Contact Us / Request a Quote Download Manuals
Advanced Cell Diagnostics Advanced Cell Diagnostics

Search form

Please sign in
  • Log In
  • Register
  • How to Order
  • What to Buy
0 My Cart
X

You have no items in your shopping cart.

Menu
X
  • Products +
    RNAscope™/BaseScope™/ miRNAscope™
    +
    • Assay Selection Guide
    Target Probes
    +
    • All About Probes
    • Catalog Probes
    • Probe Sets
    • New Probe Request
    Manual Assays
    +
    RNAscope™ Chromogenic
    • Overview
    • RNAscope™ 2.5 HD Assay-Brown
    • RNAscope™ 2.5 HD Assay-Red
    • RNAscope™ 2.5 HD Duplex Assay
    RNAscope™ Multiplex Fluorescent
    • Overview
    • RNAscope™ HiPlex v2 Assay
    • RNAscope™ Multiplex Fluorescent V2
    BaseScope™
    • Overview
    • BaseScope™ Assay Red
    • BaseScope™ Duplex Assay
    miRNAscope™
    • Overview
    • miRNAscope™ Assay red
    • RNAscope™ Plus smRNA-RNA Assay
    DNAscope™
    • Overview
    • DNAscope™ Duplex Assay
    Automated Assays
    +
    For Lunaphore COMET™
    • RNAscope™ HiPlex Pro for COMET™
    For Leica systems
    • Overview
    • RNAscope™ 2.5 LS Assay-Brown
    • RNAscope™ 2.5 LS Assay-Red
    • RNAscope™ 2.5 LS Duplex Assay
    • RNAscope™ Multiomic LS Assay
    • RNAscope™ 2.5 LS Fluorescent Multiplex Assay
    • RNAscope™ 2.5 LSx Reagent Kit-BROWN
    • RNAscope™ 2.5 LSx Reagent Kit-RED
    • BaseScope™ LS Reagent Kit – RED
    • miRNAscope LS Reagent Kit Red
    • RNAscope™ Plus smRNA-RNA LS Assay
    Roche DISCOVERY ULTRA system
    • Overview
    • RNAscope™ VS Universal HRP
    • RNAscope™ VS Universal AP
    • RNAscope™ VS Duplex Assay
    • BaseScope™ VS Reagent Kit – RED
    RNA-Protein Co-Detection Assay
    +
    • RNAscope HiPlex-IMC™ Co-Detection
    • Integrated Codetection Assay
    • Sequential RNA Protein Detection
    Software
    +
    • Overview
    • Aperio RNA ISH Algorithm
    • HALO® image analysis platform
    Controls & Accessories
    +
    • RNAscope™
    • BaseScope™
    • miRNAscope™
    • Accessories
    How to Order
    +
    • Ordering Instructions
    • What to Buy
  • Services +
    Professional Assay Services
    +
    • Our Services
    • Multiomic Services
    • Biomarker Assay Development
    • Cell & Gene Therapy Services
    • Clinical Assay Development
    • Tissue Bank & Sample Procurement
    • Image Analysis
    Benefits
    +
    • Your Benefits
    • Certified Providers
    How to Order
    +
    • Ordering Process
    • Contact Services
  • Areas of Research +
    Most Popular
    +
    • COVID-19 Coronavirus
    • Single Cell Analysis
    • Whole-Mount
    • Anatomic Pathology Panels
    • Neuroscience
    • Inflammation
    • Gene Therapy/AAV
    • Stem Cell
    • Immuno-oncology
    • Liver Research
    • Cardiovascular & Skeletal Muscle Research
    Cell & Gene Therapy
    +
    • Gene Therapy
    • Gene Therapy/AAV
    • siRNA/ASO
    • Cell Therapy
    Cancer
    +
    • Breast Cancer
    • EGFRvIII Splice Variant
    • HPV Related Cancer
    • Immuno-oncology
    • Lung Cancer
    • PDx
    • Prostate Cancer
    • Point Mutation
    • CDR3 for TCR
    Viral
    +
    • COVID-19 Coronavirus
    • HIV & SIV
    • Infectious Disease
    • Zika Virus
    Pathways
    +
    • AKT
    • JAK STAT
    • WNT B-Catenin
    Neuroscience
    +
    Neuroscience
    • Neural Development
    • Neuronal Cell Types
    • Learning and Memory
    • G-protein-coupled Receptors & Ion Channels
    • Post-mortem Brain Tissue
    Other
    +
    • Circular RNA
    • Gene Fusions
    • HT Transcript Validation
    • Long Non-coding RNA
    • RNAseq Validation
    • Single Cell Analysis
    • Splice Variant
    • miRNA
    RNA & Protein
    +
    • Antibody Challenges
    • Dual ISH + IHC Methods
    • No Antibodies
    • RNA & Protein Analysis
    Customer Innovations
    +
    • Dual RNA+DNA ISH
    • Very old FFPE ISH
    • Wholemount ISH
    Animal Models
    +
    • Any Species
    • Mouse Model
    • Preclincal Safety
  • Technology +
    Overview
    +
    • How it Works
    • Data Image Gallery
    • Technology Video
    • Webinars
    RNA Detection
    +
    • Why RNA?
    • RNA ISH and IHC
    Pretreatment Options
    +
    • RNAscope™ Pretreatment
    • PretreatPro™
    Spotlights
    +
    • Researchers Spotlights
    • RNA & DNA
    • WISH
    • FFPE
    • Testimonials
    Publications, Guides & Posters
    +
    • Search publications
    • RNAscope™ Reference Guide
    • RNAscope™ Data Analysis Guide
    • Download RNAscope™ Posters
  • Support +
    Overview
    +
    • Get Started
    • How to Order
    • Distributors
    • Contact Support
    Troubleshooting
    +
    • Troubleshooting Guide
    • FAQs
    • User Manuals, SDS and Product Inserts
    • Documents and Downloads
    Imaging Resource
    +
    • Image Analysis
    • Image Registration Software
    • QuPath
    • HALO® image analysis platform
    Learn More
    +
    • Webinars
    • Training Videos
  • Partners +
    Partners
    +
    • Overview
    Partners Directory
    +
    Automation Partners
    • Leica Biosystem
    • Roche Diagnostics
    Workflow Partners
    • NanoString
    Software Partners
    • indica labs
    Become a Partner
    +
    • Learn How
  • Diagnostics +
    Diagnostics
    +
    • Diagnostics
    • Literature
    • Diagnostics ASR Probes
    • Diagnostics CE-IVD Probes
    • Diagnostics CE-IVD Detection
    • Companion Diagnostics
  • Image Calendar +
    Image Calendar
    +
    • Image Contest
    • Data Image Gallery
Search

