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Bdnf and TrkB co-localize in CA1 neurons resistant to transient forebrain ischemia in the adult gerbil

AuthorsFerrer, Isidre; Ballabriga, Jordi; Martí, Eulàlia; Pozas, Esther ; Planas, Anna M. ; Blasi, Juan
Delayed cell death
Transient forebrain ischemia
Issue DateJul-1997
PublisherAmerican Association of Neuropathologists
CitationJournal of Neuropathology and Experimental Neurology 56(7): 790-797 (1997)
AbstractDelayed cell death of projection cells in the CA1 area of the hippocampus is produced in the adult gerbil following 5 minutes (min) of transient forebrain ischemia. Parvalbumin-immunoreactive local-circuit neurons are resistant to the ischemic insult. Brain-Derived Neurotrophic Factor (BDNF) immunoreactivity is localized in all neurons of the CA1 area in control gerbils. However, TrkB immunoreactivity is observed in a minority of BDNF-immunoreactive neurons in the CA1 are. The number of BDNF-immunoreactive cells in CA1 is dramatically reduced in ischemic gerbils as early as 24 h after ischemia, but the number of TrkB-immunoreactive cells in the CA1 area is maintained following ischemia. Moreover, about 90%, of BDNF-immunoreactive cells and about 85% of TrkB-immunoreactive cells in ischemic gerbils co- localize the calcium-binding protein parvalbumin. Finally, BDNF and TrkB are coexpressed in about 95% of CA1 neurons surviving the ischemic insult. These results indicate that a subpopulation of CA1 hippocampal neurons coexpressing TrkB, parvalbumin and BDNF is resistant to transient forebrain ischemia in the gerbil. These results also suggest that a subpopulation of CA1 hippocampal neurons in the gerbil hippocampus is endowed with a putative BDNF/TrkB autocrine regulatory loop that may be involved in both cell survival and synaptic remodeling of the damaged gerbil hippocampus following transient forebrain ischemia.
Identifiersissn: 0022-3069
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