Methods: 

In the mammalian olfactory bulb, axonless granule cells mediate self- and lateral inhibitory interactions between mitral/tufted cells via reciprocal dendrodendritic synapses. We use whole-cell electrophysiological recordings in conjunction with two-photon calcium imaging to characterize granule cell signals.

Results: 

We find that strong synaptic activation of the sensory input via mitral/tufted cells causes sodium action potentials in juvenile and adult mouse granule cells. Such synaptic action potentials are followed by a long-lasting depolarization linked to a long-lasting postsynaptic calcium signal throughout the cell. These signals were not observed after current-evoked action potentials in the same cells. Both required NMDA receptor activation and were entirely missing in transgenic mice deficient for both TRPC channel subtypes 1 and 4. Single knockouts of either TRPC1 or TRPC4 showed only partial blocking effects on the long-lasting signals. TRPC1 and TRPC4 also play a role in synaptic transmission in the olfactory bulb, since recurrent inhibition of mitral cells via granule cells was decreased in amplitude and had a faster time-course in TRPC1/4 knockout animals compared to wild type.

Conclusion: 

We propose that the long-lasting postsynaptic signals are likely to be mediated by a combination of TRPC1 and TRPC4 channels and also contribute to the special calcium dynamics that are responsible for asynchronous release from the granule cell spine.