GO:0004938 alpha2-adrenergic receptor activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0004938 (alpha2-adrenergic receptor activity) is a molecular function defined as binding epinephrine or norepinephrine to initiate a cellular change via activation of a Gi alpha subunit of a heterotrimeric G protein.
• The term is synonymous with alpha2 adrenoceptor and is distinct from beta-adrenergic receptors because signaling proceeds through Gi-mediated inhibition of adenylyl cyclase.
• Alpha2-adrenergic receptors are established pharmacological targets for analgesia and sedation, exemplified by agonists such as clonidine and dexmedetomidine.
• Activation of alpha2-adrenergic receptors can suppress thermogenesis and modulate neuronal circuits, linking the receptor to metabolic and neurological control.
• Recent work shows that alpha2-adrenergic receptor activation can trigger tumour immune rejection, expanding the relevance of this GO term into immuno-oncology.
• Studying GO:0004938 requires combining pharmacological tools, genetic models, and CRISPR-based editing of the receptor genes and their downstream Gi signaling components.
Description
Alpha2-adrenergic receptor activity (GO:0004938) is a molecular function in which a receptor binds epinephrine or norepinephrine and transmits the signal to the Gi alpha subunit of a heterotrimeric G protein, thereby initiating a change in cell activity. This definition places the term at the interface of catecholamine sensing and Gi-mediated intracellular signaling, a position that makes it central to pharmacology, neuroscience, and cardiovascular biology. Researchers studying this activity are interested not only in ligand recognition but also in how receptor engagement is converted into downstream cellular responses such as inhibition of adenylyl cyclase and modulation of ion channels. The term is often referred to by its synonym, alpha2 adrenoceptor, and is experimentally distinguished from other adrenergic activities by its pharmacological profile and Gi coupling. Because alpha2-adrenergic receptors are expressed in diverse tissues, their activity has been implicated in processes ranging from analgesia and sedation to thermoregulation and immune surveillance. The discovery that activation of these receptors can promote tumour immune rejection has further broadened interest in GO:0004938 as a potential therapeutic node. At the same time, the receptor's role in oxidative stress protection and in neuronal survival after ischemia highlights its importance in disease contexts. Understanding the precise molecular and cellular mechanisms of alpha2-adrenergic receptor activity is therefore essential for interpreting both physiological and pathological catecholamine signaling.
alpha2-adrenergic receptor activity At A Glance
| GO ID | GO:0004938 |
|---|---|
| GO term | alpha2-adrenergic receptor activity |
| Ontology | molecular_function |
| Synonym | alpha2 adrenoceptor |
| Definition | Combining with epinephrine or norepinephrine to initiate a change in cell activity via activation of a G protein, with pharmacological characteristics of alpha2-adrenergic receptors; the activity involves transmitting the signal to the Gi alpha subunit of a heterotrimeric G protein. |
| Major function | Catecholamine sensing and Gi-mediated signal transduction that alters cellular activity. |
| Ligands | Epinephrine and norepinephrine. |
| G protein coupling | Gi alpha subunit of a heterotrimeric G protein. |
| Pharmacological class | Alpha2-adrenergic receptors, targeted by agonists such as clonidine and dexmedetomidine. |
| Representative processes | Analgesia, sedation, thermoregulation, immune modulation. |
What Is GO:0004938?
In plain terms, GO:0004938 describes the function of a receptor that recognizes epinephrine or norepinephrine and then activates a Gi protein to change what the cell does. The QuickGO definition specifies that this activity involves transmitting the signal to the Gi alpha subunit of a heterotrimeric G protein, which distinguishes it from adrenergic receptors that couple to other G proteins. The term is a molecular function, not a biological process or a cellular component, and its synonym alpha2 adrenoceptor reflects the pharmacological class of the receptor. When this activity is triggered, the Gi alpha subunit typically inhibits adenylyl cyclase and reduces cyclic AMP levels, although the exact downstream effects depend on the cell type and the complement of effector proteins present. This definition is used by annotators to assign the function to specific gene products, and it provides a controlled vocabulary for comparing receptor activities across species and experimental systems.
Why Is alpha2-adrenergic receptor activity Important in Cell Biology?