Probes for INS

ACD can configure probes for the various manual and automated assays for INS for RNAscope Assay, or for Basescope Assay compatible for your species of interest.

  • Probes for INS (0)
  • Kits & Accessories (0)
  • Support & Documents (0)
  • Publications (40)
  • Image gallery (0)
Refine Probe List

Content for comparison

Gene

  • TBD (137) Apply TBD filter
  • Gad1 (85) Apply Gad1 filter
  • vGlut2 (75) Apply vGlut2 filter
  • Slc17a6 (72) Apply Slc17a6 filter
  • SLC32A1 (70) Apply SLC32A1 filter
  • FOS (62) Apply FOS filter
  • Sst (57) Apply Sst filter
  • VGAT (56) Apply VGAT filter
  • TH (55) Apply TH filter
  • Gad2 (50) Apply Gad2 filter
  • DRD2 (49) Apply DRD2 filter
  • Slc17a7 (49) Apply Slc17a7 filter
  • PVALB (46) Apply PVALB filter
  • tdTomato (44) Apply tdTomato filter
  • DRD1 (36) Apply DRD1 filter
  • GFAP (33) Apply GFAP filter
  • Chat (33) Apply Chat filter
  • Crh (32) Apply Crh filter
  • egfp (31) Apply egfp filter
  • Npy (28) Apply Npy filter
  • (-) Remove Pomc filter Pomc (25)
  • VGluT1 (25) Apply VGluT1 filter
  • Cre (24) Apply Cre filter
  • Penk (23) Apply Penk filter
  • AGRP (22) Apply AGRP filter
  • Rbfox3 (21) Apply Rbfox3 filter
  • CCK (21) Apply CCK filter
  • Oxtr (21) Apply Oxtr filter
  • OPRM1 (21) Apply OPRM1 filter
  • TAC1 (20) Apply TAC1 filter
  • Pdyn (20) Apply Pdyn filter
  • C-fos (20) Apply C-fos filter
  • GLP1R (19) Apply GLP1R filter
  • Aldh1l1 (18) Apply Aldh1l1 filter
  • GFP (18) Apply GFP filter
  • Vip (18) Apply Vip filter
  • Nts (17) Apply Nts filter
  • (-) Remove Prkcd filter Prkcd (15)
  • Trpv1 (15) Apply Trpv1 filter
  • CALCA (14) Apply CALCA filter
  • Drd1a (14) Apply Drd1a filter
  • Bdnf (14) Apply Bdnf filter
  • MBP (14) Apply MBP filter
  • Tmem119 (14) Apply Tmem119 filter
  • Piezo2 (13) Apply Piezo2 filter
  • SOX2 (13) Apply SOX2 filter
  • Gal (13) Apply Gal filter
  • ESR1 (13) Apply ESR1 filter
  • PDGFRA (13) Apply PDGFRA filter
  • Aif1 (13) Apply Aif1 filter

