Pathway candidateNCBI-verifiedprotein-coding

GABRA1

gamma-aminobutyric acid type A receptor subunit alpha1

NCBI Gene: 2554 Ensembl GeneCards UniProt: P14867

Pathway candidate — not linked to PFS or PSSD by any record here

GABRA1 is in the library because it belongs to the neurotransmission family. No study, report or commentary in the corpus names it, so a variant in GABRA1 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 5 (neurotransmission). Encodes a gamma-aminobutyric acid (GABA) receptor. GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: Gamma-aminobutyric acid receptor subunit alpha-1
Function (excerpt): Alpha subunit of the heteropentameric ligand-gated chloride channel gated by Gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain. GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient. Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation.
Subcellular location: Postsynaptic cell membrane; Cell membrane; Cytoplasmic vesicle membrane.
Associated conditions: Epilepsy, childhood absence 4 (ECA4); Epilepsy, idiopathic generalized 13 (EIG13); Juvenile myoclonic epilepsy 5 (EJM5); Developmental and epileptic encephalopathy 19 (DEE19).

Source: UniProtKB/Swiss-Prot P14867, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.

Why its pathway is in the library

Monoamine, GABA, glutamate, and cholinergic systems are the direct pharmacologic targets of SSRIs/SNRIs (PSSD) and the downstream effectors of neurosteroid signaling (PFS).

Written for the whole neurotransmission family, not for GABRA1 specifically.

Mentioned in 0 corpus records

No corpus record names GABRA1 directly yet. It is in the library because it sits in a pathway the corpus tracks (Neurotransmission).

Also in neurotransmission

All 54 genes

Browse by family on the gene families page.

Protein reference (UniProt)

Protein: Gamma-aminobutyric acid receptor subunit alpha-1
Function (excerpt): Alpha subunit of the heteropentameric ligand-gated chloride channel gated by Gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter in the brain. GABA-gated chloride channels, also named GABA(A) receptors (GABAAR), consist of five subunits arranged around a central pore and contain GABA active binding site(s) located at the alpha and beta subunit interface(s). When activated by GABA, GABAARs selectively allow the flow of chloride anions across the cell membrane down their electrochemical gradient. Alpha-1/GABRA1-containing GABAARs are largely synaptic (By similarity). Chloride influx into the postsynaptic neuron following GABAAR opening decreases the neuron ability to generate a new action potential, thereby reducing nerve transmission (By similarity). GABAARs containing alpha-1 and beta-2 or -3 subunits exhibit synaptogenic activity; the gamma-2 subunit being necessary but not sufficient to induce rapid synaptic contacts formation.
Subcellular location: Postsynaptic cell membrane; Cell membrane; Cytoplasmic vesicle membrane.
Associated conditions: Epilepsy, childhood absence 4 (ECA4); Epilepsy, idiopathic generalized 13 (EIG13); Juvenile myoclonic epilepsy 5 (EJM5); Developmental and epileptic encephalopathy 19 (DEE19).