GO:0004938 is important because it defines a specific mode of catecholamine signaling that is pharmacologically tractable and physiologically widespread. Alpha2-adrenergic receptor activity is the molecular basis for the analgesic and sedative effects of clinically used agonists such as clonidine and dexmedetomidine. It also contributes to the regulation of thermogenesis and to neuronal circuit modulation, making it relevant to metabolic and neurological research. In disease, this activity has been linked to protection against oxidative stress and ischemia-reperfusion injury, as well as to tumour immune rejection, indicating that it can influence both cell survival and immune responses. Because the receptor couples to Gi proteins, its activity intersects with many downstream pathways, and understanding it is necessary for interpreting experiments that use adrenergic drugs or that manipulate catecholamine signaling. For researchers, GO:0004938 provides a precise annotation target when studying receptor function, and it guides the design of genetic and pharmacological experiments.
• Provides a defined molecular function for annotating genes that encode alpha2-adrenergic receptors and their signaling partners.
• Underlies the clinical use of alpha2-adrenergic agonists as analgesics and sedatives.
• Links catecholamine signaling to Gi-mediated inhibition of adenylyl cyclase and reduced cyclic AMP.
• Contributes to the regulation of thermogenesis and energy expenditure.
• Modulates neuronal activity in brain regions such as the diagonal band, relevant to arousal and cognition.
• Can protect cardiomyocytes and neurons against oxidative stress and ischemia-reperfusion injury.
• Has been shown to trigger tumour immune rejection, connecting the receptor to cancer immunology.
• Is a target for pharmacological tools that help dissect adrenergic contributions to complex phenotypes.
• Supports comparative studies of adrenergic-like receptors in model organisms such as Drosophila.
• Guides CRISPR-based knockout, knock-in, and point-mutation experiments to test causality of receptor activity.
Molecular Mechanism of alpha2-adrenergic receptor activity
Ligand binding and receptor activation
In simple terms: The receptor first catches epinephrine or norepinephrine, which flips it into an active state.
Alpha2-adrenergic receptor activity begins with the binding of epinephrine or norepinephrine to the receptor, a step that is required for initiating a change in cell activity. This binding event is the defining feature of the molecular function and is what distinguishes the term from other adrenergic activities. Pharmacological characterization of alpha2-adrenergic receptors has been central to understanding their analgesic effects, as agonists such as clonidine mimic the natural ligands. In experimental systems, ligand binding is often assessed using radioligand binding or functional assays that report receptor activation.
Gi protein coupling and signal transmission
In simple terms: Once active, the receptor passes the signal to a Gi protein inside the cell.
The QuickGO definition specifies that alpha2-adrenergic receptor activity involves transmitting the signal to the Gi alpha subunit of a heterotrimeric G protein. This coupling is a key mechanistic step because it determines the downstream effects, which typically include inhibition of adenylyl cyclase and a reduction in cyclic AMP. The Gi coupling also distinguishes alpha2-adrenergic receptors from beta-adrenergic receptors, which generally couple to Gs and stimulate cyclic AMP production. Experimental evidence for Gi coupling comes from pharmacological and genetic studies that manipulate receptor activity and measure downstream signaling.
Downstream cellular responses
In simple terms: The Gi signal changes what the cell does, such as altering excitability or metabolism.
After Gi activation, alpha2-adrenergic receptor activity can lead to diverse cellular responses depending on the cell type. In neurons, this activity modulates neuronal activity in brain regions such as the horizontal limbs of the diagonal band, as shown using dexmedetomidine in mice. In thermoregulation, alpha2-adrenergic receptor-mediated inhibition of thermogenesis has been demonstrated, linking the receptor to metabolic control. In cardiomyocytes, alpha2-adrenergic receptor-dependent protection against oxidative stress has been reported, and this protection can be diminished by nicotine. These examples illustrate that the downstream consequences of GO:0004938 are context-dependent but consistently involve Gi-mediated signaling.
Pharmacological modulation
In simple terms: Drugs can turn this receptor activity up or down, which is why it is a drug target.
Alpha2-adrenergic receptor activity is pharmacologically tractable, with agonists such as clonidine and dexmedetomidine used to activate the receptor. Clonidine has been shown to protect against cerebral ischemia/reperfusion-induced neuronal apoptosis in rats, an effect attributed to alpha2-adrenergic receptor activation. Dexmedetomidine modulates neuronal activity via alpha2-adrenergic receptors in mice, demonstrating the utility of selective agonists for probing receptor function. Conversely, antagonists can be used to block the activity and test its contribution to a phenotype. These pharmacological tools are essential complements to genetic approaches when studying GO:0004938.