Product

  • RNAscope Fluorescent Multiplex Assay (13) Apply RNAscope Fluorescent Multiplex Assay filter
  • RNAscope Multiplex Fluorescent Assay (11) Apply RNAscope Multiplex Fluorescent Assay filter
  • RNAscope (2) Apply RNAscope filter
  • RNAscope 2.5 HD Duplex (2) Apply RNAscope 2.5 HD Duplex filter
  • RNAscope 2.5 HD Brown Assay (1) Apply RNAscope 2.5 HD Brown Assay filter
  • RNAscope 2.5 HD Red assay (1) Apply RNAscope 2.5 HD Red assay filter
  • RNAscope 2.5 LS Assay (1) Apply RNAscope 2.5 LS Assay filter
  • RNAscope Fluorescent Multiplex Reagent kit (1) Apply RNAscope Fluorescent Multiplex Reagent kit filter
  • RNAscope HiPlex v2 assay (1) Apply RNAscope HiPlex v2 assay filter
  • RNAscope Multiplex Fluorescent v2 (1) Apply RNAscope Multiplex Fluorescent v2 filter

Research area

  • (-) Remove Neuroscience filter Neuroscience (40)
  • Obesity (2) Apply Obesity filter
  • Addiction (1) Apply Addiction filter
  • Alcohol Use disorder (1) Apply Alcohol Use disorder filter
  • Alcohol Withdrawl (1) Apply Alcohol Withdrawl filter
  • behavioral (1) Apply behavioral filter
  • Bioinformatics (1) Apply Bioinformatics filter
  • Cross Species Evolution (1) Apply Cross Species Evolution filter
  • Endocrinology (1) Apply Endocrinology filter
  • Evolution (1) Apply Evolution filter
  • Feeding Behavior (1) Apply Feeding Behavior filter
  • Metabolism (1) Apply Metabolism filter
  • Other: Metabolism (1) Apply Other: Metabolism filter
  • Pain (1) Apply Pain filter
  • Psychiatry (1) Apply Psychiatry filter
  • Stem cell (1) Apply Stem cell filter
  • Transcriptomics (1) Apply Transcriptomics filter

Category

  • Publications (40) Apply Publications filter
Hypothalamic POMC or MC4R deficiency impairs counterregulatory responses to hypoglycemia in mice.

Molecular Metabolism

2018 Nov 20

Tooke BP, Yu H, Adams JM, Jones GL, Sutton-Kennedy T, Mundada L, Qi NR, Low MJ, Chhabra KH.
PMID: - | DOI: 10.1016/j.molmet.2018.11.004

Abstract

Objective

Life-threatening hypoglycemia is a major limiting factor in the management of diabetes. While it is known that counterregulatory responses to hypoglycemia are impaired in diabetes, molecular mechanisms underlying the reduced responses remain unclear. Given the established roles of the hypothalamic proopiomelanocortin (POMC)/melanocortin 4 receptor (MC4R) circuit in regulating sympathetic nervous system (SNS) activity and the SNS in stimulating counterregulatory responses to hypoglycemia, we hypothesized that hypothalamic POMC as well as MC4R, a receptor for POMC derived melanocyte stimulating hormones, is required for normal hypoglycemia counterregulation.

Methods

To test the hypothesis, we induced hypoglycemia or glucopenia in separate cohorts of mice deficient in either POMC or MC4R in the arcuate nucleus (ARC) or the paraventricular nucleus of the hypothalamus (PVH), respectively, and measured their circulating counterregulatory hormones. In addition, we performed a hyperinsulinemic-hypoglycemic clamp study to further validate the function of MC4R in hypoglycemia counterregulation. We also measured Pomc and Mc4r mRNA levels in the ARC and PVH, respectively, in the streptozotocin-induced type 1 diabetes mouse model and non-obese diabetic (NOD) mice to delineate molecular mechanisms by which diabetes deteriorates the defense systems against hypoglycemia. Finally, we treated diabetic mice with the MC4R agonist MTII, administered stereotaxically into the PVH, to determine its potential for restoring the counterregulatory response to hypoglycemia in diabetes.

Results

Stimulation of epinephrine and glucagon release in response to hypoglycemia or glucopenia was diminished in both POMC- and MC4R-deficient mice, relative to their littermate controls. Similarly, the counterregulatory response was impaired in association with decreased hypothalamic Pomc and Mc4r expression in the diabetic mice, a phenotype that was not reversed by insulin treatment which normalized glycemia. In contrast, infusion of an MC4R agonist in the PVH restored the counterregulatory response in diabetic mice.

Conclusion

In conclusion, hypothalamic Pomc as well as Mc4r, both of which are reduced in type 1 diabetic mice, are required for normal counterregulatory responses to hypoglycemia. Therefore, enhancing MC4R function may improve hypoglycemia counterregulation in diabetes.

