Peter Cain

Dr. Peter Cain

Professor Emeritus - Cognitive, Developmental, and Brain Sciences


  • Bio

  • Publications

  • Research

Biographical Information

I attended Northeastern University in Boston, initially in the Engineering program and then in the Psychology degree program. The years I spent in Engineering taught me the importance of understanding basic science and engineering for whatever I might do in a career, and have been invaluable in my subsequent career in Neuroscience. The new field of Neuroscience, which was then called Physiological Psychology, proved to be the right field for my interests, and I left Engineering for Psychology. I was fortunate to be able to work in an active research lab at Northeastern at a time when formal Honours programs involving lab research were yet to be developed. After graduating I moved to Montreal and worked in Dalbir Bindra's lab at McGill University, doing research on the brain mechanisms of learning. I subsequently completed the MSc and PhD programs in Psychology at McGill under Bindra's supervision, and moved to the University of British Columbia Faculty of Medicine for postdoctoral training with Juhn Wada. During that time I worked with rats and primates and learned research techniques involved in the study of a form of brain plasticity known as kindling, which is epileptic in nature. After completion of the postdoctoral training I moved to the University of Western Ontario, where I have been ever since, apart from sabbatical and other periods spent in other labs. I am currently Professor of Psychology and a member of the Graduate Program in
Neuroscience, and I supervise students in both the Psychology and Neuroscience programs.

Selected Publications

Saucier D, Cain DP. Spatial learning without NMDA receptor-dependent long-term potentiation. Nature, 1995, 378: 186-189.

Cain DP , Grant SGN, Saucier D, Hargreaves EL, Kandel ER. Fyn tyrosine kinase is required for normal seizure kindling. Epilepsy Research, 1995, 22: 107-114.

Hargreaves EL, Cain DP. MK801-induced hyperactivity: Duration of effects in rats. Pharmacology Biochemistry and Behavior, 1995, 51: 13-19.

Cain DP , Saucier D. The neuroscience of spatial navigation: Focus on behavior yields advances. Reviews in the Neurosciences, 1996, 7: 215-231.

Cain DP , SaucierD, Hall J, Hargreaves EL, Boon F. Detailed behavioral analysis of water maze acquisition under APV or CNQX: Contribution of sensorimotor disturbances to drug-induced acquisition deficits. Behavioral Neuroscience, 1996, 110: 86-102.

Kornelsen RA, Boon F, Leung LS, Cain DP. The effects of a single neonatally induced convulsion on spatial navigation, locomotor activity and convulsion susceptibility in the adult rat. Brain Research, 1996, 706: 155-159.

Saucier D, Cain DP. NMDA receptor activity is not required for cholinergic kindling with carbachol. Epilepsy Research, 1996, 24: 9-18.

Saucier D, Hargreaves EL, Boon F, Vanderwolf CH, Cain DP. Detailed behavioral analysis of water maze acquisition under systemic NMDA or muscarinic antagonism: Nonspatial pretraining eliminates spatial learning deficits. Behavioral Neuroscience, 1996, 110: 103-116.

Cain DP , Beiko J, Boon F. Navigation in the water maze: The role of proximal and distal visual cues, path integration, and magnetic field information. Psychobiology, 1997, 25: 286-293.

Beiko J, Candusso L, Cain DP. The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism. Behavioral Brain Research, 1997, 88: 201-211.

Cain DP . Prior nonspatial pretraining eliminates sensorimotor disturbances and impairments in water maze learning caused by diazepam. Psychopharmacology, 1997, 130: 313-319.

Cain DP , Saucier D, Boon F. Testing hypotheses of spatial learning: The role of NMDA receptors and NMDA-mediated long term potentiation. Behavioral Brain Research, 1997, 84: 179-193.

Cain DP. LTP, NMDA, genes, and learning. Current Opinion in Neurobiology, 1997, 7: 235-242.

Hoh T, Cain DP. Fractionating the nonspatial pretraining effect in the water maze task. Behavioral Neuroscience, 1997, 111: 1285-1291.

