Target intelligence / Profile preview

Glutamate receptor ionotropic, NMDA 3A (GRIN3A)

Target
GRIN3A
Molecular classification
Ion channel, Receptor
01

Overview

Glutamate receptor ionotropic, NMDA 3A (GRIN3A), also known as GluN3A, is a subunit of NMDA-type ionotropic glutamate receptors. NMDA receptors are ligand-gated cation channels crucial for excitatory neurotransmission and synaptic plasticity in the central nervous system. The GluN3A subunit assembles with other subunits (GluN1, GluN2) to form receptor complexes with altered properties, such as reduced calcium permeability and weaker magnesium block. It is involved in the refinement of synaptic connections during neural development and restricts dendritic spine maturation. GRIN3A variants are linked to neurological disorders including epilepsy and neuropsychiatric conditions. Currently, no drugs are approved that specifically target GluN3A; all clinically used NMDA receptor antagonists act more broadly[1][2][3][6].

Other names
Glutamate ionotropic receptor NMDA type subunit 3AGluN3ANMDAR3ANR3ANMDAR-Lglutamate [NMDA] receptor subunit 3AKIAA1973glutamate receptor ionotropic, NMDA 3AN-methyl-D-aspartate receptor subtype 3Aglutamate receptor, ionotropic, N-methyl-D-aspartate 3AmKIAA1973chi-1NR3
02

Mechanism of action

Antagonism or modulation of NMDA receptor ion channel activity; for drugs like ketamine, blockade of NMDA receptor-mediated excitatory neurotransmission[1][6].

03

Biological functions

Signal transductionSynaptic transmissionSynapse development
04

Disease associations

EpilepsyNeuropsychiatric disordersNeurodevelopmental disordersOther (potential, see description)
05

Safety considerations

NMDA receptor antagonism generally linked to neuropsychiatric side effects, cognitive impairment, and possible neurotoxicity with chronic blockade (safety for GluN3A-specific targeting not established; see description)[1].
06

Interacting drugs

No clinically approved drugs directly and selectively antagonize or modulate GluN3A; NMDA receptor antagonists (e.g., ketamine, memantine, dextromethorphan) may exert indirect effects but these target the receptor complex generally, not specifically the 3A subunit[1][2][6].
07

Biomarkers

No established biomarkers for routine patient selection or monitoring based specifically on GRIN3A[1][4].

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