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Last update 08 May 2025

μ opioid receptor x NK1R

Last update 08 May 2025

Basic Info

Related Targets

μ opioid receptorNK1R

Drugs associated with μ opioid receptor x NK1R

MB-301

Target

NK1R x μ opioid receptor

Mechanism

NK1R antagonists [+1]

Active Org.

Mainline Biosciences, Inc.

Originator Org.

Mainline Biosciences, Inc.

Active Indication

Pain

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Delta/mu opioid receptor agonists and neurokinin-1 receptor antagonists(University of Arizona)

Target

NK1R x δ opioid receptor x μ opioid receptor

Mechanism

NK1R antagonists [+2]

Active Org.-

Originator Org.

University of Arizona

Active Indication-

Inactive Indication

Chronic Pain

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ESP7

Target

NK1R x μ opioid receptor

Mechanism

NK1 agonists [+1]

Active Org.-

Originator Org.-

Active Indication-

Inactive Indication

Pain

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with μ opioid receptor x NK1R

100 Translational Medicine associated with μ opioid receptor x NK1R

0 Patents (Medical) associated with μ opioid receptor x NK1R

120

Literatures (Medical) associated with μ opioid receptor x NK1R

01 Jul 2024·Journal of Neurophysiology

Anatomical distribution of µ-opioid receptors, neurokinin-1 receptors, and vesicular glutamate transporter 2 in the mouse brainstem respiratory network

Article

Author: Furdui, Andreea ; Montandon, Gaspard ; da Silveira Scarpellini, Carolina

Opioid drugs can cause serious respiratory side-effects by binding to µ-opioid receptors (MORs) in brainstem regions that control breathing. To better understand the regions and their cellular subpopulations that may be vulnerable to modulation by opioids, we provide a comprehensive map of Oprm1 (gene encoding MORs) mRNA expression throughout brainstem regions that control and modulate breathing. Notably, we identify glutamatergic and neurokinin-1 receptor-expressing cells as potentially vulnerable to modulation by opioid drugs and worthy of further investigation using targeted approaches.

01 Jul 2023·eNeuro

Differential Modulation of GABAergic and Glutamatergic Neurons in the Ventral Pallidum by GABA and Neuropeptides.

Article

Author: Kalivas, Peter ; Neuhofer, Daniela

The ventral pallidum (VP) is an integral locus in the reward circuitry and a major target of GABAergic innervation of both D1-medium spiny neurons (MSNs) and D2-MSNs from the nucleus accumbens. The VP contains populations of GABAergic [VPGABA, GAD2(+), or VGluT(-)] and glutamatergic [VPGlutamate, GAD2(-), or VGluT(+)] cells that facilitate positive reinforcement and behavioral avoidance, respectively. MSN efferents to the VP exert opponent control over behavioral reinforcement with activation of D1-MSN afferents promoting and D2-MSN afferents inhibiting reward seeking. How this afferent-specific and cell type-specific control of reward seeking is integrated remains largely unknown. In addition to GABA, D1-MSNs corelease substance P to stimulate neurokinin 1 receptors (NK1Rs) and D2-MSNs corelease enkephalin to activate μ-opioid receptors (MORs) and δ-opioid receptors. These neuropeptides act in the VP to alter appetitive behavior and reward seeking. Using a combination of optogenetics and patch-clamp electrophysiology in mice, we found that GAD2(-) cells receive weaker GABA input from D1-MSN, but GAD2(+) cells receive comparable GABAergic input from both afferent types. Pharmacological activation of MORs induced an equally strong presynaptic inhibition of GABA and glutamate transmission on both cell types. Interestingly, MOR activation hyperpolarized VPGABA but not VGluT(+). NK1R activation inhibited glutamatergic transmission only on VGluT(+) cells. Our results indicate that the afferent-specific release of GABA and neuropeptides from D1-MSNs and D2-MSNs can differentially influence VP neuronal subtypes.

01 Feb 2023·Neuroscience & Biobehavioral Reviews

Crosstalk between Mu-Opioid receptors and neuroinflammation: Consequences for drug addiction and pain

Review

Author: Polache, Ana ; Cuitavi, Javier ; Campos-Jurado, Yolanda ; Lorente, Jesús David ; Agustín-Pavón, Carmen ; Hipólito, Lucía ; Andrés-Herrera, Paula ; Torres-Pérez, Jose Vicente

Mu-Opioid Receptors (MORs) are well-known for participating in analgesia, sedation, drug addiction, and other physiological functions. Although MORs have been related to neuroinflammation their biological mechanism remains unclear. It is suggested that MORs work alongside Toll-Like Receptors to enhance the release of pro-inflammatory mediators and cytokines during pathological conditions. Some cytokines, including TNF-α, IL-1β and IL-6, have been postulated to regulate MORs levels by both avoiding MOR recycling and enhancing its production. In addition, Neurokinin-1 Receptor, also affected during neuroinflammation, could be regulating MOR trafficking. Therefore, inflammation in the central nervous system seems to be associated with altered/increased MORs expression, which might regulate harmful processes, such as drug addiction and pain. Here, we provide a critical evaluation on MORs' role during neuroinflammation and its implication for these conditions. Understanding MORs' functioning, their regulation and implications on drug addiction and pain may help elucidate their potential therapeutic use against these pathological conditions and associated disorders.

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