RATIONALE: Previous studies have shown the beneficial effects of enriched environment (EE) in rescuing behavioral deficits such as pre-pulse inhibition and locomotor hyperactivity associated with N-methyl-D-aspartate (NMDA) receptor blockade; however, cognitive deficits remain unresponsive. OBJECTIVES: We designed experiments to determine the consequences of raising rat pups in an EE on several behavioral aberrations, mainly cognitive deficits, observed in rats postnatally exposed to MK-801 (NMDA receptor antagonist). METHODS: Male Wistar rats were injected with MK-801 (1 mg/kg) from postnatal day (P) 6-10. Rat pups were housed in an EE from birth up to the time of behavioral experiments at P28-34. The effects of EE in correcting MK-801-associated behaviors were assessed by rotarod, wire grip, open filed, and Morris water maze tests. RESULTS: We found that EE not only has beneficial effects on cognitive performance of normal rats but also prevents spatial learning and memory deficits in Morris water maze induced by MK-801. Postnatal MK-801 treatment also led to motor deficits both in wire grip and accelerating rotarod tests. These deficits were not observed in MK-801-treated rats raised in EE. In the open field test, EE prevented increase in "frequency of grooming" and decrease in "time spent in the center" associated with MK-801. CONCLUSIONS: Our results suggest that exposure to an EE would be strongly beneficial in correcting deficits, notably cognitive, associated with MK-801. Given that the postnatal MK-801 treatment represents an animal model of schizophrenia, we propose timely environmental interventions might be an effective strategy in the protection against schizophrenia.
RATIONALE: Previous studies have shown the beneficial effects of enriched environment (EE) in rescuing behavioral deficits such as pre-pulse inhibition and locomotor hyperactivity associated with N-methyl-D-aspartate (NMDA) receptor blockade; however, cognitive deficits remain unresponsive. OBJECTIVES: We designed experiments to determine the consequences of raising rat pups in an EE on several behavioral aberrations, mainly cognitive deficits, observed in rats postnatally exposed to MK-801 (NMDA receptor antagonist). METHODS: Male Wistar rats were injected with MK-801 (1 mg/kg) from postnatal day (P) 6-10. Rat pups were housed in an EE from birth up to the time of behavioral experiments at P28-34. The effects of EE in correcting MK-801-associated behaviors were assessed by rotarod, wire grip, open filed, and Morris water maze tests. RESULTS: We found that EE not only has beneficial effects on cognitive performance of normal rats but also prevents spatial learning and memory deficits in Morris water maze induced by MK-801. Postnatal MK-801 treatment also led to motor deficits both in wire grip and accelerating rotarod tests. These deficits were not observed in MK-801-treated rats raised in EE. In the open field test, EE prevented increase in "frequency of grooming" and decrease in "time spent in the center" associated with MK-801. CONCLUSIONS: Our results suggest that exposure to an EE would be strongly beneficial in correcting deficits, notably cognitive, associated with MK-801. Given that the postnatal MK-801 treatment represents an animal model of schizophrenia, we propose timely environmental interventions might be an effective strategy in the protection against schizophrenia.
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