Glutamate and Synaptic Plasticity at Mammalian Primary Olfactory Synapsesa

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Abstract
Glutamate is the transmitter at synapses from the olfactory nerve (ON) to mitral (Mi)/tufted cells, but very little is known about the functional properties of this synapse. This report summarizes in vitro physiological and computational modeling studies investigating glutamatergic neurotransmission at ON → Mi cell synapses. Single ON shocks in rat main olfactory bulb (MOB) slices elicit distinct early and late spiking components triggered, respectively, by (RS)‐α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA)/kainic acid (KA) and N‐methyl‐d‐aspartate (NMDA) receptor activation. Modeling simulations showed that the placement of both AMPA/KA and NMDA receptors on Mi apical dendrites replicates the experimentally observed early and late Mi spiking responses to ON shocks. Brief, tetanic ON stimulation in vitro induced robust, selective long‐term potentiation (LTP) of NMDA receptor‐dependent spiking. Modeling experiments disclosed several potential mechanisms underlying the selective LTP of NMDA receptor‐dependent spiking. These findings demonstrate that ON → Mi cell transmission exhibits a novel form of plasticity whereby high frequency synaptic activity induces selective LTP of NMDA receptor‐dependent spiking.