Paper Information

Title: 

THE DELETION OF ACAMKII IN CA3 AREA OF HIPPOCAMPUS AND IT’S EFFECT ON SYNAPTIC PLASTICITY IN CA1 AREA OF HIPPOCAMPUS IN MICE

Type: SPEECH
Author(s): HOJATI M.R.*,BUITENDIJK G.,ELGERSMA Y.
 
 *DEPARTMENT OF PHYSIOLOGY, MEDICAL FACULTY, SHAHREKORD UNIVERSITY OF MEDICAL SCIENCES, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Calcium/Calmodulin-dependent protein kinase II (aCaMKII) is a multifunctional serine/threonine kinase that is found in most tissues. This enzyme is highly expressed in neurons in the brain. In mammals, aCaMKII is encoded by four genes and two isoforms of this kinase (a and b) are predominant in the brain. Previous studies have shown that aCaMKII can phosphorylate many different synaptic proteins and it is involved in synaptic plasticity in hippocampus. Although postsynaptic role of aCaMKII in synaptic plasticity has been well described, but less studies have been execute to demonstrate its presynaptic role in mammals.
In this study we have made use of mutant mice, in which
aCaMKII has been deleted from CA3 area of the hippocampus. fEPSP recordings from CA1 area showed that basic synaptic transmission is normal in these mice. Paired Pulse Facilitation (PPF) was also normal in time intervals of 10-400 ms. long-term potentiation (LTP) is the most promising mechanism for learning and memory. We applied 10Hz and 100Hz stimulation protocols to induce LTP in hippocampal slices. Our results demonstrated that LTP was not significantly changed in mutant mice compared to the wild type mice. In conclusion, our study shows that the deletion of aCaMKII from CA3 area of hippocampus has no effect on basic synaptic transmission, PPF and LTP in mice.

 
Keyword(s): NEUROFIBROMATOSIS TYPE 1 (NF1), αCAMKII, HIPPOCAMPUS, LTP, PPF, SYNAPTIC PLASTICITY
 
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