Regulation of receptor activity
In simple terms: The strength and duration of the signal can be tuned by the cell.
The activity of alpha2-adrenergic receptors can be regulated at multiple levels, including receptor expression, desensitization, and interactions with other signaling pathways. For example, nicotine has been shown to diminish alpha2-adrenergic receptor-dependent protection against oxidative stress in H9c2 cardiomyocytes, indicating that other stimuli can modulate the protective signaling. Social stress has been linked to beta-adrenergic-driven oxidative stress in intestinal mucosal compartments, highlighting that adrenergic signaling is subject to environmental and physiological regulation. While the exact mechanisms of regulation for alpha2-adrenergic receptors are complex, experimental evidence supports the idea that their activity is not fixed but can be influenced by other inputs.
Evolutionary and comparative aspects
In simple terms: Similar receptors exist in other animals, helping researchers study the same function.
Alpha2-adrenergic-like receptors are found in invertebrate model organisms such as Drosophila melanogaster, where the octopamine receptor exhibits biological functions related to alpha2-adrenergic signaling. This conservation allows researchers to use genetic tools in flies to dissect the fundamental mechanisms of this receptor class. Comparative studies can reveal core features of the molecular function that are shared across species, while also highlighting differences in pharmacology and physiology. Such work complements mammalian studies and can inform the interpretation of GO:0004938 annotations across taxa.
Key Genes Involved in GO:0004938 alpha2-adrenergic receptor activity
The following genes and proteins are central to alpha2-adrenergic receptor activity, including the receptors themselves, their endogenous ligands, and the Gi protein components that transmit the signal.
| Gene | Major Role | Research Relevance |
|---|---|---|
| ADRA2A | Alpha2A-adrenergic receptor; binds catecholamines and couples to Gi | Target of clonidine and dexmedetomidine; studied in analgesia, sedation, and neuronal modulation |
| ADRA2B | Alpha2B-adrenergic receptor; mediates Gi signaling in vascular and other tissues | Implicated in thermoregulation and cardiovascular responses |
| ADRA2C | Alpha2C-adrenergic receptor; modulates neurotransmitter release | Studied in neuronal circuits and stress responses |
| GNAI1 | Gi alpha subunit 1; transmits signal from receptor to effectors | Key downstream component of GO:0004938 |
| GNAI2 | Gi alpha subunit 2; inhibits adenylyl cyclase | Central to Gi-mediated signaling in many cell types |
| GNAI3 | Gi alpha subunit 3; participates in receptor coupling | Potential modifier of alpha2-adrenergic responses |
| GNAO1 | Go alpha subunit; related Gi family member in neurons | May contribute to neuronal effects of alpha2-adrenergic activity |
| GNB1 | G protein beta subunit 1; part of heterotrimeric G protein | Required for receptor-G protein coupling |
| GNG2 | G protein gamma subunit 2; part of heterotrimeric G protein | Modulates Gi signaling specificity |
| ADCY1 | Adenylyl cyclase 1; downstream effector inhibited by Gi | Readout of alpha2-adrenergic receptor activity |
| ADCY5 | Adenylyl cyclase 5; cyclic AMP production | Effector whose inhibition reflects receptor activity |
| SLC6A2 | Norepinephrine transporter; regulates ligand availability | Indirectly influences receptor activation |
| TH | Tyrosine hydroxylase; rate-limiting enzyme in catecholamine synthesis | Determines epinephrine/norepinephrine supply |
| DBH | Dopamine beta-hydroxylase; converts dopamine to norepinephrine | Affects ligand availability for alpha2-adrenergic receptors |
| PNMT | Phenylethanolamine N-methyltransferase; synthesizes epinephrine | Contributes to epinephrine supply |
| COMT | Catechol-O-methyltransferase; degrades catecholamines | Regulates ligand levels and receptor activity |
| MAOA | Monoamine oxidase A; degrades norepinephrine and epinephrine | Modulates catecholamine tone |
| OCTOPAMINE_R | Drosophila alpha2-adrenergic-like octopamine receptor | Model for studying conserved receptor functions |
How Is alpha2-adrenergic receptor activity Regulated?
