The selective delayed neuronal death of CA1 pyramidal cells after transient global ischemia in the gerbil brain can be prevented by preconditioning with a short sublethal period of ischemia 1–7 days prior to a subsequent, usually lethal ischemia of 5 min duration. Since changes of neuronal gene expression may play a crucial role in this tolerance induction, we investigated the postischemic expression profile of the fos, jun and Krox transcription factor families. We have previously reported that a single 5 min period of cerebral ischemia does not cause a de novo synthesis of immediate early gene (IEG) encoded proteins in CA1 neurons. In the present study, two experimental groups of Mongolian gerbils were investigated: one group was subjected to a single tolerance‐inducing 2.5 min period of ischemia by bilateral occlusion of the common carotid artery. The second (combined ischemia) group was subjected to 2.5 min of ischemia, followed by 5 min of ischemia 4 days later. Postischemic expression of c‐FOS, FOS B, c‐JUN, JUN B, JUN D and KROX‐24 was investigated by in situ hybridization and immunocytochemistry up to 48 h of recirculation. In contrast to a single 5 min period of ischemia, 2.5 min caused a postischemic expression of c‐JUN protein, but no other IEGs, in CA1 neurons (peak at 6 h). Similarly, a selective but delayed c‐JUN expression (peak at 18 h) was observed in animals subjected to combined ischemia. These results indicate that the induction of an endogenous neuroprotective state in CA1 neurons is associated with the activation of a genetic program which involves the expression of specific transcription factors.
Brain Pathology – Wiley
Published: Apr 1, 1995
It’s your single place to instantly
discover and read the research
that matters to you.
Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.
All for just $49/month
Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly
Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.
Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.
Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.
All the latest content is available, no embargo periods.
“Hi guys, I cannot tell you how much I love this resource. Incredible. I really believe you've hit the nail on the head with this site in regards to solving the research-purchase issue.”Daniel C.
“Whoa! It’s like Spotify but for academic articles.”@Phil_Robichaud
“I must say, @deepdyve is a fabulous solution to the independent researcher's problem of #access to #information.”@deepthiw
“My last article couldn't be possible without the platform @deepdyve that makes journal papers cheaper.”@JoseServera