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Differential effect of glutamate receptor blockade on dendritic outgrowth in developing chicken lumbar motoneurons
Author(s) -
Ni Xianglian,
MartinCaraballo Miguel
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.791.5
Subject(s) - cnqx , ampa receptor , nmda receptor , receptor , glutamate receptor , long term depression , chemistry , microbiology and biotechnology , silent synapse , dendritic spine , biology , neuroscience , biochemistry , hippocampal formation
Glutamate receptor‐mediated changes in intracellular Ca 2+ may have important implications for activity‐dependent regulation of early embryonic development. Although NMDA receptors were originally considered to be the sole source of Ca 2+ influx through glutamate receptors, AMPA receptors also allow a significant influx of Ca 2+ ions. Previously, we have demonstrated that chicken lumbar motoneurons express Ca 2+ permeable AMPA receptors at embryonic day (E) 6. By E11, the Ca 2+ permeability of AMPA receptors decreases three‐fold. In this study we have explored the role of transiently expressed Ca 2+ permeable AMPA receptors in regulating the dendritic outgrowth of developing motoneurons. The AMPA receptor blocker CNQX (1 mg/day), when applied between E5 and E8, causes a significant increase in dendritic outgrowth as compared with vehicle‐treated embryos. CNQX causes both an increase in dendritic length and branching. Inhibition of NMDA receptor function with MK‐801 (0.2 mg/day) during this period, however, does not have any effect on dendritic or cell body morphology. Treatment of chicken embryos with CNQX between E8 and E11 (when most receptors become Ca 2+ impermeable) did not have any effect on dendritic outgrowth. However, MK‐801 application to chicken embryos between E8 and E11 causes a significant reduction in dendritic length and branching. These findings indicate AMPA receptor activation limits dendritic outgrowth at early stages of development, whereas NMDA receptor activation is involved in dendritic remodeling after the establishment of synaptic contacts with sensory afferents.