Mitochondrial cristae-remodeling protein OPA1 in POMC neurons couples Ca2+ homeostasis with adipose tissue lipolysis

Cell metabolism

2021 Jul 27

Gómez-Valadés, AG;Pozo, M;Varela, L;Boudjadja, MB;Ramírez, S;Chivite, I;Eyre, E;Haddad-Tóvolli, R;Obri, A;Milà-Guasch, M;Altirriba, J;Schneeberger, M;Imbernón, M;Garcia-Rendueles, AR;Gama-Perez, P;Rojo-Ruiz, J;Rácz, B;Alonso, MT;Gomis, R;Zorzano, A;D'Agostino, G;Alvarez, CV;Nogueiras, R;Garcia-Roves, PM;Horvath, TL;Claret, M;
PMID: 34343501 | DOI: 10.1016/j.cmet.2021.07.008

Appropriate cristae remodeling is a determinant of mitochondrial function and bioenergetics and thus represents a crucial process for cellular metabolic adaptations. Here, we show that mitochondrial cristae architecture and expression of the master cristae-remodeling protein OPA1 in proopiomelanocortin (POMC) neurons, which are key metabolic sensors implicated in energy balance control, is affected by fluctuations in nutrient availability. Genetic inactivation of OPA1 in POMC neurons causes dramatic alterations in cristae topology, mitochondrial Ca2+ handling, reduction in alpha-melanocyte stimulating hormone (α-MSH) in target areas, hyperphagia, and attenuated white adipose tissue (WAT) lipolysis resulting in obesity. Pharmacological blockade of mitochondrial Ca2+ influx restores α-MSH and the lipolytic program, while improving the metabolic defects of mutant mice. Chemogenetic manipulation of POMC neurons confirms a role in lipolysis control. Our results unveil a novel axis that connects OPA1 in POMC neurons with mitochondrial cristae, Ca2+ homeostasis, and WAT lipolysis in the regulation of energy balance.
Defining potential targets of prenatal androgen excess: expression analysis of androgen receptor on hypothalamic neurons in the fetal female mouse brain

Journal of Neuroendocrinology

2023 May 18

Watanabe, Y;Fisher, L;Campbell, R;Jasoni, C;
| DOI: 10.1111/jne.13302

Polycystic ovary syndrome (PCOS) is a female endocrine disorder that is associated with prenatal exposure to excess androgens. In prenatally androgenized (PNA) mice that model PCOS, GABAergic neural transmission to and innervation of GnRH neurons is increased. Evidence suggests that elevated GABAergic innervation originates in the arcuate nucleus (ARC). We hypothesised that GABA-GnRH circuit abnormalities are a direct consequence of PNA, resulting from DHT binding to androgen receptor (AR) in the prenatal brain. However, whether prenatal ARC neurons express AR at the time of PNA treatment is presently unknown. We used RNAScope _in situ_ hybridization to localize AR mRNA (_Ar_)-expressing cells in healthy gestational day (GD) 17.5 female mouse brains and to assess co-expression levels in specific neuronal phenotypes. Our study revealed that less than 10% of ARC GABA cells expressed _Ar_. In contrast, we found that ARC kisspeptin neurons, critical regulators of GnRH neurons, were highly co-localised with _Ar_. Approximately 75% of ARC _Kiss1_-expressing cells also expressed _Ar_ at GD17.5, suggesting that ARC kisspeptin neurons are potential targets of PNA. Investigating other neuronal populations in the ARC we found that approximately 50% of pro-opiomelanocortin (_Pomc_) cells, 22% of tyrosine hydroxylase (_Th_) cells, 8% of agouti-related protein (_Agrp_) cells and 8% of somatostatin (_Sst_) cells express _Ar_. Lastly, RNAscope in coronal sections showed _Ar_ expression in the medial preoptic area (mPOA), and the ventral part of the lateral septum (vLS). These _Ar_-expressing regions were highly GABAergic, and 22% of GABA cells in the mPOA and 25% of GABA cells in the vLS also expressed _Ar_. Our findings identify specific neuronal phenotypes in the ARC, mPOA and vLS that are androgen sensitive in late gestation. PNA-induced functional changes in these neurons may be related to the development of impaired central mechanisms associated with PCOS-like features.
Lipopolysacharide rapidly and completely suppresses AgRP neuron-mediated food intake in male mice

Endocrinology.

2016 Apr 25

Liu Y, Huang Y, Liu T, Wu H, Cui H, Gautron L.
PMID: 27111742 | DOI: -

While Agouti-related peptide (AgRP) neurons play a key role in the regulation of food intake, their contribution to the anorexia caused by pro-inflammatory insults has yet to be identified. Using a combination of neuroanatomical and pharmacogenetics experiments, this study sought to investigate the importance of AgRP neurons and downstream targets in the anorexia caused by the peripheral administration of a moderate dose of lipopolysaccharide (LPS; 100 μ g/kg, ip). First, in the C57/Bl6 mouse, we demonstrated that LPS induced c-fos in select AgRP-innervated brain sites involved in feeding, but not in any arcuate proopiomelanocortin neurons. Double immunohistochemistry further showed that LPS selectively induced c-Fos in a large subset of melanocortin 4 receptor-expressing neurons in the lateral parabrachial nucleus. Secondly, we used pharmacogenetics to stimulate the activity of AgRP neurons during the course of LPS-induced anorexia. In AgRP-Cre mice expressing the designer receptor hM3Dq-Gq only in AgRP neurons, the administration of the designer drug clozapine-N-oxide (CNO) induced robust food intake. Strikingly, CNO-mediated food intake was rapidly and completely blunted by the coadministration of LPS. Neuroanatomical experiments further indicated that LPS did not interfere with the ability of CNO to stimulate c-Fos in AgRP neurons. In summary, our findings combined together support the view that the stimulation of select AgRP-innervated brain sites and target neurons, rather than the inhibition of AgRP neurons themselves, is likely to contribute to the rapid suppression of food intake observed during acute bacterial endotoxemia.

