Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Maternal care in the rat influences the development of cognitive function in the offspring through neural systems known to mediate activity-dependent synaptic plasticity. The offspring of mothers that exhibit increased levels of pup licking/grooming (high-LG mothers) show increased hippocampal N-methyl-D-aspartate (NMDA) subunit mRNA expression, enhanced synaptogenesis and improved hippocampal-dependent spatial learning in comparison with animals reared by low-LG mothers. The effects of reduced maternal care on cognitive function are reversed with peripubertal environmental enrichment; however, the neural mechanisms mediating this effect are not known. In these studies we exposed the offspring of high- and low-LG mothers to environmental enrichment from days 22 to 70 of life, and measured the expression of genes encoding for glutamate receptor subunits and synaptophysin expression as a measure of synaptic density. Environmental enrichment reversed the effects of maternal care on synaptic density and this effect was, in turn, associated with a reversal of the effect of maternal care on the NR2A and NR2B subunits of the NMDA receptor, as well as effects on (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunits. Finally, direct infusion of an NR2B-specific NMIDA receptor antagonist into the hippocampus eliminated the effects of maternal care on spatial learning/memory in the Morris water maze. These findings suggest that: (1) the effects of maternal care are mediated by changes in NR2B gene expression; and (2) that environmental enrichment reverses the effects of reduced maternal care through the same genomic target, the NR2B gene, and possibly effects on other subunits of the NMIDA and AMPA receptors

Aged rats. --- Ampa receptors. --- Animal. --- Animals. --- Care. --- Cognitive function. --- Density. --- Dentate gyrus. --- Development. --- Enrichment. --- Environmental enrichment. --- Expression. --- Function. --- Gene-expression. --- Gene. --- Genes. --- Glutamate receptors. --- Glutamate. --- Hippocampal. --- Hippocampus. --- Immediate-early gene. --- Learning. --- Level. --- Life. --- Long-term potentiation. --- Maternal care. --- Maternal-care. --- Maternal. --- Mechanisms. --- Memory consolidation. --- Messenger-rna. --- Morris water maze. --- Mother. --- Mothers. --- Neural systems. --- Nmda receptor. --- Plasticity. --- Rat hippocampus. --- Rat. --- Receptor antagonist. --- Receptor. --- Receptors. --- Spatial learning. --- Spatial memory. --- Spatial. --- Synaptic plasticity. --- System. --- Systems. --- Time. --- Water maze.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Abstract Cognitive impairment is common after ischemic stroke. In rodent stroke models using occlusion of the middle cerebral artery (MCA) this is reflected by impaired spatial memory associated with the size of the ischemic lesion. Housing in an enriched environment enhances brain plasticity and improves recovery of sensorimotor functions after experimental stroke in rats. In this study we report that postischemic housing in an enriched environment also attenuates the long-term spatial memory impairment after MCA occlusion and extinguishes the association between spatial memory and infarct volume. An enriched environment did not significantly alter the expression of selected neuronal plasticity-associated genes 1month after MCA occlusion, indicating that most of the adaptive changes induced by an enriched environment have already occurred at this time point. We conclude that the attenuated memory impairment induced by environmental enrichment after MCA occlusion provides a useful model for further studies on the neurobiological mechanisms of recovery of cognitive functions after ischemic stroke

Association. --- Brain. --- Cerebral ischemia. --- Cerebral-ischemia. --- Cognitive function. --- Cognitive impairment. --- Enriched environment. --- Enriched. --- Enrichment. --- Environment. --- Environmental enrichment. --- Expression. --- Function. --- Gene. --- Genes. --- Housing. --- Infarct. --- Ischemia. --- Ischemic stroke. --- Learning. --- Lesion. --- Long-term. --- Mechanisms. --- Memory. --- Model. --- Models. --- Morris water maze. --- Neuronal. --- Plasticity. --- Rat. --- Rats. --- Recovery. --- Rodent. --- Size. --- Spatial memory. --- Spatial. --- Stroke. --- Time.

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

The mammalian brain has a high degree of plasticity, with dentate granule cell neurogenesis(1) and glial(2,3) proliferation stimulated by an enriched environment combining both complex inanimate and social stimulation. Moreover, rodents exposed to an enriched environment both before and after a cerebral insult show improved cognitive performance(1,4). One of the most robust associations of environmental enrichment is improved learning and memory in the Morris water maze, a spatial task that mainly involves the hippocampus(5). Furthermore, clinical evidence showing an association between higher educational attainment and reduced risk of Alzheimer(6) and Parkinson-related dementia(7) indicates that a stimulating environment has positive effects on cerebral health that may provide some resilience to cerebral insults. Here we show that in addition to its effects on neurogenesis, an enriched environment reduces spontaneous apoptotic cell death in the rat hippocampus by 45%. Moreover, these environmental conditions protect against kainate-induced seizures and excitotoxic injury. The enriched environment induces expression of glial-derived neurotrophic factor and brain-derived neurotrophic factor and increases phosphorylation of the transcription factor cyclic-AMP response element binding protein, indicating that the; influence of the environment on spontaneous apoptosis and cerebral resistance to insults may be mediated through transcription factor activation and induction of growth factor expression

Activation. --- Adult-rat. --- Association. --- Brain. --- Cell-death. --- Death. --- Enriched environment. --- Enriched. --- Enrichment. --- Environment. --- Environmental enrichment. --- Expression. --- Fibroblast growth-factor. --- Generated granule cells. --- Growth. --- Health. --- Hippocampal-neurons. --- Hippocampus. --- Increase. --- Increases. --- Induction. --- Injuries. --- Injury. --- Learning. --- Memory. --- Morris water maze. --- Neurogenesis. --- Neurotrophic factor. --- Nmda receptor activation. --- Phosphorylation. --- Plasticity. --- Progenitor cells. --- Protein. --- Rat dentate gyrus. --- Rat hippocampus. --- Rat. --- Resistance. --- Response. --- Risk. --- Rodent. --- Rodents. --- Seizure. --- Seizures. --- Social. --- Spatial task. --- Spatial. --- Stimulation. --- Task. --- Transcription.