UBP141, GluN2D antagonist

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Glutamate Receptor 1 (AMPA subtype) also known as GluR1 is a subunit of the AMPA receptor complex which mediates fast synaptic transmission in the central nervous system. It is an ionotropic receptor for glutamate functioning by opening ion channels to allow the flow of Na+ and Ca2+ ions across the cell membrane contributing to excitatory neurotransmission. The GluR1 subunit has a molecular mass of approximately 100 kDa. This receptor is commonly expressed in the brain regions such as the hippocampus and the cerebral cortex playing an important role in synaptic plasticity and memory formation.

Biological function summary

The GluR1 subunit is an essential component of the AMPA receptor complex which typically forms as a tetramer. This complex modulates synaptic strength and plasticity processes critical for learning and memory. The activity of AMPA receptors including those containing GluR1 is regulated by several auxiliary proteins and is essential for post-synaptic responses. The GluR1 subunit also interacts with other proteins such as TARPs which modulate its trafficking and channel properties.

Pathways

The GluR1-containing AMPA receptors participate significantly in the glutamatergic signaling pathway which is vital for fast excitatory synaptic transmission in the brain. This pathway also involves the NMDA receptors which work together with AMPA receptors to regulate synaptic plasticity and neuronal communication. Additionally the GluR1 interacts within the long-term potentiation (LTP) pathway contributing to the strengthening of synapses an essential mechanism underlying learning and memory.

Dysfunction in GluR1 and associated AMPA receptors has been implicated in conditions like Alzheimer's disease and epilepsy. Alzheimer's disease exhibits decreased synaptic transmission and plasticity linked to impaired GluR1 function and its interactions with NMDA receptors. In epilepsy abnormal GluR1 activity may contribute to heightened neuronal excitability and seizure propagation. Targeting GluR1 or associated pathways offers potential for therapeutic interventions in these disorders possibly through drugs such as memantine and NBQX which modulate receptor activity.