Premium
Multiple neurotrophic signals converge in surviving CA1 neurons of the gerbil hippocampus following transient forebrain ischemia
Author(s) -
Ferrer I.,
López E.,
Pozas E.,
Ballabriga J.,
Martí E.
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19980518)394:4<416::aid-cne2>3.0.co;2-4
Subject(s) - tropomyosin receptor kinase b , gerbil , biology , parvalbumin , tropomyosin receptor kinase c , brain derived neurotrophic factor , neurotrophin 3 , neurotrophic factors , synaptophysin , endocrinology , medicine , neurotrophin , tropomyosin receptor kinase a , hippocampus , neuroscience , nissl body , microbiology and biotechnology , ischemia , growth factor , immunohistochemistry , receptor , immunology , platelet derived growth factor receptor , biochemistry , staining , genetics
Delayed cell death involving the CA1 area of the hippocampus was produced following 5 minutes of transient forebrain ischemia in gerbils. Cell death mainly affected CA1 pyramidal neurons, whereas parvalbumin‐immunoreactive (parv‐ir) cells were spared. Synaptophysin immunoreactivity was observed in the strata oriens and radiatum of CA1 for months, although immunoreactivity decreased in gerbils surviving 1 year post‐ischemia. Golgi studies disclosed a few pyramidal neurons with dendrites, variably covered with dendritic spines, in the CA1 area of 1‐year surviving gerbils. In the normal gerbil, the majority of CA1 neurons expressed brain‐derived neurotrophic factor (BDNF), tyrosine protein kinase C (TrkC), fibroblast growth factor receptor 1 (Flg), transforming growth factor‐alpha (TGF‐alpha), and epidermal growth factor‐receptor (EGF‐R), but only a minority of cells were tyrosine protein kinase B (TrkB)‐immunoreactive. Marked reduction in the number of BDNF‐, TrkC‐, Flg‐, TGF‐alpha‐, and EGF‐R‐ir cells was observed in CA1 from 24 hours to 1 year after ischemia. In contrast, TrkB‐ir cells survived the ischemic insult. Double‐labeling immunohistochemistry disclosed that about 90% of surviving BDNF‐ir and 85% of TrkB‐ir neurons co‐localized parvalbumin in the CA1 area. In control gerbils, only about 5% of BDNF‐ir cells in CA1 co‐expressed TrkB. However, TrkB co‐localized in about 95% of surviving BDNF‐ir neurons in CA1 in ischemic gerbils. In addition, parvalbumin was co‐expressed in about 90% of TrkC‐, 95% Flg‐, and 85% EGF‐R‐ir surviving neurons in the stratum pyramidale of CA1. Finally, basic fibroblast growth factor (bFGF) was expressed by reactive astrocytes from day 4 onwards. These data show that the subpopulation of TrkB‐/parv‐ir neurons in CA1 survive the ischemic episode and that multiple neurotrophic signals converge in surviving neurons of the gerbil hippocampus following transient forebrain ischemia. J. Comp. Neurol. 394:416–430, 1998. © 1998 Wiley‐Liss, Inc.