Source data for: Presynaptic NMDARs cooperate with local spikes toward GABA release from the reciprocal olfactory bulb granule cell spine

In the rodent olfactory bulb the smooth dendrites of the principal
glutamatergic mitral cells (MCs) form reciprocal dendrodendritic synapses
with large spines on GABAergic granule cells (GC), where unitary release
of glutamate can trigger postsynaptic local activation of voltage-gated
Na+-channels (Navs), i.e. a spine spike. Can such single MC input evoke
reciprocal release? We find that unitary-like activation via two-photon
uncaging of glutamate causes GC spines to release GABA both synchronously
and asynchronously onto MC dendrites. This release indeed requires
activation of Navs and high-voltage-activated Ca2+-channels (HVACCs), but
also of NMDA receptors (NMDAR). Simulations show temporally overlapping
HVACC- and NMDAR-mediated Ca2+-currents during the spine spike, and
ultrastructural data prove NMDAR presence within the GABAergic presynapse.
The cooperative action of presynaptic NMDARs allows to implement
synapse-specific, activity-dependent lateral inhibition and thus could
provide an efficient solution to combinatorial percept synthesis in a
sensory system with many receptor channels.