Behaviorally induced synaptogenesis and dendritic growth in the hippocampal region following transient global cerebral ischemia are accompanied by improvement in spatial learning

Briones, Teresita L.; Suh, Eugene; Józsa, L; Woods, Julie

doi:10.1016/j.expneurol.2005.12.032

Cited by 42 publications

(25 citation statements)

References 39 publications

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“…However, one therapeutic strategy that has been overlooked in cerebral ischemia and oxidative stress studies is the use of enriched environment (EE) housing. Compelling evidence exists for the influence of EE housing on enhanced neuronal growth and restructuring and recovery following central nervous system (CNS) injury (Briones et al, 2000(Briones et al, , 2004(Briones et al, , 2006aSaucier et al, 2010;Will et al 2004;Xu et al, 2009;) yet little is known about whether EE housing has protective effects against oxidative damage. Interestingly, reports show that the neural plasticity seen after EE housing is mediated by glutamate through activation of NMDAR signaling (Andin et al, 2007;Li et al, 2007;(Wood et al, 2005).…”

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confidence: 99%

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Briones

Rogozinska

Woods

2011

Journal of Neurotrauma

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In this study, we examined whether enriched environment (EE) housing has direct neuroprotective effects on oxidative damage following transient global cerebral ischemia. Fifty-two adult male Wistar rats were included in the study and received either ischemia or sham surgery. Once fully awake, rats in each group were randomly assigned to either: EE housing or socially paired housing (CON). Animals remained in their assigned environment for 7 days, and then were killed. Our data showed that glutamate receptor expression was significantly higher in the hippocampus of the ischemia CON group than in the ischemia EE group. Furthermore, the oxidative DNA damage, protein oxidation, and neurodegeneration in the hippocampus of the ischemia CON group were significantly increased compared to the ischemia EE group. These results suggest that EE housing possibly modulated the ischemia-induced glutamate excitotoxicity, which then attenuated the oxidative damage and neurodegeneration in the ischemia EE rats.

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confidence: 99%

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Briones

Rogozinska

Woods

2011

Journal of Neurotrauma

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“…Mixed repeated measures ANOVAs on MAL scores demonstrated that the CI therapy group showed far greater use of the more affected arm in the life situation than the comparison therapy group (F (1,32) ϭ26.0; PϽ0.0001; Table). Follow-up analyses of simple main effects revealed that CI therapy recipients showed a significant improvement in real-world arm use (t (15) ϭ9.36; PϽ0.0001; dЈϭ2.34) that was 2.88-times greater than that seen in comparison therapy patients, although the comparison group also made a clinically significant improvement on the MAL 28 (t (19) ϭ4.54; PϽ0.001; dЈϭ1.02; Figure 1a).…”

Section: Clinical Resultsmentioning

confidence: 99%

“…24 One might speculate that the increases in gray matter observed in the hippocampal region or sensory and motor areas of the brain are mediated in part by increased production of neuronal or glial stem cells that might migrate to an infarcted area and participate in its repair. 31 Alternatively or in addition, gray matter increases may result from rehabilitation-induced increases in dendritic arborization and synaptic density, 32 and possibly gliosis or angiogenesis. Notably, the gray matter increases that we observed occurred over the course of just 2 weeks of therapy, emphasizing the rapid time course in which structural neuroplastic changes can take place.…”

Section: Discussionmentioning

confidence: 99%

Remodeling the Brain

Gauthier

Taub

Perkins

et al. 2008

Stroke

355

151

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Background and Purpose-Studies on adult stroke patients have demonstrated functional changes in cortical excitability, metabolic rate, or blood flow after motor therapy, measures that can fluctuate rapidly over time. This study evaluated whether evidence could also be found for structural brain changes during an efficacious rehabilitation program. Methods-Chronic stroke patients were randomly assigned to receive either constraint-induced movement therapy (nϭ16) or a comparison therapy (nϭ20). Longitudinal voxel-based morphometry was performed on structural MRI scans obtained immediately before and after patients received therapy. Results-The group receiving constraint-induced movement therapy exhibited far greater improvement in use of the more affected arm in the life situation than the comparison therapy group. Structural brain changes paralleled these improvements in spontaneous use of the more impaired arm for activities of daily living. There were profuse increases in gray matter in sensory and motor areas both contralateral and ipsilateral to the affected arm that were bilaterally symmetrical, as well as bilaterally in the hippocampus. In contrast, the comparison therapy group failed to show gray matter increases. Importantly, the magnitude of the observed gray matter increases was significantly correlated with amount of improvement in real-world arm use. Conclusions-These findings suggest that a previously overlooked type of brain plasticity, structural remodeling of the human brain, is harnessed by constraint-induced movement therapy for a condition once thought to be refractory to treatment: motor deficit in chronic stroke patients. Key Words: constraint-induced movement therapy Ⅲ hemiplegia Ⅲ imaging Ⅲ motor activity Ⅲ MRI Ⅲ stroke rehabilitation Ⅲ voxel-based morphometry M erzenich et al 1 and other investigators 2 showed in animals that altering behaviorally relevant afferent input to the central nervous system can produce plastic changes in the function and organization of the brain. Sustained increased use of a body part by an animal leads to an increase in the brain's cortical representation of that body part, 3 whereas decreased input reduces the representational zone of that body part, as occurs after amputation of a digit 1 or somatosensory deafferentation of an entire forelimb in monkeys. 4 Similar phenomena have been demonstrated in humans after both increased use 5 and decreased use resulting from upper extremity amputation 6 or stroke 7 using functional imaging or mapping techniques.A neurorehabilitation technique termed Constraint-Induced Movement therapy (CI therapy) was developed in this laboratory from basic research with monkeys. 8 This treatment has been shown to substantially increase the amount of use of an affected upper extremity after stroke 9 -12 and also greatly alter the size of the regional brain activity or activation pattern associated with the more affected arm. 7,[13][14][15] Until now, neuroanatomical evaluations of treatment changes in humans have relied solely on funct...

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“…By contrast, cytoarchitectural adjustments such as axonal and dendritic sprouting, increase of number of dendritic spines and synapses, changes in the relative proportion of spine types, are interpreted as compensatory plastic responses of surviving neurons. They contribute to neuronal circuit remodeling and functional recovery, and have been correlated with preservation of cognitive functions after the ischemic insult, even in absence of neuroprotective procedures (Briones et al, 2006;Jourdain et al, 2002;Mudrick & Baimbridge, 1989;Neigh et al, 2004;Onodera et al, 1990;Ruan et al, 2006;Skibo & Nikonenko, 2010;Sorra & Harris, 2000). In addition, neurogenesis and integration of newly differentiated neurons into neuronal circuits in the Ammon's horn may contribute to recovery of hippocampal-dependent cognitive functions (Bendel et al, 2005;Bernabeu & Sharp, 2000).…”

Section: Cellular Mechanisms Of Neuronal Plasticity and Repairmentioning

confidence: 99%

“…Different parameters of the glial reaction elicited by global cerebral ischemia have been used as indexes of brain damage or neuroprotection de Yebra et al, 2006;Duan et al, 2011;Korzhevskii et al, 2005;Piao et al, 2002;Soltys et al, 2003). Neuronal cytoarchitecture and fine structure parameters of synaptic connectivity have also been used for histopathological assessment after brain damage and neuroprotection (Briones et al, 2006;García-Chávez et al, 2008;González-Burgos et al, 2007;Johansson & Belichenko, 2002;Kovalenko et al, 2006, Moralí et al, 2011aNikonenko et al, 2009;Ruan et al, 2006).…”

Section: Histopathological Assessmentmentioning

confidence: 99%