Dorsal BNST α2A-adrenergic receptors produce HCN-dependent excitatory actions that initiate anxiogenic behaviors.

J Neurosci.

2018 Aug 27

Harris NA, Isaac AT, Günther A, Merkel K, Melchior J, Xu M, Eguakun E, Perez R, Nabit BP, Flavin S, Gilsbach R, Shonesy B, Hein L, Abel T, Baumann A, Matthews R, Centanni SW, Winder DG.
PMID: 30150361 | DOI: 10.1523/JNEUROSCI.0963-18.2018

Stress is a precipitating agent in neuropsychiatric disease and initiates relapse to drug-seeking behavior in addicted patients. Targeting the stress system in protracted abstinence from drugs of abuse with anxiolytics may be an effective treatment modality for substance use disorders. α2A-adrenergic receptors (α2A-ARs) in extended amygdala structures play key roles in dampening stress responses. Contrary to early thinking, α2A-ARs are expressed at non-noradrenergic sites in the brain. These non-noradrenergic α2A-ARs play important roles in stress-responses, but their cellular mechanisms of action are unclear. In humans, the α2A-AR agonist guanfacine reduces overall craving and uncouples craving from stress yet minimally affects relapse, potentially due to competing actions in the brain. Here we show that heteroceptor α2A-ARs postsynaptically enhance dorsal BNST (dBNST) neuronal activity in mice of both sexes. This effect is mediated by hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels, as inhibition of these channels is necessary and sufficient for excitatory actions. Finally, this excitatory action is mimicked by clozapine-N-oxide activation of the Gi-coupled DREADD hM4Di in dBNST neurons, and its activation elicits anxiety-like behavior in the elevated plus maze. Together, this data provides a framework for elucidating cell-specific actions of GPCR signaling and provides a potential mechanism whereby competing anxiogenic and anxiolytic actions of guanfacine may affect its clinical utility in the treatment of addiction.SIGNIFICANCE STATEMENTStress impacts the development of neuropsychiatric disorders including anxiety and addiction. Guanfacine is an α2A-adrenergic receptor (α2A-AR) agonist with actions in the bed nucleus of the stria terminalis (BNST) that produces antidepressant actions and uncouples stress from reward-related behaviors. Here we show that guanfacine increases dBNST neuronal activity through actions at postsynaptic α2A-ARs via a mechanism that involves hyperpolarization-activated cyclic nucleotide gated cation (HCN) channels. This action is mimicked by activation of the designer receptor hM4Di expressed in the BNST, which also induces anxiety-like behaviors. Together, these data suggest 1) that postsynaptic α2A-ARs in BNST have excitatory actions on BNST neurons, and 2) these actions can be phenocopied by the so-called "inhibitory" DREADDs, suggesting care must be taken regarding interpretation of data obtained with these tools.

Insulin signalling in tanycytes gates hypothalamic insulin uptake and regulation of AgRP neuron activity

Nature metabolism

2021 Dec 01

Porniece Kumar, M;Cremer, AL;Klemm, P;Steuernagel, L;Sundaram, S;Jais, A;Hausen, AC;Tao, J;Secher, A;Pedersen, TÅ;Schwaninger, M;Wunderlich, FT;Lowell, BB;Backes, H;Brüning, JC;
PMID: 34931084 | DOI: 10.1038/s42255-021-00499-0

Insulin acts on neurons and glial cells to regulate systemic glucose metabolism and feeding. However, the mechanisms of insulin access in discrete brain regions are incompletely defined. Here we show that insulin receptors in tanycytes, but not in brain endothelial cells, are required to regulate insulin access to the hypothalamic arcuate nucleus. Mice lacking insulin receptors in tanycytes (IR∆Tan mice) exhibit systemic insulin resistance, while displaying normal food intake and energy expenditure. Tanycytic insulin receptors are also necessary for the orexigenic effects of ghrelin, but not for the anorexic effects of leptin. IR∆Tan mice exhibit increased agouti-related peptide (AgRP) neuronal activity, while displaying blunted AgRP neuronal adaptations to feeding-related stimuli. Lastly, a highly palatable food decreases tanycytic and arcuate nucleus insulin signalling to levels comparable to those seen in IR∆Tan mice. These changes are rooted in modifications of cellular stress responses and of mitochondrial protein quality control in tanycytes. Conclusively, we reveal a critical role of tanycyte insulin receptors in gating feeding-state-dependent regulation of AgRP neurons and systemic insulin sensitivity, and show that insulin resistance in tanycytes contributes to the pleiotropic manifestations of obesity-associated insulin resistance.
Angiotensin AT1A receptors on leptin receptor-expressing cells control resting metabolism

J Clin Invest.