Anderson R, Barnes JC, Bliss TVP, Cain DP, Cambron K, Davies HA, Errington ML, Fellows LA, Gray RA, Hoh T, Stewart M, Large CH, Higgins GA. Behavioural, physiological and morphological analysis of ApoE knockout mice. Neuroscience, 1998, 85: 93-110.

Beiko J, Cain DP. The effect of water maze spatial training on posterior parietal cortex transcallosal evoked field potentials in the rat. Cerebral Cortex, 1998, 8: 407-414.

Cain DP. Testing the NMDA, long term potentiation, and cholinergic hypotheses of spatial learning. Neuroscience and Biobehavioral Reviews, 1998, 22: 181-193.

Hoh T, Beiko J, Boon F, Cain DP. Complex behavioral strategy and reversal learning in the water maze without NMDA receptor-dependent long-term potentiation. Journal of Neuroscience, 1999, 19: RC2.

Cain DP , Ighanian K, Boon F. Individual and combined manipulation of muscarinic, NMDA and benzodiazepine receptor activity in the water maze task: Implications for a rat model of Alzheimer dementia. Behavioral Brain Research, 2000, 111: 125-137.

Williams MT, Vorhees CV, Boon F, Saber A, Cain DP. Methamphetamine exposure from postnatal day 11 to 20 causes impairments in both behavioral strategies and spatial learning in adult rats. Brain Research, 2002, 958: 312-321.

Cain DP , Finlayson C, Boon F, Bekio J. Ethanol impairs behavioral strategy use in naive rats but does not prevent spatial learning in the water maze in pretrained rats. Psychopharmacology, 2002, 164: 1-9.

Bredy TW, Humpartzoomian RA, Cain DP, Meaney MJ. Partial reversal of the effect of maternal care on cognitive function through environmental enrichment. Neuroscience, 2003, 118: 571-576.

Cain DP, Boon F. Detailed behavioral analysis reveals both task strategies and spatial memory impairments in rats given bilateral middle cerebral artery stroke. Brain Research, 2003, 972: 64-74.

Hoh TE, Kolb B, Eppel A, Vanderwolf CH, Cain DP. Role of the neocortex in the water maze task in the rat: A detailed behavioral and Golgi-Cox analysis. Behavioural Brain Research, 2003, 138: 81-94.

Saber AJ, Cain DP. Combined B-adrenergic and cholinergic antagonism produces behavioral and cognitive impairments in the water maze: Implications for Alzheimer disease and pharmacotherapy with B-adrenergic antagonists. Neuropsychophramacology, 2003, 28:1247-1256.

Beiko J, Lander R, Hampson E, Boon F, Cain DP. Contribution of sex differences in the acute stress response to sex differences in water maze performance in the rat. Behavioural Brain Research, 2004, 151: 239-253.

Cain DP, Boon F, Corcoran ME. Thalamic and hippocampal mechanisms in spatial navigation: A dissociation between brain mechanisms for learning how vs. learning where to navigate. Behavioural Brain Research 2006, 170: 241-256.

Cain DP , Humpartzoomian R, Boon F. Retrosplenial cortex lesions impair water maze strategies learning or spatial place learning depending on prior experience of the rat. Behavioural Brain Research, 2006, 170: 316-325.

MacFabe DF, Cain DP, Rodriguez-Capote K, Franklin AE, Hoffman JE, Kavaliers M, Ossenkopp KP. Neurobiological effects of intraventricular propionic acid in rats: Possible role of short chain fatty acids on the pathogenesis and characteristics of autism spectrum disorders. Behavioural Brain Research, 2007, 176: 149-169.

Dyer K, Cain DP. Water maze impairments after combined depletion of somatostatin and serotonin in the rat. Behavioural Brain Research, 2007, 181: 85-95.

Kenton L, Boon F, Cain DP. Combined but not individual administration of β-adrenergic and serotonergic antagonists impairs water maze acquisition in the rat. Neuropsychopharmacology, 2008, 33: 1298-1311. 

