In vivo odorant input induces distinct synaptic plasticity of GABAergic synapses in developing zebrafish olfactory bulb.

In the first station of central odor processing, the main olfactory bulb, signal processing is regulated by synaptic interactions between glutamatergic and GABAergic inputs of the mitral cells (MCs), the major projection neurons. Our previous study has found that repetitive postsynaptic spiking within a critical time window after presynaptic activation by natural odorant stimulation results in persistent enhancement of glutamatergic inputs of MCs in larval zebrafish. Here we observed a long-term depression of GABAergic synapses induced by the same protocol. This long-term depression was mediated by presynaptic NMDA receptors (NMDARs). Further dissecting GABAergic neurotransmission revealed that the STDP-induction protocol induced persistent modification in recurrent and lateral inhibition with opposite directions and distinct requirements on NMDARs. Thus, at the plasticity level, different types of GABAergic inhibition may utilize different mechanisms to cooperate or compete with excitatory inputs to optimize patterns of olfactory bulb output.