Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Lushnikova, Iryna; Воронин, К. В.; Malyarevskyy, P.Y.; Skibo, G. G.

doi:10.1111/j.1582-4934.2004.tb00279.x

Cited by 21 publications

(26 citation statements)

References 38 publications

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“…Oxygen-glucose deprivation (OGD) paradigm was used to model ischemia in vitro. The cultures were placed in the interface chamber filled with N 2 and perfused with a medium containing 10 mM sucrose instead of glucose for 10 min (Jourdain et al, 2002;Lushnikova et al, 2004). After that, they were washed with warm regular culture medium, placed back in the normal conditions in the incubator for 15 min or 2 h, and fixed and processed for electron microscopy (EM).…”

Section: In Vitro Brain Ischemia Modelingmentioning

confidence: 99%

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

et al. 2006

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Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen-glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity.

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Section: In Vitro Brain Ischemia Modelingmentioning

confidence: 99%

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

et al. 2006

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“…Unlike long-term deprivation that causes irreversible cell death, transient OGD induces mild and reversible damage such as decreased metabolic activity (Lushnikova et al, 2004), inhibition of transmitter release (Fowler, 1989), and increased postsynaptic Ca 2ϩ influx, spontaneous miniature EPSC amplitude, evoked AMPA and NMDA receptor-mediated excitatory responses, and AMPA/NMDA responses ratio (Quintana et al, 2006). The impact of OGD was evaluated by measuring f-EPSPs evoked in area CA1 by electrical stimulation of Schaffer collaterals (Raley-Susman and Lipton, 1990;Lobner and Lipton, 1993).…”

Section: Pharmacological and Genetic Inhibition Of Pp1 Reduces Recovementioning

confidence: 99%

Protein Phosphatase 1-Dependent Bidirectional Synaptic Plasticity Controls Ischemic Recovery in the Adult Brain

Hédou¹,

Koshibu²,

Farinelli³

et al. 2008

J. Neurosci.

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Protein kinases and phosphatases can alter the impact of excitotoxicity resulting from ischemia by concurrently modulating apoptotic/ survival pathways. Here, we show that protein phosphatase 1 (PP1), known to constrain neuronal signaling and synaptic strength (Mansuy et al., 1998; Morishita et al., 2001), critically regulates neuroprotective pathways in the adult brain. When PP1 is inhibited pharmacologically or genetically, recovery from oxygen/glucose deprivation (OGD) in vitro, or ischemia in vivo is impaired. Furthermore, in vitro, inducing LTP shortly before OGD similarly impairs recovery, an effect that correlates with strong PP1 inhibition. Conversely, inducing LTD before OGD elicits full recovery by preserving PP1 activity, an effect that is abolished by PP1 inhibition. The mechanisms of action of PP1 appear to be coupled with several components of apoptotic pathways, in particular ERK1/2 (extracellular signal-regulated kinase 1/2) whose activation is increased by PP1 inhibition both in vitro and in vivo. Together, these results reveal that the mechanisms of recovery in the adult brain critically involve PP1, and highlight a novel physiological function for long-term potentiation and long-term depression in the control of brain damage and repair.

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“…The somata of СА1 neurons possessed a typical pyramidal shape. As was mentioned above, the slices under study were subjected to 10-min-long OGD with subsequent normoxic reoxygenation for 1 h. In our previous studies, we found that in such case neurons in the СА1 area undergo gradual delayed significant structural damage [2]. These delayed destructive consequences are based on certain primary reactions and mechanisms, in particular disorders of biochemical cascades providing production of adenosine triphosphate (ATP), disorders of the processes of ion exchange, significant excessive release of glutamate, accumulation of Са 2+ in the cells, intensification of oxidative processes, etc.…”

Section: Resultsmentioning

confidence: 99%

“…To induce the state of LTP, we arranged episodes of OGD using a technique described earlier [2,3]. The duration of these episodes was 10 min; then, the slices were returned to normal conditions of culturing for 1 h (period of normoxic reoxygenation).…”

Section: Methodsmentioning

confidence: 99%

“…In experiments with modeling of ischemia conditions (in vitro, oxygen-glucose deprivation, OGD, and in vivo, occlusion of the carotid arteries), it was shown that the insufficiency of oxygen and glucose supply results in significant late (time-delayed) neurodegenerative modifications in the hippocampus [1][2][3]. Short episodes of anoxia/hypoglycemia induced long-lasting intensification of evoked electrical responses (long-term potentiation, LTP) in the СА1 area of the hippocampus.…”

Section: Introductionmentioning

confidence: 98%

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Structural plasticity of synapses in hippocampal slices after oxygen-glucose deprivation

2011

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We analyzed structural rearrangements of synaptic contacts in the stratum radiatum of the СА1 area of cultured rat hippocampal slices under conditions of the development of potentiation of synaptic transmission induced by short-term (10 min) oxygen-glucose deprivation (OGD). Studies were carried out using electron microscopy and 3D reconstruction of cellular compartments. Within the 1st h after OGD, we observed increases in the volume of pre-synaptic terminals and post-synaptic spines and also in the area of postsynaptic densities (PSDs) in both asymmetric excitatory and symmetric inhibitory synapses, especially in the case were the PSD was perforated. We also observed significant activation of glial cells (increases in their volume and area of contacts of their processes with the components of synapses). Therefore, OGD results in activationassociated structural rearrangements of both excitatory and inhibitory synapses of the hippocampal СА1 area. Such rearrangements are accompanied by a clearly pronounced reaction of the glia, which correlates with an important role of the latter in modulation of the functioning of neurons.

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Morphological and functional changes in rat hippocampal slice cultures after short‐term oxygen‐glucose deprivation

Cited by 21 publications

References 38 publications

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

Protein Phosphatase 1-Dependent Bidirectional Synaptic Plasticity Controls Ischemic Recovery in the Adult Brain

Structural plasticity of synapses in hippocampal slices after oxygen-glucose deprivation

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