Abnormal synaptic transmission in the olfactory bulb of Fyn-kinase
deficient mice.
HIROMASA KITAZAWA, TAKASHI YAGI, TSUYOSHI MIYAKAWA, HIROAKI NIKI, AND NOBUFUMI
KAWAI.
Department of Physiology, Jichi Medical School, Tochigi 329-04; Department
of Neurobiology, National Institute of Physiology Okazaki,444 and Department
of Letters, University of Tokyo, Tokyo 113, Japan.
APStracts 4:273N, 1997.
ABSTRACT
We studied synaptic transmission in the granule cells in the olfactory bulb of
the homozygous Fyn-deficient (fynz /fynzjand heterozygous Fyn-deficient (+
/fynz) mice using slice preparations from the olfactory bulb. Stimulation to
the lateral olfactory tract and/or centrifugal fibers to the olfactory bulb
evoked field excitatory postsynaptic potentials (fEPSPs) in the granule cells.
In +/fynz mice, fEPSPs were augmented by bicuculline, a GABAA antagonist and
picrotoxin, whereas fEPSPs in fynz /fynz mice were much less sensitive to
bicuculline and picrotoxin. Application of D-2-amino-5-phosphonopentanoic acid
(APV) had no effect but 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) produced
almost complete block of fEPSPs in both + /fynz mice and fynz /fynz mice. (1S,
3R)-1-aminocyclo-pentane-1.3-dicarboxylate (1S, 3R-ACPD), an agonist of
metabotropic glutamate receptors caused a similar depression of fEPSPs in both
+ /fynz and fynz /fynz mice. In + /fynz mice tetanic stimulation to the
lateral olfactory tract and/or centrifugal fibers induced NMDA-dependent long-
term potentiation (LTP) of fEPSPs, whereas LTP was impaired in fynz /fynz
mice. Our results demonstrate altered functions of GABAA and NMDA receptors in
the olfactory system of Fyn-deficient mice.
Received 13 March 1997; accepted in final form 24 September 1997.
APS Manuscript Number J220-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 7 October 1997