Related Experiment Video
Updated: Jun 23, 2026

04:48
A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
Published on: July 10, 2018
Uncoupling dendrite growth and patterning: single-cell knockout analysis of NMDA receptor 2B
J Sebastian Espinosa1, Damian G Wheeler, Richard W Tsien
1Department of Biology, Stanford University, Stanford, CA 94305, USA.
Neuron
|May 5, 2009
Summary
NR2B, a key N-methyl-D-aspartate receptor (NMDAR) subunit, cell-autonomously controls dendrite patterning in developing neurons. This ensures proper sensory information representation by regulating dendrite pruning and targeting.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- N-methyl-D-aspartate receptors (NMDARs) are crucial for neural development.
- NR2B is the primary NR2 subunit in the developing brain, influencing neuronal function.
- Understanding NR2B's role is vital for comprehending neural circuit formation.
Purpose of the Study:
- To investigate the cell-autonomous function of NR2B in dendrite development.
- To determine how NR2B regulates dendrite patterning in specific neuronal populations.
- To differentiate mechanisms of activity-dependent patterning from general growth.
Main Methods:
- Mosaic analysis with double markers (MADM) was employed.
- NR2B was knocked out in isolated single cells.
- Dendritic morphology of mutant and control cells (dentate gyrus granule cells and barrel cortex layer 4 spiny stellate cells) was analyzed.
Main Results:
- NR2B knockout did not affect overall dendritic growth rate, total length, or branch number.
- Mutant cells exhibited impaired pruning, leading to supernumerary primary dendrites.
- Mutant cells failed to restrict dendritic growth to a single barrel, unlike controls.
Conclusions:
- NR2B plays a cell-autonomous role in regulating dendrite patterning, not general growth.
- Proper dendrite patterning by NR2B is essential for accurate sensory information representation in the cortex.
- Mechanisms governing activity-dependent dendrite patterning are separable from those controlling overall dendrite growth.

