Anti-alpha 1 Glycine Receptor/GLRA1 antibody

Supplementary info

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

Activity summary

The alpha 1 Glycine Receptor also known as GLRA1 is a ligand-gated ion channel receptor. It plays an important role in transmitting inhibitory neurotransmission by binding glycine a neurotransmitter. The receptor possesses a mass around 48 kDa and is mainly expressed in the central nervous system particularly in the spinal cord and brainstem. This receptor helps regulate chloride ion influx which stabilizes neuronal membrane potential by reducing the likelihood of neuron firing.

Biological function summary

The GLRA1 facilitates inhibitory synapses in the central nervous system. Working as part of a larger receptor complex it couples with glycine to enable chloride anion flow across the neuronal membrane. This results in hyperpolarization which decreases the neuronal excitability. The receptor operates within a pentameric configuration often interacting with other subunits like beta glycine receptor subunits to form heteromeric channels.

Pathways

The GLRA1 is essential in the glycinergic pathway which serves to modulate excitatory signals in the nervous system by providing inhibitory control. It closely relates to other ligand-gated ion channels such as the GABAA receptor which shares a similar inhibitory function. The proper functioning of GLRA1 ensures balance in neurotransmission and prevents excessive neuronal firing which can lead to disorders.

Associated diseases and disorders

Dysfunctional GLRA1 contributes to hyperekplexia also known as startle disease a genetic neurological disorder affecting muscle control. Mutations in the GLRA1 affect its ability to bind glycine effectively leading to impaired inhibitory neurotransmission. This receptor also shows a connection to disorders involving neurotransmission imbalance when linked with the protein gephyrin which anchors and clusters the glycine receptors at synaptic sites to ensure proper inhibitory signaling.