2017 Mar 06

Claflin KE, Sandgren JA, Lambertz AM, Weidemann BJ, Littlejohn NK, Burnett CM, Pearson NA, Morgan DA, Gibson-Corley KN, Rahmouni K, Grobe JL.
PMID: 28263184 | DOI: 10.1172/JCI88641

Leptin contributes to the control of resting metabolic rate (RMR) and blood pressure (BP) through its actions in the arcuate nucleus (ARC). The renin-angiotensin system (RAS) and angiotensin AT1 receptors within the brain are also involved in the control of RMR and BP, but whether this regulation overlaps with leptin's actions is unclear. Here, we have demonstrated the selective requirement of the AT1A receptor in leptin-mediated control of RMR. We observed that AT1A receptors colocalized with leptin receptors (LEPRs) in the ARC. Cellular coexpression of AT1A and LEPR was almost exclusive to the ARC and occurred primarily within neurons expressing agouti-related peptide (AgRP). Mice lacking the AT1A receptor specifically in LEPR-expressing cells failed to show an increase in RMR in response to a high-fat diet and deoxycorticosterone acetate-salt (DOCA-salt) treatments, but BP control remained intact. Accordingly, loss of RMR control was recapitulated in mice lacking AT1A in AgRP-expressing cells. We conclude that angiotensin activates divergent mechanisms to control BP and RMR and that the brain RAS functions as a major integrator for RMR control through its actions at leptin-sensitive AgRP cells of the ARC.

Molecular and cellular evolution of the amygdala across species analyzed by single-nucleus transcriptome profiling

Cell discovery

2023 Feb 14

Yu, B;Zhang, Q;Lin, L;Zhou, X;Ma, W;Wen, S;Li, C;Wang, W;Wu, Q;Wang, X;Li, XM;
PMID: 36788214 | DOI: 10.1038/s41421-022-00506-y

The amygdala, or an amygdala-like structure, is found in the brains of all vertebrates and plays a critical role in survival and reproduction. However, the cellular architecture of the amygdala and how it has evolved remain elusive. Here, we generated single-nucleus RNA-sequencing data for more than 200,000 cells in the amygdala of humans, macaques, mice, and chickens. Abundant neuronal cell types from different amygdala subnuclei were identified in all datasets. Cross-species analysis revealed that inhibitory neurons and inhibitory neuron-enriched subnuclei of the amygdala were well-conserved in cellular composition and marker gene expression, whereas excitatory neuron-enriched subnuclei were relatively divergent. Furthermore, LAMP5+ interneurons were much more abundant in primates, while DRD2+ inhibitory neurons and LAMP5+SATB2+ excitatory neurons were dominant in the human central amygdalar nucleus (CEA) and basolateral amygdalar complex (BLA), respectively. We also identified CEA-like neurons and their species-specific distribution patterns in chickens. This study highlights the extreme cell-type diversity in the amygdala and reveals the conservation and divergence of cell types and gene expression patterns across species that may contribute to species-specific adaptations.
Activation of GABAB receptors in central amygdala attenuates activity of PKCδ + neurons and suppresses punishment-resistant alcohol self-administration in rats

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2023 Feb 04

Domi, E;Xu, L;Toivainen, S;Wiskerke, J;Coppola, A;Holm, L;Augier, E;Petrella, M;Heilig, M;
PMID: 36739350 | DOI: 10.1038/s41386-023-01543-1

Alcohol use despite negative consequences is a core phenomenon of alcohol addiction. We recently used alcohol self-administration that is resistant to footshock punishment as a model of this behavior, and found that activity of PKCδ + GABAergic neurons in the central amygdala (CeA) is a determinant of individual susceptibility for punishment resistance. In the present study, we examined whether activation of GABAB receptors in CeA can attenuate the activity of PKCδ + neurons in this region, and whether this will result in suppression of punishment- resistant alcohol self-administration in the minority of rats that show this behavior. Systemic administration of the clinically approved GABAB agonist baclofen (1 and 3 mg/kg) dose- dependently reduced punishment-resistant alcohol self-administration. Bilateral microinjections of baclofen into CeA (64 ng in 0.3 µl/side) reduced the activity of PKCδ + neurons, as measured by Fos expression. This manipulation also selectively suppressed punished alcohol self-administration in punishment-resistant rats. Expression analysis indicated that virtually all CeA PKCδ + neurons express the GABAB receptor. Using in vitro electrophysiology, we found that baclofen induced hyperpolarization of CeA neurons, reducing their firing rate in response to depolarizing current injections. Together, our findings provide a potential mechanism that contributes to the clinical efficacy of baclofen in alcohol addiction. Therapeutic use of baclofen itself is limited by problems of tolerance and need for dose escalation. Our findings support a mechanistic rationale for developing novel, improved alcohol addiction medications that target GABAB receptors, and that lack these limitations, such as e.g., GABAB positive allosteric modulators (PAM:s).
Cell-type specific changes in PKC-delta neurons of the central amygdala during alcohol withdrawal

