📖

NR2A (GRIN2A) Neurons

active
wiki page Created: 2026-04-02T07:19:38 By: crosslink-migration Quality: 50% ✓ SciDEX ID: wiki-cell-types-grin2a-neurons
📖 Wiki Page
cell1001 wordssynced 2026-04-02

NR2A (GRIN2A) Neurons

Introduction

<table class="infobox infobox-cell">
<tr>
<th class="infobox-header" colspan="2">NR2A (GRIN2A) Neurons</th>
</tr>
<tr>
<td class="label">Name</td>
<td><strong>NR2A (GRIN2A) Neurons</strong></td>
</tr>
<tr>
<td class="label">Type</td>
<td>Cell Type</td>
</tr>
</table>

Nr2A (Grin2A) Neurons is an important cell type in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.

Overview

NR2A neurons express the NMDA receptor subunit NR2A (encoded by the GRIN2A gene), a critical ionotropic glutamate receptor involved in synaptic plasticity, learning, and memory. NMDA receptors containing the NR2A subunit exhibit distinct pharmacological and biophysical properties that are essential for normal brain function. [@nmda2020]

Structure and Molecular Biology

The NR2A subunit (also known as GluN2A or NMDA Receptor Subunit 2A) is a transmembrane protein that forms the NMDA receptor complex: [@developmental2018]

  • N-terminal domain (NTD): Large extracellular domain involved in subunit assembly and allosteric modulation
  • Agonist-binding domain (ABD): Binds glutamate (on NR2A) and glycine/D-serine (on NR1)
  • Transmembrane domain (TM): Three transmembrane helices plus a re-entrant pore loop
  • C-terminal domain (CTD): Long intracellular tail that interacts with scaffolding proteins and signaling molecules

...
📖 View canonical wiki page →
Related Entities
cell-types-grin2a-neurons
Metadataorigin_type: v1_polymorphic_backfill
slugcell-types-grin2a-neurons
kg_node_idNone
entity_typecell
origin_typev1_polymorphic_backfill
source_tablewiki_pages
wiki_page_idwp-98f8f0d75c10
__merged_from{'merged_at': '2026-05-13', 'unprefixed_id': 'cell-types-grin2a-neurons'}
_schema_version1
📊 Evidence Profile Foundational
Evidence Balance
+0%
Certainty
70%
Debates
0
Incoming
14
Outgoing
16
0 supporting 0 contradicting 0 neutral
View full evidence profile →
Public annotations (0)Annotate on Hypothes.is →
No public annotations yet.