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Last update 08 May 2025

CHRNA4

Last update 08 May 2025

Basic Info

Synonyms

acetylcholine receptor, nicotinic, alpha 4 (neuronal), BFNC, cholinergic receptor nicotinic alpha 4 subunit

+ [8]

Introduction

After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane permeable to sodium ions.

Drugs associated with CHRNA4

NESS 29-64FD

Target

CHRNA4 x CHRNB2

Mechanism

CHRNA4 modulators [+1]

Active Org.-

Originator Org.

PharmaNess Neuroscience

Active Indication-

Inactive Indication

Neurodegenerative Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CHRNA4

100 Translational Medicine associated with CHRNA4

0 Patents (Medical) associated with CHRNA4

344

Literatures (Medical) associated with CHRNA4

01 Mar 2025·Brain and Behavior

Transcriptomic Dysregulation in Animal Models of Attention‐Deficit Hyperactivity Disorder and Nicotine Dependence Suggests Shared Neural Mechanisms

Article

Author: Van Horn, Sarah ; Toufexis, Donna J ; Driscoll, Heather

ABSTRACTIntroductionAttention‐deficit‐hyperactivity disorder (ADHD) is highly heritable and increases the likelihood of nicotine dependence (ND). The self‐medication hypothesis of nicotine use in ADHD proposes that ADHD patients seek nicotine for its ability to improve their symptoms, and they have less success quitting, possibly due to the worsening of ADHD symptoms in withdrawal.MethodsThe present analysis compared transcriptomic data from the brains of rodent models of ADHD and those of ND, with a focus on striatal gene expression. Differential expression analysis, pathway enrichment analysis, and gene‐network mapping identified signaling networks and candidate genes that may contribute to the high co‐occurrence between ADHD and ND.ResultsWe identified novel differentially expressed genes (PRKAG2, MAPK1), and genes with known associations to either ADHD or ND (ANK3, CALD1, CHRNA4, CHRNA7, CMTM8, DLG4, DUSP6, GNG3, GNG11, GRIK5, GRINA2, GRM5, ICAM2, KCNJ6, PRKAB1, SNAP25, SYNPO, SYT1, VAMP2). In addition, synaptic transmission (hsa04728, R‐HAS‐112315, R‐HSA‐442755) and MAPK signaling pathways (hsa04010, hsa04014, hsa04015, R‐HSA‐5673001, R‐HSA‐5684996) were enriched in both ADHD and ND.ConclusionThe signaling pathways implicated by this analysis mediate neurological mechanisms known to contribute to ND. The association of analogous differently expressed genes and common signaling pathways suggests an important causal relationship between ND and ADHD that may be clinically important.

01 Jan 2025·Journal of Neurochemistry

Clinical, molecular, physiologic, and therapeutic feature of patients with CHRNA4 and CHRNB2 deficiency: A systematic review

Review

Author: Rezazadeh, Maryam ; Ghafouri‐Fard, Soudeh ; Jalaiei, Abbas ; Asadi, Mohammad Reza ; Daneshmandpour, Yousef

AbstractThe α4β2 nAChRs are crucial ion channels that control neurotransmitter release and play a role in various physiologic and pathologic processes. CHRNA4 encodes the α4‐nAChRs, while CHRNB2 encodes the β2‐nAChRs. Recent studies have found different variants of α4β2‐nAChRs in individuals with conditions such as AD, ADHD, ALS, PD, and brain abnormalities. We conducted a scoping review following a six‐stage methodology structure and adhering to PRISMA guidelines. We systematically reviewed articles using relevant keywords up to October 2, 2023. In this summary, we cover the clinical symptoms reported, the genes and protein structure of CHRNA4 and CHRNB2, mutations in these genes, inheritance patterns, the functional impact of mutations and polymorphisms in CHRNA4 and CHRNB2, and the epidemiology of these diseases. Recent research indicates that nAChRs may play a significant role in neurodegenerative disorders, possibly impacting neuronal function through yet undiscovered regulatory pathways. Studying how nAChRs interact with disease‐related aggregates in neurodegenerative conditions may lead to new treatment options for these disorders.

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01 Nov 2024·Biochemistry (Moscow)

Prenatal Hypoxia Predisposes to Impaired Expression of the chrna4 and chrna7 Genes in Adult Rats without Affecting Acetylcholine Metabolism during Embryonic Development

Article

Author: Vetrovoy, Oleg V ; Tyulkova, Ekaterina I ; Stratilov, Viktor A ; Potapova, Sofiia S

Previous studies have shown that the combined effect of fetal hypoxia and maternal stress hormones predetermines tendency to nicotine addiction in adulthood. This study in rats aimed to investigate the effect of prenatal severe hypoxia (PSH) on acetylcholine metabolism in the developing brain, as well as on expression of acetylcholine receptors chrna4 and chrna7 in both the developing brain and adult brain structures following nicotine consumption. In the developing brain of PSH rats, no changes were found in the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) or disturbances in the acetylcholine levels. However, decreased chrna4 expression was detected on the day 15 of pregnancy, while elevation in the chrna7 expression was observed on the days 15 and 16 of embryogenesis. In adulthood, the consequences of PSH were manifested as decreased expression of chrna4 in the medial prefrontal cortex (PFC), nucleus accumbens (NAacc), and hypothalamus (HT), decreased expression of chrna7 in the PFC and hippocampus (HPC). Whereas, nicotine consumption did not decrease the expression levels of chrna4 and chrna7 compared to the control group in the adult PSH rats. Thus, prenatal hypoxia predisposes to impaired expression of the chrna4 and chrna7 genes in adult rats without affecting acetylcholine metabolism during embryonic development.

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CHRNA4

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