Premium
Differential NR2A and NR2B expression between trigeminal neurons during early postnatal development
Author(s) -
Turman Jack E.,
Lee Ophelia K.,
Chandler Scott H.
Publication year - 2002
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10059
Subject(s) - nmda receptor , brainstem , neuroscience , biology , receptor , glutamate receptor , medicine , endocrinology , anatomy , biochemistry
Abstract N ‐methyl‐D‐aspartate (NMDA) receptors play an important role in the production of rhythmical trigeminal motor activity resembling suckling and chewing. The developmental relationship between the expression of NMDA receptor subunits and the function of neurons comprising brainstem oral–motor circuitry is not clear. We conducted receptor immunohistochemistry studies to demonstrate the expression of NR2A and NR2B subunits in trigeminal motoneurons (Mo5) and mesencephalic trigeminal neurons (Me5) during the first 2 weeks of development. During this time period, rats begin the transition from suckling to chewing, two distinct motor behaviors. In Mo5, NR2A and NR2B immunoreactivity was observed throughout the time frame sampled. A significant increase in the NR2A:NR2B ratio occurred between P3–4 and P11 due to a reduction in the number of NR2B immunoreactive neurons. The temporal and spatial expression of NR2A and NR2B was differentially regulated between caudal and rostral regions of Me5. In contrast to Mo5, the NR2A:NR2B ratio decreased between P0–1 and P11 in caudal Me5 due to a concurrent increase in the number of NR2A and NR2B immunoreactive neurons. In rostral Me5, NR2A and NR2B immunoreactivity emerged at P3 and P11, respectively. Our data provides further insight into the molecular changes of trigeminal neurons during the transition from suckling to chewing behaviors. The differences in the NR2A:NR2B ratio between Mo5 and Me5 suggest functional differences in these neurons during NMDA‐mediated neurotransmission. Synapse 44:76–85, 2002. © 2002 Wiley‐Liss, Inc.