ArticleNeurobiology of learning and memory2016
Memory deficits with intact cognitive control in the methylazoxymethanol acetate (MAM) exposure model of neurodevelopmental insult.
Article in Neurobiology of learning and memory, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Roles of Lcn2 and neuroinflammation in a scopolamine-induced cognitive impairment animal model: implication of the NLRP3 inflammasome pathway.Genes & genomics · 2026Article
- Cognitive control of behavior and hippocampal information processing without medial prefrontal cortex.eLife · 2025Article
- Serotonin 5-HTPsychopharmacology · 2021Article
- Fine Spike Timing in Hippocampal-Prefrontal Ensembles Predicts Poor Encoding and Underlies Behavioral Performance in Healthy and Malformed Brains.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Synaptic plasticity/dysplasticity, process memory and item memory in rodent models of mental dysfunction.Schizophrenia research · 2019Review
- Sub-circuit alterations in dorsal hippocampus structure and function after global neurodevelopmental insult.Brain structure & function · 2018Article
- Phencyclidine Discoordinates Hippocampal Network Activity But Not Place Fields.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- MAM-E17 rat model impairments on a novel continuous performance task: effects of potential cognitive enhancing drugs.Psychopharmacology · 2017Article
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3 authors.
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Abstract
Cognitive impairments are amongst the most debilitating deficits of schizophrenia and the best predictor of functional outcome. Schizophrenia is hypothesized to have a neurodevelopmental origin, making animal models of neurodevelopmental insult important for testing predictions that early insults will impair cognitive function. Rats exposed to methylazoxymethanol acetate (MAM) at gestational day 17 display morphological, physiological and behavioral abnormalities relevant to schizophrenia. Here we investigate the cognitive abilities of adult MAM rats. We examined brain activity in MAM rats by histochemically assessing cytochrome oxidase enzyme activity, a metabolic marker of neuronal activity. To assess cognition, we used a hippocampus-dependent two-frame active place avoidance paradigm to examine learning and spatial memory, as well as cognitive control and flexibility using the same environment and evaluating the same set of behaviors. We confirmed that adult MAM rats have altered hippocampal morphology and brain function, and that they are hyperactive in an open field. The latter likely indicates MAM rats have a sensorimotor gating deficit that is common to many animal models used for schizophrenia research. On first inspection, cognitive control seems impaired in MAM rats, indicated by more errors during the two-frame active place avoidance task. Because MAM rats are hyperactive throughout place avoidance training, we considered the possibility that the hyperlocomotion may account for the apparent cognitive deficits. These deficits were reduced on the basis of measures of cognitive performance that account for motor activity differences. However, though other aspects of memory are intact, the ability of MAM rats to express trial-to-trial memory is delayed compared to control rats. These findings suggest that spatial learning and cognitive abilities are largely intact, that the most prominent cognitive deficit is specific to acquiring memory in the MAM neurodevelopmental model, and that hyperactivity can confound assessments of cognition in animal models of mental dysfunction.
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