MacFabe DF, Rodriguez-Capote K, Hoffman JE, Franklin AE, Mohammad-Asef Y, Taylor AR, Boon F, Cain DP, Kavaliers M, Possmayer F, Ossenkopp KP. A novel rodent model of autism: Intraventricular infusions of propionic acid increase locomotor activity and induce neuroinflammation and oxidative stress in discrete regions of adult rat brain.  American Journal of Biotechnology and Biochemistry, 2008, 4: 146-166.

Snihur A, Hampson E, Cain DP. Estradiol and corticosterone independantly impair spatial navigation in the Morris water maze in adult female rats. Behavioural Brain Research, 2008, 187: 56-66.

Shultz SR, MacFabe D, Ossenkopp K-P, Scratch S, Whalen J, Cain DP. Intracerebroventricular injection of propionic acid, an enteric bacterial metabolic end-product, impairs social behavior in the rat: Implications for an animal model of autism. Neuropharmacology, 2008, 54: 901-911.

Lazar NL, Rajakumar N, Cain DP. Injections of NGF into neonatal frontal cortex decrease social interaction as adults: A rat model of schizophrenia. Schizophrenia Bulletin, 2008, 34: 127-136.

Shultz SR, MacFabe DF, Martin S, Jackson J, Taylor R, Boon F, Ossenkopp KP, Cain DP. Intracerebroventricular injections of the enteric bacterial metabolic product propionic acid impair cognition and sensorimotor ability in the Long-Evans rat: Further development of a rodent model of autism. Behavioural Brain Research, 2009, 200: 33-41.


My work at Western has had two main phases, both focussed on mechanisms of neural plasticity and behaviour. The first phase involved kindling research, which gradually progressed to the study of a lab model of neural plasticity known as Long Term Potentiation (LTP) as a possible underlying mechanism of kindling. Since LTP was being actively studied as a possible neural mechanism of learning by many researchers, I gradually returned to my original interest of studying the neural mechanisms of learning, with emphasis on the study of LTP in intact, behaving animals. This describes the core of the second phase of my research career. We are continuing to do research on the neural basis of learning and memory in my laboratory. In addition we are developing animal models of a variety of human neurological disorders including Alzheimers disease, schizophrenia, and autism.

I have learned a number of important lessons during this phase, which guide the research I do:

1) Many people are studying brain slices, cells, and molecules. Since natural selection actually selects behaviour, not cells or molecules, it is important and useful to study neural mechanisms of learning in intact, behaving animals.

2) If you are going to study neural mechanisms of learning in behaving animals, it is no good to use the latest complex techniques involving slices, cells, or molecules, and then use a simplistic measure of "learning" like search time in the water maze. Behaviour must be studied in detail, so that the information from behaviour is as rich and detailed as the information on the neural mechanisms. Otherwise the risk of making erroneous inferences about whether learning has been blocked by some treatment, for example, are too high.

3) Properly used, the water maze may be the best laboratory task to use to study the brain mechanisms of learning in small mammals. This necessarily involves employing a detailed behavioural analysis, as discussed above. Use of the water maze in this way has reminded us of the important insight from Krechevsky, Whishaw, and others that acquiring appropriate general behavioural strategies for a task must preceed acquisition of the specific crucial (spatial) information necessary for solving the task, and has allowed these two forms of learning to be studied separately. Using this approach has revealed that many experimental treatments severely impair naive rats in acquiring the necessary general behavioural strategies but do not affect spatial learning at all in rats that already know the behavioural strategies.

4) Two principles of good scientific thinking should always be kept in mind: SCEPTICISM about results and especially interpretations of those results (including one's own), and PARSIMONY, keeping in mind that the simplest explanation is always the best one, at least until a better, more encompassing explanation comes along.

5) We are largely supported by public money. Therefore it is important to apply good behavioural neuroscience research techniques to neurological problems in the population. This illuminates both the disorders and basic brain-behaviour mechanisms. One way to accomplish this is to develop good animals models of Alzheimers disease, schizophrenia, Autism and other common disorders.