BDNF AND TRKB CO-LOCALIZE IN CA1 NEURONS RESISTANT TO TRANSIENT FOREBRAIN ISCHEMIA IN THE ADULT GERBIL

Delayed cell death of projection cells in the CA1 area of the hippocam pus is produced in the adult gerbil following 5 minutes (min) of trans ient forebrain ischemia. Parvalbumin-immunoreactive local-circuit neur ons are resistant to the ischemic insult. Brain-Derived Neurotrophic F actor (BDNF) immunoreactivity is localized in all neurons of the CA1 a rea in control gerbils. However, TrkB in immunoreactivity is observed in a minority of BDNF-immunoreactive neurons in the CA1 area. The numb er of BDNF-immunoreactive cells in CA1 is dramatically reduced in isch emic gerbils as early as 24 h after ischemia, but the number of TrkB-i mmunoreactive 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-bindi ng protein parvalbumin. Finally, BDNF and TrkB are coexpressed in abou t 95% of CA1 neurons surviving the ischemic insult. These results indi cate 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 hi ppocampal neurons in the gerbil hippocampus is endowed with a putative BDNF/TrkB autocrine regulatory loop thar may be involved in both cell survival and synaptic remodeling of the damaged gerbil hippocampus fo llowing transient forebrain ischemia.