Translational psychiatry

2022 Jul 20

Dilly, GA;Kittleman, CW;Kerr, TM;Messing, RO;Mayfield, RD;
PMID: 35859068 | DOI: 10.1038/s41398-022-02063-0

The central amygdala (CeA) contains a diverse population of cells, including multiple subtypes of GABAergic neurons, along with glia and epithelial cells. Specific CeA cell types have been shown to affect alcohol consumption in animal models of dependence and may be involved in negative affect during alcohol withdrawal. We used single-nuclei RNA sequencing to determine cell-type specificity of differential gene expression in the CeA induced by alcohol withdrawal. Cells within the CeA were classified using unbiased clustering analyses and identified based on the expression of known marker genes. Differential gene expression analysis was performed on each identified CeA cell-type. It revealed differential gene expression in astrocytes and GABAergic neurons associated with alcohol withdrawal. GABAergic neurons were further subclassified into 13 clusters of cells. Analyzing transcriptomic responses in these subclusters revealed that alcohol exposure induced multiple differentially expressed genes in one subtype of CeA GABAergic neurons, the protein kinase C delta (PKCδ) expressing neurons. These results suggest that PKCδ neurons in the CeA may be uniquely sensitive to the effects of alcohol exposure and identify a novel population of cells in CeA associated with alcohol withdrawal.
The central fibroblast growth factor receptor/beta klotho system: comprehensive mapping in mus musculus and comparisons to non-human primate and human samples using an automated in situ hybridization platform.

J Comp Neurol.

2019 Feb 27

Hultman K, Scarlett JM, Baquero AF, Cornea A, Zhang Y, Salinas CBG, Brown J, Morton GJ, Whalen EJ, Grove KL, Koegler FH, Schwartz MW, Mercer AJ.
PMID: 30809795 | DOI: 10.1002/cne.24668

Central activation of fibroblast growth factor (FGF) receptors regulates peripheral glucose homeostasis and reduces food intake in preclinical models of obesity and diabetes. The current work was undertaken to advance our understanding of the receptor expression, as sites of ligand action by FGF19, FGF21, and FGF1 in the mammalian brain remains unresolved. Recent advances in automated RNAscope in situ hybridization and droplet digital PCR (ddPCR) technology allowed us to interrogate central FGFR/beta klotho (Klb) system at the cellular level in the mouse, with relevant comparisons to nonhuman primate and human brain. FGFR1-3 gene expression was broadly distributed throughout the CNS in Mus musculus, with FGFR1 exhibiting the greatest heterogeneity. FGFR4 expression localized only in the medial habenula and subcommissural organ of mice. Likewise, Klb mRNA was restricted to the suprachiasmatic nucleus (SCh) and select midbrain and hindbrain nuclei. ddPCR in the rodent hypothalamus confirmed that, although expression levels are indeed low for Klb, there is nonetheless a bonafide subpopulation of Klb+ cells in the hypothalamus. In NHP and human midbrain and hindbrain, Klb + cells are quite rare, as is expression of FGFR4. Collectively, these data provide the most robust central map of the FGFR/Klb system to date and highlight central regions that may be of critical importance to assess central ligand effects with pharmacological dosing, such as the putative interactions between the endocrine FGFs and FGFR1/Klb, or FGF19 with FGFR4.

Mild Impairment of Mitochondrial OXPHOS Promotes Fatty Acid Utilization in POMC Neurons and Improves Glucose Homeostasis in Obesity.

Cell Rep.

2018 Oct 09

Timper K, Paeger L, Sánchez-Lasheras C, Varela L, Jais A, Nolte H, Vogt MC, Hausen AC, Heilinger C, Evers N, Pospisilik JA, Penninger JM, Taylor EB, Horvath TL, Kloppenburg P, Brüning JC.
PMID: 30304679 | DOI: 10.1016/j.celrep.2018.09.034

Mitochondrial oxidative phosphorylation (OXPHOS) and substrate utilization critically regulate the function of hypothalamic proopiomelanocortin (POMC)-expressing neurons. Here, we demonstrate that inactivation of apoptosis-inducing factor (AIF) in POMC neurons mildly impairs mitochondrial respiration and decreases firing of POMC neurons in lean mice. In contrast, under diet-induced obese conditions, POMC-Cre-specific inactivation of AIF prevents obesity-induced silencing of POMC neurons, translating into improved glucose metabolism, improved leptin, and insulin sensitivity, as well as increased energy expenditure in AIFΔPOMC mice. On a cellular level, AIF deficiency improves mitochondrial morphology, facilitates the utilization of fatty acids for mitochondrial respiration, and increases reactive oxygen species (ROS) formation in POMC neurons from obese mice, ultimately leading to restored POMC firing upon HFD feeding. Collectively, partial impairment of mitochondrial function shifts substrate utilization of POMC neurons from glucose to fatty acid metabolism and restores their firing properties, resulting in improved systemic glucose and energy metabolism in obesity.

