Biomedical subjects

Pascal Jourdain

Publications and source records attributed to Pascal Jourdain.

3 recordsLinked to original sources

PubMed2002

Remodeling of hippocampal synaptic networks by a brief anoxia-hypoglycemia.

Cerebral ischemia is a major cause of brain dysfunction. Using a model of delayed death induced by a brief, transient oxygen and glucose deprivation, we studied here how this affected the structural organization of hippocampal synaptic networks. We report that brief anoxic-hypoglycemic episodes rapidly modified the structure of synapses. This was characterized, at the electron microscopic level, by a transient increase in the proportion of perforated synapses, followed after 2 hr by an increase in images of multiple synapse boutons. These changes were considerable because 10-20% of all synapses were affected. This structural remodeling was correlated by three kinds of modifications observed using two-photon confocal microscopy: the growth of filopodia, occurring shortly (5-20 min) after anoxia-hypoglycemia, enlargements of existing spines, and formation of new spines, both seen mainly 20-60 min after the insult. All of these structural changes were calcium and NMDA receptor dependent and thus reproduced, to a larger scale, those associated with synaptic plasticity. Concomitantly and related to the severity of anoxia-hypoglycemia, we could also observe spine loss and images of spine, dendrite, or presynaptic terminal swellings that evolved up to membrane disruption. These changes were also calcium dependent and reduced by NMDA receptor antagonists. Thus, short anoxic-hypoglycemic episodes, through NMDA receptor activation and calcium influx, resulted in a profound structural remodeling of synaptic networks, through growth, formation, and elimination of spines and synapses.

Animals↗

PubMed2002

Activity-induced changes of spine morphology.

Spine morphology has been shown in recent years to exhibit a high degree of plasticity. In developing tissue such as organotypic slice cultures, shape changes in spines as well as reorganization of the postsynaptic density (PSD) occur within minutes. Furthermore, several studies have shown that these and other changes can be induced by or are dependent on synaptic activation. Formation of filopodia, enlargement of spines, formation of spines with perforated PSDs, appearance of new spines, and formation of specific types of synapses such as multiple synapse boutons (MSBs), in which two spines contact the same terminal, have all been reported to be induced in an activity-dependent manner. The common denominator of most of these different processes is that they are calcium and NMDA receptor dependent. Their time course, however, may vary. Some appear quite rapidly after stimulation (e.g., filopodia, perforated synapses), while others are clearly more delayed (e.g., formation of spines, appearance of MSBs). How these different structural changes relate to each other, as well as their functional significance, have therefore become intriguing issues. The characteristics of these different types of morphological changes are reviewed, with a discussion of the possibility that structural plasticity contributes to changes in synaptic efficacy.

Animals↗

PubMed2002

LTP, memory and structural plasticity.

Our current understanding of the mechanisms of information processing and storage in the brain, based on the concept proposed more than fifty years ago by D. Hebb, is that a key role is played by changes in synaptic efficacy induced by coincident pre- and postsynaptic activity. Decades of studies of the properties of long-term potentiation (LTP) have shown that this form of plasticity adequately fulfills these requirements and is likely to contribute to several models of learning and memory. Recent analyses of the molecular events implicated in LTP are consistent with the view that modifications of receptor properties or insertion of new receptors account for the potentiation of synaptic transmission. These experiments, however, have also uncovered an unexpected structural plasticity of synapses. Dendritic spines appear to be dynamic structures that can be formed, modified in their shape or eliminated under the influence of activity. Furthermore, recent studies suggest that LTP, in addition to changes in synaptic function, is also associated with mechanisms of synaptogenesis. We review here the evidence pointing to this activity-dependent remodeling and discuss the possible role of this structural plasticity for synaptic potentiation, learning and memory.

Animals↗