We studied synaptic transmission in the granule cells in the olfactory bulb of the homozygous Fyn (a nonreceptor type tyrosine kinase)-deficient (fyn2/fyn2) and heterozygous Fyn-deficient (+/fyn2) 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 +/fyn2 mice, fEPSPs were augmented by bicuculline, a γ-aminobutyric acid (GABA(A)) antagonist and picrotoxin, whereas fEPSPs in fyn2/fyn2 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 +/fyn2 mice and fyn2/fyn2 mice. (1S, 3R)-1-aminocyclo-pentane-1.3-dicarboxylate, an agonist of metabotropic glutamate receptors caused a similar depression of fEPSPs in both +/fyn2 and fyn2/fyn2 mice. In +/fyn2 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 fyn2/fyn2 mice. Our results demonstrate altered functions of GABA(A) and NMDA receptors in the olfactory system of Fyn deficient mice.
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