Alpha2-adrenergic receptor activity is regulated at multiple levels, including ligand availability, receptor expression, and downstream signaling cross-talk. Nicotine has been shown to diminish alpha2-adrenergic receptor-dependent protection against oxidative stress in H9c2 cardiomyocytes, indicating that other signaling inputs can modulate the protective effects of receptor activation. Social stress has been linked to beta-adrenergic-driven oxidative stress in intestinal mucosal compartments, illustrating that adrenergic signaling is influenced by environmental factors. These examples suggest that the activity of alpha2-adrenergic receptors is not constitutive but can be tuned by physiological and pharmacological contexts.
alpha2-adrenergic receptor activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| ADRA2A | Neuroprotection in ischemia-reperfusion injury | Rat model of cerebral ischemia with clonidine treatment |
| ADRA2A | Oxidative stress in cardiomyocytes | H9c2 cardiomyocytes with nicotine exposure |
| ADRA2A/B/C | Tumour immune rejection | Mouse tumour models with alpha2-adrenergic agonists |
| ADRA2B | Thermogenesis and metabolic control | Mouse models of thermoregulation |
| ADRA2A | Neuronal activity and sedation | Mouse diagonal band neurons with dexmedetomidine |
Alpha2-adrenergic receptors in cancer and immune rejection
Activation of alpha2-adrenergic receptors has been shown to trigger tumour immune rejection, revealing a role for this molecular function in cancer immunology. This finding suggests that pharmacological or genetic manipulation of GO:0004938 could influence anti-tumour immunity. The mechanism likely involves Gi-mediated signaling in immune cells, although the precise pathways require further investigation. This connection expands the disease relevance of alpha2-adrenergic receptor activity beyond classical neurological and cardiovascular contexts.
Neuroprotection and ischemia-reperfusion injury
Alpha2-adrenergic receptor activation by clonidine protects against cerebral ischemia/reperfusion-induced neuronal apoptosis in rats, indicating a neuroprotective role for this activity. This effect is consistent with the ability of alpha2-adrenergic agonists to reduce excitotoxicity and oxidative stress. In cardiomyocytes, alpha2-adrenergic receptor-dependent protection against oxidative stress has been demonstrated, and this protection is diminished by nicotine. These studies highlight the potential of targeting GO:0004938 in ischemic and oxidative stress-related diseases.
Metabolic and thermoregulatory disorders
Alpha2-adrenergic receptor-mediated inhibition of thermogenesis has been described, linking this molecular function to metabolic control. Dysregulation of thermogenesis contributes to obesity and metabolic disorders, making alpha2-adrenergic receptors potential targets for modulating energy expenditure. The receptor's role in thermoregulation is likely mediated by Gi signaling in thermogenic tissues, although the exact cell types and circuits continue to be studied. This connection underscores the importance of GO:0004938 in metabolic physiology.
Neurological and psychiatric conditions
Dexmedetomidine modulates neuronal activity via alpha2-adrenergic receptors in the horizontal limbs of the diagonal band in mice, a region implicated in arousal and cognition. This suggests that alpha2-adrenergic receptor activity can influence neurological functions relevant to sedation and potentially to psychiatric conditions. Alpha2-adrenergic agonists are used clinically for sedation and analgesia, further supporting the relevance of this activity to brain function. Understanding how GO:0004938 modulates neuronal circuits may inform the development of therapies for disorders of arousal and cognition.
