Rapid Alterations in Dendrite Morphology during Sublethal Hypoxia or Glutamate Receptor Activation

Park, James S.; Bateman, Michael C.; Goldberg, Mark P.

doi:10.1006/nbdi.1996.0022

Cited by 196 publications

(201 citation statements)

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“…Moreover, inhibition of Rho GTPases or their effectors protects against ischemia/reperfusion injury in vivo in both brain (Laufs et al, 2000;Trapp et al, 2001) and other tissues (Bao et al, 2004). Based on these findings, we offer the speculation that modulation of Rho GTPase signaling cascades by Slit has the net effect of maintaining cellular integrity and functioning in ischemic brain secondary to its ability to prevent or reduce synaptic disruption and other changes in dendritic morphology crucial to neuronal viability (Hasbani et al, 2001;Park et al, 1996).…”

Section: Discussionmentioning

confidence: 86%

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Altay

McLaughlin

et al. 2007

Experimental Neurology

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Cerebrovascular inflammation contributes to secondary brain injury following ischemia. Recent in vitro studies of cell migration and molecular guidance mechanisms have indicated that the Slit family of secreted proteins can exert repellant effects on leukocyte recruitment in response to chemoattractants. Utilizing intravital microscopy, we addressed the role of Slit in modulating leukocyte dynamics in the mouse cortical venular microcirculation in vivo following TNFα application or global cerebral ischemia. We also studied whether Slit affected neuronal survival in the mouse global ischemia model as well as in mixed neuronal-glial cultures subjected to oxygenglucose deprivation. We found that systemically administered Slit significantly attenuated cerebral microvessel leukocyte-endothelial adherence occurring 4 h after TNFα and 24 h after global cerebral ischemia. Administration of RoboN, the soluble receptor for Slit, exacerbated the acute chemotactic response to TNFα. These findings are indicative of a tonic repellant effect of endogenous Slit in brain under acute proinflammatory conditions. Three days of continuous systemic administration of Slit following global ischemia significantly attenuated the delayed neuronal death of hippocampal CA1 pyramidal cells. Moreover, Slit abrogated neuronal death in mixed neuronal-glial cultures exposed to oxygen-glucose deprivation. The ability of Slit to reduce the recruitment of immune cells to ischemic brain and to provide cytoprotective effects suggests that this protein may serve as a novel anti-inflammatory and neuroprotective target for stroke therapy.

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Section: Discussionmentioning

confidence: 86%

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Altay

McLaughlin

et al. 2007

Experimental Neurology

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“…Golgi-Cox staining have been used to describe the beaded morphology of ischemic neuronal dendrites (Hasbani et al, 2001;Park et al, 1996). Zhang and colleagues (2005) show that dendritic tufts and spines located within the infarct undergo severe morphological change and swelling within 10 minutes of ischemia onset.…”

Section: Cellular Changesmentioning

confidence: 99%

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

et al. 2010

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“…Synaptic pathology precedes cell death in Alzheimer's disease and is a clinical hallmark of neuropsychiatric diseases (Gasic and Nicotera, 2003). Similarly, dramatic and rapidly reversible structural changes are observed in dendritic spine morphology after excitotoxic or hypoxic stress (Hasbani et al, 2001;Park et al, 1996). It was observed that structural (Park et al, 1996) and biochemical conditions (Martone et al, 1999) at the synapse rapidly return to normal following the stressor.…”

Section: Introductionmentioning

confidence: 99%

“…Furthermore, synaptic structure and function is extraordinarily sensitive to cerebral ischemia (Hasbani et al, 2001;Park et al, 1996). Lastly, synaptic signals are important determinants of neuronal fate during pathological conditions (Mattson et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Cerebral Ischemia Causes Dysregulation of Synaptic Adhesion in Mouse Synaptosomes

Costain

Rasquinha

Sandhu

et al. 2007

J Cereb Blood Flow Metab

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Synaptic pathology is observed during hypoxic events in the central nervous system in the form of altered dendrite structure and conductance changes. These alterations are rapidly reversible, on the return of normoxia, but are thought to initiate subsequent neuronal cell death. To characterize the effects of hypoxia on regulators of synaptic stability, we examined the temporal expression of cell adhesion molecules (CAMs) in synaptosomes after transient middle cerebral artery occlusion (MCAO) in mice. We focused on events preceding the onset of ischemic neuronal cell death ( < 48 h). Synaptosome preparations were enriched in synaptically localized proteins and were free of endoplasmic reticulum and nuclear contamination. Electron microscopy showed that the synaptosome preparation was enriched in spheres (E650 nm in diameter) containing secretory vesicles and postsynaptic densities. Forebrain mRNA levels of synaptically located CAMs was unaffected at 3 h after MCAO. This is contrasted by the observation of consistent downregulation of synaptic CAMs at 20 h after MCAO. Examination of synaptosomal CAM protein content indicated that certain adhesion molecules were decreased as early as 3 h after MCAO. For comparison, synaptosomal Agrn protein levels were unaffected by cerebral ischemia. Furthermore, a marked increase in the levels of p-Ctnnb1 in ischemic synaptosomes was observed. p-Ctnnb1 was detected in hippocampal fiber tracts and in cornu ammonis 1 neuronal nuclei. These results indicate that ischemia induces a dysregulation of a subset of synaptic proteins that are important regulators of synaptic plasticity before the onset of ischemic neuronal cell death.

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Rapid Alterations in Dendrite Morphology during Sublethal Hypoxia or Glutamate Receptor Activation

Cited by 196 publications

References 0 publications

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Slit modulates cerebrovascular inflammation and mediates neuroprotection against global cerebral ischemia

Thinning, movement, and volume loss of residual cortical tissue occurs after stroke in the adult rat as identified by histological and magnetic resonance imaging analysis

Cerebral Ischemia Causes Dysregulation of Synaptic Adhesion in Mouse Synaptosomes

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