Glutamate Transporter Studies Reveal the Pruning of Metabotropic Glutamate Receptors and Absence of AMPA Receptor Desensitization at Mature Calyx of Held Synapses

• DOI: 10.1523/jneurosci.1848-05.2005
• Publication Date: 2005-09-14T22:12:44Z
• Authors: Robert Renden; Holger Taschenberger; Nagore Puente; Dmitri A. Rusakov; Robert Duvoisin; Lu-Yang Wang; Knut P. Lehre; Henrique von Gers...
• Keywords: Silent synapse; Long-term depression

We examined the effect of glutamate transporter blockade at calyx Held synapse. In immature synapses [defined as postnatal day 8 (P8) to P10 rats], causes tonic activation NMDA receptors and strong inhibition AMPA receptor-mediated EPSC amplitude. was blocked with a metabotropic receptor (mGluR) antagonist [1 microm LY341495 (2S-2-amino-2-(1S,2S-2-carboxycycloprop-1-yl)-3-(xanth-9-yl)propanoic acid)], suggesting that elevated resting concentration specifically activates group II III mGluRs. Using mGluR subtype-specific agonists antagonists, we determined increased presynaptic mGluR2/3 mGluR8 but not mGluR4, although this is present. Surprisingly, in older animals (P16-P18), had no on amplitude because developmental downregulation II/III rats mice. contrast other CNS synapses, observed decay kinetics, expression transporters nearby glial processes both P9 P17. Finally, using low-affinity (gamma-D-glutamylglycine), show desensitization occurs P8-P10 absent P16-P18, even during trains high-frequency (100-300 Hz) stimulation. suggest diffusion are insufficient clear synaptically released calyces, resulting significant desensitization. Thus, mGluRs may be expressed help limit release. more mature calyx, there far smaller diffusional barrier attributable highly fenestrated synaptic terminal morphology, so avoided mGluR-mediated necessary.