Last update 01 Nov 2024

nAChRs x DRDs

Last update 01 Nov 2024

Basic Info

Related Targets

Drugs associated with nAChRs x DRDs

Target

5-HT2 receptor x D2 receptor x H1 receptor x Muscle-type nAChRs x δ opioid receptor x κ opioid receptor x μ opioid receptor x σ1 receptor

Mechanism

5-HT2 receptor antagonists [+7]

Active Org.-

Originator Org.

Mitsubishi Tanabe Pharma Corp.

Active Indication-

Inactive Indication

Attention Deficit Disorder With Hyperactivity

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Deuterated bupropion(DeuteRx)

Target

DRDs x nAChRs

Mechanism

DRDs agonists [+1]

Active Org.-

Originator Org.

Deuteria Pharmaceuticals, Inc.

Active Indication-

Inactive Indication

Depressive Disorder [+1]

Drug Highest PhaseDiscontinued

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with nAChRs x DRDs

NCT01174355 / CompletedPhase 1/2

A Multicenter, Open Label, Escalating Dose Study to Assess the Tolerability and the Safety and to Explore the Efficacy and the Pharmacokinetics of ND0801 in Adult Patients With Attention Deficit/Hyperactivity Disorder (ADHD)

A multicenter, open label, escalating dose study to assess the tolerability and the safety and to explore the efficacy and the pharmacokinetics of ND0801 in adult patients with attention deficit/hyperactivity disorder (ADHD).

Start Date01 Oct 2010

Sponsor / Collaborator

NeuroDerm Ltd.

100 Clinical Results associated with nAChRs x DRDs

100 Translational Medicine associated with nAChRs x DRDs

0 Patents (Medical) associated with nAChRs x DRDs

147

Literatures (Medical) associated with nAChRs x DRDs

01 Oct 2024·CNS Neuroscience & Therapeutics

Alterations in Neuronal Nicotinic Acetylcholine Receptors in the Pathogenesis of Various Cognitive Impairments

Review

Author: Guan, Zhi‐Zhong

ABSTRACTCognitive impairment is a typical symptom of both neurodegenerative and certain other diseases. In connection with these different pathologies, the etiology and neurological and metabolic changes associated with cognitive impairment must differ. Until these characteristics and differences are understood in greater detail, pharmacological treatment of the different forms of cognitive impairment remains suboptimal. Neurotransmitter receptors, including neuronal nicotinic acetylcholine receptors (nAChRs), dopamine receptors, and glutamine receptors, play key roles in the functions and metabolisms of the brain. Among these, the role of nAChRs in the development of cognitive impairment has attracted more and more attention. The present review summarizes what is presently known concerning the structure, distribution, metabolism, and function of nAChRs, as well as their involvement in major cognitive disorders such as Alzheimer's disease, Parkinson's disease, vascular dementia, schizophrenia, and diabetes mellitus. As will be discussed, the relevant scientific literature reveals clearly that the α4β2 and α7 nAChR subtypes and/or subunits of the receptors play major roles in maintaining cognitive function and in neuroprotection of the brain. Accordingly, focusing on these as targets of drug therapy can be expected to lead to breakthroughs in the treatment of cognitive disorders such as AD and schizophrenia.

01 Aug 2024·European Journal of Pharmacology

17-β-estradiol potentiates the neurotrophic and neuroprotective effects mediated by the dopamine D3/acetylcholine nicotinic receptor heteromer in dopaminergic neurons

Article

Author: Fiorentini, Chiara ; Fadel, Dounia ; Mutti, Veronica ; Bono, Federica ; Sbrini, Giulia ; Missale, Cristina ; Tomasoni, Zaira

Dopaminergic neurons express a heteromer composed of the dopamine D3 receptor and the α4β2 nicotinic acetylcholine receptor, the D3R-nAChR heteromer, activated by both nicotine and dopamine D2 and D3 receptors agonists, such as quinpirole, and crucial for dopaminergic neuron homeostasis. We now report that D3R-nAChR heteromer activity is potentiated by 17-β-estradiol which acts as a positive allosteric modulator by binding a specific domain on the α4 subunit of the nicotinic receptor protomer. In mouse dopaminergic neurons, in fact, 17-β-estradiol significantly increased the ability of nicotine and quinpirole in promoting neuron dendritic remodeling and in protecting neurons against the accumulation of α-synuclein induced by deprivation of glucose, with a mechanism that does not involve the classical estrogen receptors. The potentiation induced by 17-β-estradiol required the D3R-nAChR heteromer since either nicotinic receptor or dopamine D3 receptor antagonists and interfering TAT-peptides, but not the estrogen receptor antagonist fulvestrant, specifically prevented 17-β-estradiol effects. Evidence of estrogens neuroprotection, mainly mediated by genomic mechanisms, have been provided, which is in line with epidemiological data reporting that females are less likely to develop Parkinson's Disease than males. Therefore, potentiation of D3R-nAChR heteromer activity may represent a further mechanism by which 17-β-estradiol reduces dopaminergic neuron vulnerability.

01 Jun 2024·Heliyon

The association of genetic polymorphisms within the dopaminergic system with nicotine dependence: A narrative review

Review

Author: Chen, Huan ; Wang, Hongjuan ; Hu, Qingyuan ; Hou, Hongwei ; Yang, Jingjing

Nicotine, the main compound in cigarettes, leads to smoking addiction. Nicotine acts on the limbic dopamine reward loop in the midbrain by binding to nicotinic acetylcholine receptors, promoting the release of dopamine, and resulting in a rewarding effect or satisfaction. This satisfaction is essential for continued and compulsive tobacco use, and therefore dopamine plays a crucial role in nicotine dependence. Numerous studies have identified genetic polymorphisms of dopaminergic pathways which may influence susceptibility to nicotine addiction. Dopamine levels are greatly influenced by synthesis, storage, release, degradation, and reuptake-related genes, including genes encoding tyrosine hydroxylase, dopamine decarboxylase, dopamine transporter, dopamine receptor, dopamine 3-hydroxylase, catechol-O-methyltransferase, and monoamine oxidase. In this paper, we review research progress on the effects of polymorphisms in the above genes on downstream smoking behavior and nicotine dependence, to offer a theoretical basis for the elucidation of the genetic mechanism underlying nicotine dependence and future personalized treatment for smoking cessation.

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