It is widely held that the soma and basal dendrites of olfactory bulb mitral cells receive exclusively inhibitory synaptic input from local interneurons. However, the mitral somatodendritic membrane exhibits immunoreactivity for a variety of glutamate receptors, and blocking GABA receptors unmasks mitral cell self excitation. This excitation is proposed to be mediated either by diffuse spillover of the mitral cells own released glutamate, or by punctate transmission from glutamate-releasing granule cells. This study examined the pharmacology and kinetics of glutamate sensitivity of mitral cells by flash photolysis of nitroindoline caged glutamates, which facilitate reliable activation of receptors in the synaptic cleft. Wide-field laser uncaging (3.5 ms flash) of ~0.5-1 mM glutamate onto the soma activated large currents with fast (3.4 ms rise, 7.5 ms decay) and slow (64 ms rise, >10s decay) components. In 100 µM APV, slow currents were reduced to 53 % of control (257 ms rise , 2 s decay), displayed outward rectification in 1.3 mM Mg²⁺, and block by 15 µM 5,7-dichlorokynurenate. Responses to < ~100 µM glutamate were fully antagonized by 100 µM APV, consistent with competitive inhibition at high affinity NMDA receptors. An APV-resistant NMDA receptor was not observed, refuting the punctate transmission model. Fast currents were blocked by 10 µM NBQX, boosted 3.28-fold by 100 µM cyclothiazide, and resolved into AMPA (40%) and kainate (60%) receptor components by 100 µM SYM2206. The results suggest that self excitation depends on AMPA, kainate and conventional NMDA autoreceptors on the mitral cell.