Acyl Ghrelin Improves Synapse Recovery in an In Vitro Model of XXXX .

@entity1 @entity5473 @entity75 @entity772 @entity519 @entity1167 @entity4095
UNASSIGNED: @entity772 @entity1 after @entity1167 have a poor prognosis. Approximately half never awakes as a result of severe @entity75 . 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 @entity519 and the possibility to restrict it by ghrelin treatment. Briefly, we applied @entity519 ( @entity4095 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 @entity5473 . We observed that @entity519 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 @entity519 . It raises the possibility that ghrelin or its analogs may have a therapeutic potential for treatment of postanoxic @entity75 .
