Premium
Glutamate and Synaptic Plasticity at Mammalian Primary Olfactory Synapses a
Author(s) -
ENNIS MATTHEW,
LINSTER CHRISTIANE,
ARONIADOUANDERJASKA VASSILIKI,
CIOMBOR KELLY,
SHIPLEY MICHAEL T.
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb10606.x
Subject(s) - ampa receptor , neuroscience , long term potentiation , nmda receptor , synaptic plasticity , neurotransmission , glutamatergic , glutamate receptor , kainic acid , olfactory bulb , synapse , silent synapse , long term depression , kainate receptor , biology , chemistry , receptor , central nervous system , biochemistry
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.