Increased branching of basal dendrites on pyramidal neurons in the occipital cortex of homozygous Brattleboro rats in standard and enriched environmental conditions: A Golgi study

Greer, E.Rosalie; Diamond, Marian C.; Murphy, Greer M.

doi:10.1016/0014-4886(82)90206-0

Cited by 11 publications

(4 citation statements)

References 21 publications

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“…Importantly, findings of animal studies indicate that increasing the complexity of an environment can protect against neurodegeneration. Both environmental enrichment and extensive exercise, distinct methodologically from the paradigm used here, have been shown to increase dendritic branching, neurogenesis, and the number of synapses in brain regions involved in learning and memory (Greenough et al, 1972(Greenough et al, , 1979Greer et al, 1982;Comery et al, 1996;Biernaskie and Corbett, 2001;van Praag et al, 2005). The precise mechanisms underlying this increased plasticity may include a wide variety of neuroprotective factors, including increases in neurotrophic factors such as BDNF (Falkenberg et al, 1992;Zhao et al, 2001;Alonso et al, 2002;Pham et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Learning Decreases Aβ*56 and Tau Pathology and Ameliorates Behavioral Decline in 3xTg-AD Mice

Billings¹,

Green²,

McGaugh³

et al. 2007

J. Neurosci.

126

101

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Transgenic mouse models of Alzheimer's disease (AD), such as the 3xTg-AD mice, are instrumental for elucidating genetic, pharmacologic, environmental, and behavioral factors that affect the cognitive phenotype. Here we present the novel findings that longitudinal water-maze spatial training produces a significant, albeit transient, improvement in subsequent learning performance and reduces amyloid ␤ (A␤) and tau neuropathology. The 3xTg-AD mice were trained and tested at 3 month intervals from 2 to 18 months. Separate groups of naive mice were also tested at each age. The improvement in performance seen at 6 and 12 months is dependent on spatial training, because animals that were similarly handled and exposed to swimming without a learning contingency failed to show improved performance. Training before the development of overt neuropathology is required for full expression of the training effect because we found it delays A␤ redistribution to extracellular plaques and reduces A␤ oligomers associated with cognitive decline. In addition, learning leads to decreased glycogen synthase kinase-3␤ activity, which likely underlies the reduced tau pathology. The previous training effects on both maze performance and neuropathology are attenuated at 15 and 18 months. These findings indicate that, in young and middle-aged 3xTg-AD mice, repeated spatial training can significantly delay the development of neuropathology and decline in spatial memory.

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Section: Discussionmentioning

confidence: 99%

Learning Decreases Aβ*56 and Tau Pathology and Ameliorates Behavioral Decline in 3xTg-AD Mice

Billings¹,

Green²,

McGaugh³

et al. 2007

J. Neurosci.

126

101

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“…32,33 Somatosensory deprivation reduces dendritic complexity in the neocortex of monkeys, 34 and psychosocial stress and other models of depression result in reduced neuritic and synaptic complexity. 35 Environmental enrichment can also enhance recovery and regeneration of damaged neural circuits.…”

Section: Enhancement Of Neural Plasticity and Prophylaxis Against Neumentioning

confidence: 99%

Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations

et al. 2004

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Summary: It is well established that when most types of cells, including neurons, are exposed to a mild stress they increase their ability to resist more severe stress. This "preconditioning" phenomenon involves up-regulation of genes that encode cytoprotective proteins such as heat-shock proteins and growth factors. We found that a similar beneficial cellular stress response can be induced in neurons throughout the brain by a "meal-skipping" dietary restriction (DR) regimen in rats and mice. DR is effective in protecting neurons and improving functional outcome in models of stroke, Alzheimer's, Parkinson's and Huntington's diseases. DR induces an increase in the levels of brain-derived neurotrophic factor (BDNF) and heatshock proteins in neurons. DR also stimulates neurogenesis in the hippocampus, and BDNF plays a role in this effect of DR. Physical exercise and environmental enrichment are two other manipulations that have been shown to induce BDNF expression in the brain, presumably because it is a mild cellular stress. When taken together with epidemiological and clinical studies in humans, the data from animal studies suggest that it may be possible to reduce the risk for age-related neurodegenerative disorders through dietary and behavioral modifications that act by promoting neuronal plasticity and survival.

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“…When rats or mice are housed in complex environments or exercised on a regular basis, there are increases in the complexity of dendrites in cortical neurons, and increased numbers of synapses. 32,33 Somatosensory deprivation reduces dendritic complexity in the neocortex of monkeys, 34 and psychosocial stress and other models of depression result in reduced neuritic and synaptic complexity. 35 Environmental enrichment can also enhance recovery and regeneration of damaged neural circuits.…”

Section: Enhancement Of Neural Plasticity and Prophylaxis Against Neumentioning

confidence: 99%

Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations

et al. 2004

View full text Add to dashboard Cite

It is well established that when most types of cells, including neurons, are exposed to a mild stress they increase their ability to resist more severe stress. This "preconditioning" phenomenon involves up-regulation of genes that encode cytoprotective proteins such as heat-shock proteins and growth factors. We found that a similar beneficial cellular stress response can be induced in neurons throughout the brain by a "meal-skipping" dietary restriction (DR) regimen in rats and mice. DR is effective in protecting neurons and improving functional outcome in models of stroke, Alzheimer's, Parkinson's and Huntington's diseases. DR induces an increase in the levels of brain-derived neurotrophic factor (BDNF) and heatshock proteins in neurons. DR also stimulates neurogenesis in the hippocampus, and BDNF plays a role in this effect of DR. Physical exercise and environmental enrichment are two other manipulations that have been shown to induce BDNF expression in the brain, presumably because it is a mild cellular stress. When taken together with epidemiological and clinical studies in humans, the data from animal studies suggest that it may be possible to reduce the risk for age-related neurodegenerative disorders through dietary and behavioral modifications that act by promoting neuronal plasticity and survival.

show abstract

Increased branching of basal dendrites on pyramidal neurons in the occipital cortex of homozygous Brattleboro rats in standard and enriched environmental conditions: A Golgi study

Cited by 11 publications

References 21 publications

Learning Decreases Aβ*56 and Tau Pathology and Ameliorates Behavioral Decline in 3xTg-AD Mice

Learning Decreases Aβ*56 and Tau Pathology and Ameliorates Behavioral Decline in 3xTg-AD Mice

Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations

Prophylactic activation of neuroprotective stress response pathways by dietary and behavioral manipulations

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