An ultrastructural study into the effect of global transient cerebral ischaemia on the synaptic population of the cerebellar cortex in rats

Stepanov, S. S.; Sergeyeva, Elena D.; Semchenko, V. V.; Akulinin, V. A.

doi:10.1016/s0300-9572(98)00103-8

Cited by 10 publications

(9 citation statements)

References 21 publications

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“…Furthermore no other reports are available on synaptic densities and numbers after a clinical relevant fetal inflammatory challenge. Nevertheless, similar results were found after different adverse developmental conditions, like malnutrition, hypoxia, hypothyroidism, intrauterine growth retardation, and antenatal glucocorticoids [ 14 – 21 ]. For example, Colberg and colleagues found the loss of synaptic densities in layer 3 of the cortex and CA1 of the hippocampus and the caudate nucleus [ 17 , 19 ] after antenatal betamethasone treatment in sheep.…”

Section: Discussionsupporting

confidence: 66%

Intra-Amniotic LPS Induced Region-Specific Changes in Presynaptic Bouton Densities in the Ovine Fetal Brain

Strackx

Jellema

Rieke

et al. 2015

BioMed Research International

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Rationale. Chorioamnionitis has been associated with increased risk for fetal brain damage. Although, it is now accepted that synaptic dysfunction might be responsible for functional deficits, synaptic densities/numbers after a fetal inflammatory challenge have not been studied in different regions yet. Therefore, we tested in this study the hypothesis that LPS-induced chorioamnionitis caused profound changes in synaptic densities in different regions of the fetal sheep brain. Material and Methods. Chorioamnionitis was induced by a 10 mg intra-amniotic LPS injection at two different exposure intervals. The fetal brain was studied at 125 days of gestation (term = 150 days) either 2 (LPS2D group) or 14 days (LPS14D group) after LPS or saline injection (control group). Synaptophysin immunohistochemistry was used to quantify the presynaptic density in layers 2-3 and 5-6 of the motor cortex, somatosensory cortex, entorhinal cortex, and piriforme cortex, in the nucleus caudatus and putamen and in CA1/2, CA3, and dentate gyrus of the hippocampus. Results. There was a significant reduction in presynaptic bouton densities in layers 2-3 and 5-6 of the motor cortex and in layers 2-3 of the entorhinal and the somatosensory cortex, in the nucleus caudate and putamen and the CA1/2 and CA3 of the hippocampus in the LPS2D compared to control animals. Only in the motor cortex and putamen, the presynaptic density was significantly decreased in the LPS14 D compared to the control group. No changes were found in the dentate gyrus of the hippocampus and the piriforme cortex. Conclusion. We demonstrated that LPS-induced chorioamnionitis caused a decreased density in presynaptic boutons in different areas in the fetal brain. These synaptic changes seemed to be region-specific, with some regions being more affected than others, and seemed to be transient in some regions.

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Section: Discussionsupporting

confidence: 66%

Intra-Amniotic LPS Induced Region-Specific Changes in Presynaptic Bouton Densities in the Ovine Fetal Brain

Strackx

Jellema

Rieke

et al. 2015

BioMed Research International

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“…Several causes for presynaptic and postsynaptic ischemic failure have been proposed [17]. The initial disturbances are probably located presynaptically rather than postsynaptically, with impaired transmitter release [17], decreased presynaptic dense projections [47], and isolated loss of presynaptic buttons [48]. Failure of synaptic transmission has been proposed to account for electric silence in the penumbra of a brain infarct [49] and has been associated with lasting network damage in the absence of depolarization in a rat model of cerebral infarction [45].…”

Section: Discussionmentioning

confidence: 99%

Acyl Ghrelin Improves Synapse Recovery in an In Vitro Model of Postanoxic Encephalopathy

et al. 2015

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Comatose patients after cardiac arrest have a poor prognosis. Approximately half never awakes as a result of severe diffuse postanoxic encephalopathy. Several neuroprotective agents have been tested, however without significant effect. In the present study, we used cultured neuronal networks as a model system to study the general synaptic damage caused by temporary severe hypoxia and the possibility to restrict it by ghrelin treatment. Briefly, we applied hypoxia (pO2 lowered from 150 to 20 mmHg) during 6 h in 55 cultures. Three hours after restoration of normoxia, half of the cultures were treated with ghrelin for 24 h, while the other, non-supplemented, were used as a control. All cultures were processed immunocytochemically for detection of the synaptic marker synaptophysin. We observed that hypoxia led to drastic decline of the number of synapses, followed by some recovery after return to normoxia, but still below the prehypoxic level. Additionally, synaptic vulnerability was selective: large- and small-sized neurons were more susceptible to synaptic damage than the medium-sized ones. Ghrelin treatment significantly increased the synapse density, as compared with the non-treated controls or with the prehypoxic period. The effect was detected in all neuronal subtypes. In conclusion, exogenous ghrelin has a robust impact on the recovery of cortical synapses after hypoxia. It raises the possibility that ghrelin or its analogs may have a therapeutic potential for treatment of postanoxic encephalopathy.

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“…Our observations confirm that excitotoxic changes occur primarily at the postsynaptic dendrite (Olney, 1971). However, this does not exclude the possibility that hypoxic-ischemic injury (Stepanov et al, 1998) and other acute insults may also injure presynaptic terminals.…”

Section: Significance Of Transient Spine Loss and Recoverymentioning

confidence: 96%

Dendritic Spines Lost during Glutamate Receptor Activation Reemerge at Original Sites of Synaptic Contact

et al. 2001

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During cerebral ischemia, neurons undergo rapid alterations in dendritic structure consisting of focal swelling and spine loss. We used time-lapse microscopy to determine the fate of dendritic spines that disappeared after brief, sublethal hypoxic or excitotoxic exposures. Dendrite and spine morphology were assessed in cultured cortical neurons expressing yellow fluorescent protein or labeled with the fluorescent membrane tracer, DiI. Neurons exposed to NMDA, kainate, or oxygen-glucose deprivation underwent segmental dendritic beading and loss of approximately one-half of dendritic spines. Most spine loss was observed in regions of local dendritic swelling. Despite widespread loss, spines recovered within 2 hr after termination of agonist exposure or oxygen-glucose deprivation and remained stable over the subsequent 24 hr. Recovery was slower after NMDA than AMPA/kainate receptor activation. Time-lapse fluorescence imaging showed that the vast majority of spines reemerged in the same location from which they disappeared. In addition to spine recovery, elaboration of dendritic filopodia was observed in new locations along the dendritic shaft after dendrite recovery. Spine recovery did not depend on actin polymerization because it was not blocked by application of latrunculin-A, which eliminated filamentous actin staining in spines and blocked spine motility. Throughout spine loss and recovery, presynaptic and postsynaptic elements remained in physical proximity. These results suggest that elimination of dendritic spines is not necessarily associated with loss of synaptic contacts. Rapid reestablishment of dendritic spine synapses in surviving neurons may be a substrate for functional recovery after transient cerebral ischemia.

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An ultrastructural study into the effect of global transient cerebral ischaemia on the synaptic population of the cerebellar cortex in rats

Cited by 10 publications

References 21 publications

Intra-Amniotic LPS Induced Region-Specific Changes in Presynaptic Bouton Densities in the Ovine Fetal Brain

Intra-Amniotic LPS Induced Region-Specific Changes in Presynaptic Bouton Densities in the Ovine Fetal Brain

Acyl Ghrelin Improves Synapse Recovery in an In Vitro Model of Postanoxic Encephalopathy

Dendritic Spines Lost during Glutamate Receptor Activation Reemerge at Original Sites of Synaptic Contact

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