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Developmental expression of the group III metabotropic glutamate receptor mGluR4a in the medial nucleus of the trapezoid body of the rat
Author(s) -
Elezgarai Izaskun,
Benítez Rocío,
Mateos José María,
Lázaro Esther,
Osorio Alexandra,
Azkue Jon Jatsu,
Bilbao Aurora,
Lingenhoehl Kurt,
Van Der Putten Herman,
Hampson David R.,
Kuhn Rainer,
Knöpfel Thomas,
Grandes Pedro
Publication year - 1999
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/(sici)1096-9861(19990830)411:3<431::aid-cne6>3.0.co;2-r
Subject(s) - trapezoid body , biology , metabotropic glutamate receptor , neuroscience , neurotransmission , glutamate receptor , excitatory postsynaptic potential , nucleus , receptor , anatomy , inhibitory postsynaptic potential , biochemistry
A preembedding immunocytochemical method for light microscopy was used to study the postnatal development of expression of the group III metabotropic glutamate receptor mGluR4a in the medial nucleus of the trapezoid body (MNTB) of the rat. Immunoreactivity for mGluR4a was localized in axonal endings wrapping the principal globular neurons in MNTB, known as calyces of Held. The percentage of calyces of Held immunoreactive for mGluR4a increased progressively from postnatal day 3 (PND3), showing the highest density of labeled calyces by PND9. From this postnatal age on, a gradual reduction in the number of mGluR4a‐immunopositive calyces of Held was observed, reaching the lowest level of labeled profiles in adult tissue. The developmental expression of mGluR4a in calyces of Held correlates well with previous studies in young animals showing a modulation of synaptic neurotransmission by group III mGluRs in these giant excitatory synapses made on MNTB principal neurons. All these observations together suggest that the expression of mGluR4a mainly between PND7 and PND12 might be relevant to the maturation and modulation of synaptic transmission at the calyces of Held. J. Comp. Neurol. 411:431–440, 1999. © 1999 Wiley‐Liss, Inc.