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Developmental increase in postsynaptic alpha‐amino‐3‐hydroxy‐5‐methyl‐4 isoxazolepropionic acid receptor compartmentalization at the calyx of held synapse
Author(s) -
Hermida Diana,
Elezgarai Izaskun,
Puente Nagore,
Alonso Virginia,
Anabitarte Naroa,
Bilbao Aurora,
DoñateOliver Francisco,
Grandes Pedro
Publication year - 2006
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20911
Subject(s) - ampa receptor , postsynaptic potential , biology , postsynaptic density , trapezoid body , neuroscience , neurotransmission , glutamate receptor , synapse , nmda receptor , ionotropic glutamate receptor , inhibitory postsynaptic potential , excitatory postsynaptic potential , receptor , nucleus , biochemistry
The pattern of expression of ionotropic glutamate receptor (GluR) subunits 1–4 in the medial nucleus of the trapezoid body (MNTB) has been reported to change during development. The aim of this study was to compare the distribution of the GluR1–4 subunits in the MNTB at postnatal day (P) 9, before high‐frequency signal transmission in the auditory system has developed, with that observed in mature adult rats. GluR1–4 subunits were studied by preembedding and postembedding immunocytochemical methods. Increased levels of GluR1, 2/3, and 4 associated with development were evident only at postsynaptic sites of MNTB principal cell bodies receiving calyces of Held synapses, whereas receptor density at nonsynaptic sites was found to remain unaltered. Taken together, the expression pattern of GluR subunits and the density of immunoparticles in postsynaptic specializations are indicative of a compartmentalization of alpha‐amino‐3‐hydroxy‐5‐methyl‐4 isoxazolepropionic acid (AMPA) subunits upon development. These developmental changes provide a morphological basis for establishment of the postsynaptic properties needed for high‐frequency synaptic transmission of auditory signals to MNTB principal neurons. J. Comp. Neurol. 495:624–634, 2006. © 2006 Wiley‐Liss, Inc.