Pages

  • 1
  • 2
  • 3
  • 4
  • next ›
  • last »
X
Description
sense
Example: Hs-LAG3-sense
Standard probes for RNA detection are in antisense. Sense probe is reverse complent to the corresponding antisense probe.
Intron#
Example: Mm-Htt-intron2
Probe targets the indicated intron in the target gene, commonly used for pre-mRNA detection
Pool/Pan
Example: Hs-CD3-pool (Hs-CD3D, Hs-CD3E, Hs-CD3G)
A mixture of multiple probe sets targeting multiple genes or transcripts
No-XSp
Example: Hs-PDGFB-No-XMm
Does not cross detect with the species (Sp)
XSp
Example: Rn-Pde9a-XMm
designed to cross detect with the species (Sp)
O#
Example: Mm-Islr-O1
Alternative design targeting different regions of the same transcript or isoforms
CDS
Example: Hs-SLC31A-CDS
Probe targets the protein-coding sequence only
EnEmProbe targets exons n and m
En-EmProbe targets region from exon n to exon m
Retired Nomenclature
tvn
Example: Hs-LEPR-tv1
Designed to target transcript variant n
ORF
Example: Hs-ACVRL1-ORF
Probe targets open reading frame
UTR
Example: Hs-HTT-UTR-C3
Probe targets the untranslated region (non-protein-coding region) only
5UTR
Example: Hs-GNRHR-5UTR
Probe targets the 5' untranslated region only
3UTR
Example: Rn-Npy1r-3UTR
Probe targets the 3' untranslated region only
Pan
Example: Pool
A mixture of multiple probe sets targeting multiple genes or transcripts

Enabling research, drug development (CDx) and diagnostics

Contact Us
  • Toll-free in the US and Canada
  • +1877 576-3636
  • 
  • 
  • 
Company
  • Overview
  • Leadership
  • Careers
  • Distributors
  • Quality
  • News & Events
  • Webinars
  • Patents
Products
  • RNAscope or BaseScope
  • Target Probes
  • Controls
  • Manual assays
  • Automated Assays
  • Accessories
  • Software
  • How to Order
Research
  • Popular Applications
  • Cancer
  • Viral
  • Pathways
  • Neuroscience
  • Other Applications
  • RNA & Protein
  • Customer Innovations
  • Animal Models
Technology
  • Overview
  • RNA Detection
  • Spotlight Interviews
  • Publications & Guides
Assay Services
  • Our Services
  • Biomarker Assay Development
  • Cell & Gene Therapy Services
  • Clinical Assay Development
  • Tissue Bank & Sample Procurement
  • Image Analysis
  • Your Benefits
  • How to Order
Diagnostics
  • Diagnostics
  • Companion Diagnostics
Support
  • Getting started
  • Contact Support
  • Troubleshooting Guide
  • FAQs
  • Manuals, SDS & Inserts
  • Downloads
  • Webinars
  • Training Videos

Visit Bio-Techne and its other brands

  • bio-technie
  • protein
  • bio-spacific
  • rd
  • novus
  • tocris
© 2025 Advanced Cell Diagnostics, Inc.
  • Terms and Conditions of Sale
  • Privacy Policy
  • Security
  • Email Preferences
  • 
  • 
  • 

For Research Use Only. Not for diagnostic use. Refer to appropriate regulations. RNAscope is a registered trademark; and HybEZ, EZ-Batch and DNAscope are trademarks of Advanced Cell Diagnostics, Inc. in the United States and other countries. All rights reserved. ©2025 Advanced Cell Diagnostics, Inc.

 

Contact Us / Request a Quote
Download Manuals
Request a PAS Project Consultation
Order online at
bio-techne.com
OK
X
Contact Us

Complete one of the three forms below and we will get back to you.

For Quote Requests, please provide more details in the Contact Sales form below

  • Contact Sales
  • Contact Support
  • Contact Services
  • Offices

Advanced Cell Diagnostics

Our new headquarters office starting May 2016:

7707 Gateway Blvd.  
Newark, CA 94560
Toll Free: 1 (877) 576-3636
Phone: (510) 576-8800
Fax: (510) 576-8798

 

Bio-Techne

19 Barton Lane  
Abingdon Science Park
Abingdon
OX14 3NB
United Kingdom
Phone 2: +44 1235 529449
Fax: +44 1235 533420

 

Advanced Cell Diagnostics China

20F, Tower 3,
Raffles City Changning Office,
1193 Changning Road, Shanghai 200051

021-52293200
info.cn@bio-techne.com
Web: www.acdbio.com/cn

For general information: Info.ACD@bio-techne.com
For place an order: order.ACD@bio-techne.com
For product support: support.ACD@bio-techne.com
For career opportunities: hr.ACD@bio-techne.com

See Distributors
×

You have already Quick ordered an Item in your cart . If you want to add a new item , Quick ordered Item will be removed form your cart. Do You want to continue?

OK Cancel
Need help?

How can we help you?