From alpha2-adrenergic receptor activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does loss of alpha2-adrenergic receptor activity alter thermogenesis? | ADRA2B knockout mouse |
| Can receptor activation protect neurons from ischemia? | Rat middle cerebral artery occlusion with clonidine |
| Does receptor activity modulate neuronal circuits? | Mouse brain slice electrophysiology with dexmedetomidine |
| Is Gi coupling required for immune rejection? | Knock-in mice expressing Gi-uncoupled receptor |
| Does nicotine modify receptor-dependent oxidative stress protection? | H9c2 cardiomyocytes with nicotine and alpha2 agonist |
| Is the Drosophila octopamine receptor functionally analogous? | Drosophila melanogaster genetic mutants |
How to Study the alpha2-adrenergic receptor activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Radioligand binding | Receptor affinity and density | Characterizing alpha2-adrenergic receptor pharmacology |
| cAMP assay | Gi-mediated inhibition of adenylyl cyclase | Measuring receptor activity in cells |
| Knockout mouse | Requirement of receptor for phenotype | Thermogenesis and immune studies |
| Electrophysiology | Neuronal activity changes | Dexmedetomidine effects on brain circuits |
| Ischemia-reperfusion model | Neuroprotection | Clonidine treatment in rats |
| Oxidative stress assay | Cardiomyocyte protection | Nicotine modulation of receptor function |
| Drosophila genetics | Conserved receptor functions | Octopamine receptor studies |
| Tumour immune assays | Immune rejection | Alpha2 agonist effects on tumour growth |
Pharmacological profiling
Pharmacological profiling using selective agonists and antagonists is a primary method to study alpha2-adrenergic receptor activity. Clonidine and dexmedetomidine are commonly used agonists that activate the receptor, while antagonists can block the activity. These tools allow researchers to test the contribution of GO:0004938 to cellular and physiological responses. Dose-response curves and competition binding assays can quantify receptor affinity and efficacy.
Genetic knockout and knockdown
Genetic approaches, including knockout and knockdown of receptor genes, are used to determine the necessity of alpha2-adrenergic receptor activity for a given phenotype. For example, knockout mice lacking specific receptor subtypes can reveal roles in thermoregulation or immune responses. These models complement pharmacological studies by removing the receptor protein entirely, avoiding off-target drug effects. CRISPR-based knockout is a powerful way to generate such models.
Signal transduction assays
Because alpha2-adrenergic receptors couple to Gi, measuring cyclic AMP levels is a standard readout of receptor activity. Inhibition of adenylyl cyclase can be assessed using cAMP sensors or biochemical assays. Downstream effects such as changes in ion channel activity or kinase signaling can also be measured to understand the cellular consequences of receptor activation. These assays are essential for linking receptor engagement to functional outcomes.
In vivo physiological measurements
In vivo measurements, such as thermoregulation studies or neuronal recordings, provide insight into the physiological roles of alpha2-adrenergic receptor activity. For example, core body temperature can be monitored in response to alpha2 agonists to study thermogenesis. Electrophysiological recordings in brain slices can assess how receptor activation modulates neuronal firing. These methods bridge molecular function to organismal physiology.
How CRISPR Can Be Used to Study GO:0004938 alpha2-adrenergic receptor activity
Knockout
CRISPR knockout of alpha2-adrenergic receptor genes (ADRA2A, ADRA2B, ADRA2C) can eliminate receptor activity and reveal its contribution to cellular and physiological processes. For example, knockout mice have been used to study thermoregulation and immune rejection. Knockout of downstream Gi subunits (GNAI1, GNAI2, GNAI3) can also disrupt the signaling pathway and help distinguish receptor-specific effects. These models are essential for establishing causality in GO:0004938 research.
Point Mutation
Point mutations can be introduced into the receptor gene to alter ligand binding or G protein coupling without eliminating the protein. For instance, mutations that uncouple the receptor from Gi can test whether Gi signaling is required for a specific phenotype. Such point-mutant models are valuable for dissecting the molecular determinants of alpha2-adrenergic receptor activity. They also help distinguish between receptor functions that are Gi-dependent and those that are not.
Knock-in
Knock-in of tagged or reporter versions of the receptor can enable visualization and tracking of receptor expression and localization. Knock-in of human receptor variants into mouse models can facilitate translational studies. Additionally, knock-in of mutant Gi subunits can be used to probe downstream signaling specificity. These approaches provide precise genetic tools for studying GO:0004938 in vivo.
Overexpression
Overexpression of alpha2-adrenergic receptors in cell lines or transgenic animals can amplify receptor activity and sensitize cells to agonists. This approach is useful for studying downstream signaling and for screening compounds that modulate receptor function. Overexpression can also reveal gain-of-function phenotypes that complement knockout studies. However, careful controls are needed to avoid artifacts from supraphysiological expression levels.
