Abnormal synaptic transmission in the olfactory bulb of Fyn-kinase-deficient mice

We studied synaptic transmission in the granule cells in the olfactory bulb of the homozygous Fyn (a nonreceptor type tyrosine kinase)-deficient (fyn(z)/fyn(z)) and heterozygous Fyn-deficient (+/fyn(z)) mice by 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 +/fyn(z) mice, fEPSPs were augmented by bicuculline, a gamma-aminobutyric acid (GABAA) antagonist and picrotoxin, whereas fEPSPs in fyn(z)/fyn(z) mice were much less sensitive to bicuculline and picrotoxin. Application of D-2-amino-5-phosphonopentanoic acid had no effect but 6-cyano-7-nitroquinoxaline-2,3-dione produced almost complete block of fEPSPs in both +/fyn(z) mice and fyn(z)/fyn(z) mice. (1S, 3R)-1-aminocyclo-pentane-1.3-dicarboxylate, an agonist of metabotropic glutamate receptors caused a similar depression of fEPSPs in both +/fyn(z) and fyn(z)/fyn(z) mice. In +/fyn(z) mice tetanic stimulation to the lateral olfactory tract and/or centrifugal fibers induced N-methyl-D-aspartate (NMDA)-dependent long-term potentiation (LTP) of fEPSPs, whereas LTP was impaired in fyn(z)/fyn(z) mice. Our results demonstrate altered functions of GABA, and NMDA receptors in the olfactory system of Fyn deficient mice.