Post insult enriched housing improves the 8-arm radial maze performance but not the Morris water maze task in ventral subicular lesioned rats

Bindu, Barkha; Jinkala, Sreerekha; Kutty, Bindu M.

doi:10.1016/j.brainres.2005.09.044

Cited by 34 publications

(23 citation statements)

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“…In the Morris water maze test, enriched mice exhibited faster learning, better adaptation during exploration and greater locomotor skills, in comparison to mice housed in standard conditions (Kempermann et al, 2002). Furthermore, rats with hippocampal damage demonstrated better cognitive performance in eight arm radial maze task but not in Morris water maze task (Dhanushkodi et al, 2007;Bindu et al, 2005) suggesting that the effects of enriched environment on distinct aspects of cognitive function may differ between intact rats and rats with hippocampal damage. Moreover, electrophysiological recordings from acute hippocampal slices of rats housed in enriched environment demonstrated enhanced long term potentiation (LTP) (Duffy et al, 2001;Tang and Zou, 2002).…”

Section: Changes In Cognitive Functionmentioning

confidence: 93%

“…However, the most conspicuous result of environmental enrichment in rats and mice has been the enhanced cognitive performance. For instance, exposure to enriched environment improves spatial learning and memory performance in the Morris water maze task (Mohammed et al, 1990;Kempermann et al, 1997;Moser et al, 1997;Nilsson et al, 1999;Pham et al, 1999a;Williams et al, 2001;Pham et al, 2002), the radial arm maze task (Bindu et al, 2005;Dhanushkodi et al, 2007) and hippocampalindependent learning tasks (Rampon et al, 2000b). In the Morris water maze test, enriched mice exhibited faster learning, better adaptation during exploration and greater locomotor skills, in comparison to mice housed in standard conditions (Kempermann et al, 2002).…”

Section: Changes In Cognitive Functionmentioning

confidence: 99%

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Is exposure to enriched environment beneficial for functional post-lesional recovery in temporal lobe epilepsy?

Dhanushkodi

Shetty

2008

Neuroscience & Biobehavioral Reviews

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Exposure to environmental enrichment has been shown to induce robust neuronal plasticity in both intact and injured adult central nervous system, including up-regulation of multiple neurotrophic factors, enhanced neurogenesis in the dentate gyrus of the hippocampus, and improved spatial learning and memory function. Neuronal plasticity, though mostly adaptive and abnormal, also occurs during certain neurodegenerative conditions such as the temporal lobe epilepsy (TLE). The TLE is characterized by hippocampal neurodegeneration, aberrant mossy fiber sprouting, spontaneous recurrent motor seizures, cognitive deficits, and abnormally enhanced neurogenesis during the early phase and dramatically declined neurogenesis during the chronic phase of the disease. As enrichment has been found to be beneficial for treating animal models of Alzheimer's, Parkinson's, and Huntington's diseases, there is considerable interest in determining the efficacy of this strategy for preventing or treating chronic TLE after the initial precipitating brain injury. This review first discusses the proof of principle behind the potential application of the environmental enrichment strategy for preventing or treating TLE after brain injury. The subsequent chapters confer the portrayed beneficial effects of enrichment for functional post-lesional recovery in TLE and the possible complications which may arise from housing epilepsy-prone or epileptic rats in enriched environmental conditions. The final segment discusses studies that are essential for further understanding the efficacy of this approach for preventing or treating TLE.

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Section: Changes In Cognitive Functionmentioning

confidence: 93%

Section: Changes In Cognitive Functionmentioning

confidence: 99%

Is exposure to enriched environment beneficial for functional post-lesional recovery in temporal lobe epilepsy?

Dhanushkodi

Shetty

2008

Neuroscience & Biobehavioral Reviews

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“…EE cages were equipped with various objects such as ladders, tunnels, wooden pieces of different shapes and sizes, interchangeable toys such as balls, building blocks, etc., to provide opportunities for both sensory and physical stimulation. These objects were rearranged every day and different objects were placed in the cages on alternate days for the novelty [29] . Food and water were provided ad libitum.…”

Section: Ee Conditionsmentioning

confidence: 99%

Extinction of Contextual Fear with Timed Exposure to Enriched Environment: A Differential Effect

Hegde¹,

O’Mara²,

Laxmi³

2017

Ann Neurosci

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Background: Extinction of fear memory depends on the environmental and emotional cues. Furthermore, consolidation of extinction is also dependent on the environmental exposure. But, the relationship of the time of the exposure to a variety of environmental cues is not well known. The important region involved in facilitation of extinction of fear memory is through diversion of the flow of information leaving the lateral nucleus of amygdala. Purpose: The study aimed to address a question to explain how these brain regions react to environmental stimulation during the retention and extinction of fear memory. Methods: An enriched environment (EE) is assumed to mediate extinction of fear memory, we examined the apparent discrepancy between the effects of defensive response, the freezing behavior induced by Pavlovian classical fear conditioning by subjecting them to variance in the timing to EE. The different timing of EE exposure was 10 days of EE either before fear conditioning and/or after extinction training to the rats. The local field potentials was recorded from CA1 hippocampus, lateral nucleus of amygdala and infralimbic region of medial prefrontal cortex (mPFC) during the fear learning and extinction from the control rats and rats exposed to EE before and after fear conditioning. Results: Exposure to EE before the fear conditioning and after extinction training was more effective in the extinction fear memory. In addition, we also found switching from exploratory locomotion to freezing during retention of contextual fear memory which was associated with decreased theta power and reduced synchronized theta oscillations in CA1-hippocampus, lateral nucleus of amygdala, and infralimbic region of mPFC. Conclusion: Thus, we propose that the timing of exposure to EE play a key role in the extinction of fear memory.

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“…Environmental enrichment (EE), a stimulation paradigm involving the combination of increased social interaction, physical exercise and continuous exposure to learning tasks (Krech et al, 1960) produces beneficial effects, like improved learning and memory of spatial tasks in rats (Bindu et al, 2005;Escorihuela et al, 1995;Kempermann et al, 1997;Leggio et al, 2005;Nilsson et al, 1999;Van Praag et al, 1999). This appears to be mediated by multiple pathways, particularly the enhancement of dendrites number, branches and spines, as well as increased glial numbers (Faherty et al, 2003;Rosenzweig and Bennett, 1996), reduced inflammatory response, enhanced microglial phagocytosis and proteasomal degradation (Ambrée et al, 2006), and increased angiogenesis (Herring et al, 2008) and neurogenesis in the hippocampus (Auvergne et al, 2002;Brown et al, 2003aBrown et al, , 2003bBruel-Jungerman et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Environmental enrichment prevents behavioral deficits and oxidative stress caused by chronic cerebral hypoperfusion in the rat

et al. 2012

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Post insult enriched housing improves the 8-arm radial maze performance but not the Morris water maze task in ventral subicular lesioned rats

Cited by 34 publications

References 38 publications

Is exposure to enriched environment beneficial for functional post-lesional recovery in temporal lobe epilepsy?

Is exposure to enriched environment beneficial for functional post-lesional recovery in temporal lobe epilepsy?

Extinction of Contextual Fear with Timed Exposure to Enriched Environment: A Differential Effect

Environmental enrichment prevents behavioral deficits and oxidative stress caused by chronic cerebral hypoperfusion in the rat

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