has been found that DA D2 receptor activation inhibits Akt activity. Inhibition of Akt prevents Akt from phosphorylating GSK-3β resulting in increased levels of GSK-3β in the brain. Interestingly, DA agonists such as amphetamine actually increase levels of GSK-3β in the brain, while antipsychotics which block DA D2 receptors prevent Akt inhibition, resulting in phosphorylation and therefore deactivation of GSK-3β. Using a GSK-3β inhibitor in the rat brain, coupled with the conditioned place preference paradigm using amphetamine would be a direct way of investigating the hypothesis that GSK-3β is implicated in incentive learning. If the rat does not show a conditioned place preference, this will implicate that the GSK-3β inhibitor has blocked the reward associated with substance use. My current research investigates this.

My previous research investigated the disposition of impulsivity and its relation to comorbid alcohol and substance use disorders and how that is related to prescribed methadone dose in methadone maintenance populations.



Sarah Simpson, B.Sc. (Hons.) 

M.D. Candidate
Queen's School of Medicine
Area of research: I am interested in the interaction of biological and environmental factors implicated in schizophrenia. Animal models offer insight into the underlying pathology and novel therapeutic approaches to schizophrenia. My research utilizes an animal model of schizophrenia-like symptoms to explore abnormalities of neurotransmission that may underlie behavioural and cognitive deficits characteristic of the disorder.

Subchronic treatment with a non-competitive glutamate NMDA-receptor antagonist or social isolation from weaning (P21) to adulthood (P56) produce deficits similar to some positive and negative symptoms of schizophrenia. The combination of these two treatments may produce a more robust animal model of symptoms. My current interests lie in the GABAergic deficits that may underlie some symptoms of schizophrenia and the ability of pro-GABA treatment to ameliorate the cognitive and behavioural deficits produced by this animal model.


Peer-reviewed Publications


Simpson, S. M., Hickey, A. J., Baker, G. B., Reynolds, J. N., & Beninger, R. J. (2012). The antidepressant phenelzine enhances memory in the double Y-maze and increases GABA levels in the hippocampus and frontal cortex of rats. Pharmacol Biochem 
Behav, 102, 109-117.


Simpson, S. M., Menard, J. L., Reynolds, J. N., & Beninger, R. J. (2010). Post-weaning social isolation increases activity in a novel environment but decreases defensive burying and subchronic MK-801 enhances the activity but not the burying effect in rats. Pharmacol Biochem 
Behav, 95, 72-79.

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