How EDITGENE Supports alpha2-adrenergic receptor activity Research
Researchers studying alpha2-adrenergic receptor activity-related genes often need to determine whether a candidate gene is causally involved in a specific signaling or disease phenotype. EDITGENE provides a comprehensive suite of CRISPR-based services to generate precisely engineered cell and animal models, enabling rigorous testing of hypotheses related to GO:0004938.
Contact EDITGENE today to design your custom CRISPR model for alpha2-adrenergic receptor activity research.
Frequently Asked Questions About alpha2-adrenergic receptor activity
What is alpha2-adrenergic receptor activity?
Alpha2-adrenergic receptor activity (GO:0004938) is a molecular function in which a receptor binds epinephrine or norepinephrine and transmits the signal to the Gi alpha subunit of a heterotrimeric G protein, initiating a change in cell activity.
What genes are involved in alpha2-adrenergic receptor activity?
The main genes include ADRA2A, ADRA2B, and ADRA2C, which encode the receptors, as well as GNAI1, GNAI2, and GNAI3, which encode Gi alpha subunits.
What is the GO ID for alpha2-adrenergic receptor activity?
The GO ID is GO:0004938.
What is the synonym for alpha2-adrenergic receptor activity?
The synonym is alpha2 adrenoceptor.
How does alpha2-adrenergic receptor activity work?
It works by binding catecholamines and activating Gi proteins, which typically inhibit adenylyl cyclase and reduce cyclic AMP levels.
What diseases are linked to alpha2-adrenergic receptor activity?
It has been linked to cancer immune rejection, neuroprotection in ischemia, oxidative stress in cardiomyocytes, and metabolic control.
What drugs target alpha2-adrenergic receptors?
Clonidine and dexmedetomidine are agonists that activate alpha2-adrenergic receptors and are used for analgesia and sedation.
How can I study alpha2-adrenergic receptor activity in the lab?
Common methods include pharmacological profiling with agonists/antagonists, cAMP assays, genetic knockout models, and electrophysiology.
What is the role of Gi proteins in alpha2-adrenergic receptor activity?
Gi proteins transmit the signal from the activated receptor to downstream effectors, such as adenylyl cyclase, leading to reduced cyclic AMP.
Can CRISPR be used to study alpha2-adrenergic receptor activity?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models can be used to dissect the function of the receptor and its signaling partners.
Conclusion
Alpha2-adrenergic receptor activity (GO:0004938) is a well-defined molecular function that couples catecholamine binding to Gi-mediated signaling. Its roles in analgesia, thermoregulation, neuroprotection, and tumour immune rejection make it a compelling target for both basic and translational research. Continued investigation using pharmacological and CRISPR-based genetic tools will further clarify how this activity contributes to health and disease.
References
- 1. Zhu J et al.. 2023. Tumour immune rejection triggered by activation of α2-adrenergic receptors.. Nature 618(7965):607-615 PMID: 37286594
- 2. Boyd RE. 2001. Alpha2-adrenergic receptor agonists as analgesics.. Curr Top Med Chem 1(3):193-7 PMID: 11895135
- 3. Caetano-Silva ME et al.. 2026. Social stress worsens colitis through β-adrenergic-driven oxidative stress in intestinal mucosal compartments.. Brain Behav Immun 132:106222 PMID: 41418891
- 4. Del Calvo G et al.. 2024. Nicotine Diminishes Alpha2-Adrenergic Receptor-Dependent Protection Against Oxidative Stress in H9c2 Cardiomyocytes.. Drug Des Devel Ther 18:71-80 PMID: 38229917
- 5. He Z et al.. 2024. The alpha2-adrenergic receptor agonist clonidine protects against cerebral ischemia/reperfusion induced neuronal apoptosis in rats.. Metab Brain Dis 39(5):741-752 PMID: 38833094
- 6. Nakagawa H et al.. 2022. Biological functions of α2-adrenergic-like octopamine receptor in Drosophila melanogaster.. Genes Brain Behav 21(6):e12807 PMID: 35411674
- 7. Madden CJ et al.. 2013. α2 Adrenergic receptor-mediated inhibition of thermogenesis.. J Neurosci 33(5):2017-28 PMID: 23365239
- 8. Zhang XW et al.. 2023. Dexmedetomidine modulates neuronal activity of horizontal limbs of diagonal band via α2 adrenergic receptor in mice.. BMC Anesthesiol 23(1):327 PMID: 37784079
