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Bio-Techne corporation crf r1 agonist stressin

Antagonism of antinociceptive effects of i.c.v. administered <t>CRF</t> by <t>CRF-R1</t> antagonist NBI 27914 and CRF-R2 antagonist K41498. In Wistar rats with 4-day FCA-induced hind paw inflammation, effects of i.c.v. administered CRF on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. application of CRF (0.5, 01.0, 1.5, 2.0 µmol) significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 445; P < 0.001). B Dose-dependent antagonism of i.c.v. CRF’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 502.9; P < 0.001). C In contrast, increasing doses of the i.c.v. CRF-R2 antagonist K41498 only partially antagonized CRF’s antinociception ( F (4, 25) = 315.7; P < 0.001). *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Crf R1 Agonist Stressin, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas"

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

Journal: Journal of Neuroinflammation

doi: 10.1186/s12974-022-02498-8

Antagonism of antinociceptive effects of i.c.v. administered CRF by CRF-R1 antagonist NBI 27914 and CRF-R2 antagonist K41498. In Wistar rats with 4-day FCA-induced hind paw inflammation, effects of i.c.v. administered CRF on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. application of CRF (0.5, 01.0, 1.5, 2.0 µmol) significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 445; P < 0.001). B Dose-dependent antagonism of i.c.v. CRF’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 502.9; P < 0.001). C In contrast, increasing doses of the i.c.v. CRF-R2 antagonist K41498 only partially antagonized CRF’s antinociception ( F (4, 25) = 315.7; P < 0.001). *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Figure Legend Snippet: Antagonism of antinociceptive effects of i.c.v. administered CRF by CRF-R1 antagonist NBI 27914 and CRF-R2 antagonist K41498. In Wistar rats with 4-day FCA-induced hind paw inflammation, effects of i.c.v. administered CRF on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. application of CRF (0.5, 01.0, 1.5, 2.0 µmol) significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 445; P < 0.001). B Dose-dependent antagonism of i.c.v. CRF’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 502.9; P < 0.001). C In contrast, increasing doses of the i.c.v. CRF-R2 antagonist K41498 only partially antagonized CRF’s antinociception ( F (4, 25) = 315.7; P < 0.001). *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Techniques Used:

Antinociceptive effects of the i.c.v. CRF-R1 agonist stressin I or CRF-R2 agonist Ucn-2 and their antagonism by the respective CRF-R1 (NBI 27914) or CRF-R2 (K41498) selective antagonists. The effects of i.c.v. CRF-R1 (stressin I) or CRF-R2 (Ucn-2) agonists on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. administration of the CRF-R1 agonist stressin I significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 552.4; P < 0.001). B i.c.v. administration of the CRF-R2 agonist Ucn-2 significantly increased nociceptive thresholds ( F (4, 25) = 389.1; P < 0.001). C Dose-dependent antagonism of i.c.v. CRF-R1 agonist’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 73.9; P < 0.001, one-way ANOVA and Dunnett’s test). D ) Dose-dependent antagonism of i.c.v. Ucn-2 antinociception by co-administered CRF-R2 antagonist K41498 was significant ( F (5, 30) = 88.4; P < 0.001), *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Figure Legend Snippet: Antinociceptive effects of the i.c.v. CRF-R1 agonist stressin I or CRF-R2 agonist Ucn-2 and their antagonism by the respective CRF-R1 (NBI 27914) or CRF-R2 (K41498) selective antagonists. The effects of i.c.v. CRF-R1 (stressin I) or CRF-R2 (Ucn-2) agonists on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. administration of the CRF-R1 agonist stressin I significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 552.4; P < 0.001). B i.c.v. administration of the CRF-R2 agonist Ucn-2 significantly increased nociceptive thresholds ( F (4, 25) = 389.1; P < 0.001). C Dose-dependent antagonism of i.c.v. CRF-R1 agonist’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 73.9; P < 0.001, one-way ANOVA and Dunnett’s test). D ) Dose-dependent antagonism of i.c.v. Ucn-2 antinociception by co-administered CRF-R2 antagonist K41498 was significant ( F (5, 30) = 88.4; P < 0.001), *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Techniques Used:

The antinociceptive effects of i.c.v. CRF and CRF-R1 agonist stressin I and their antagonism by the opioid receptor antagonist naloxone in rats with inflamed hindpaws. The effects of i.c.v. co-administration of the opioid receptor antagonist naloxone with CRF or CRF-R1 agonist stressin I on nociceptive thresholds were measured by algesiometer. A The i.c.v. CRF’s induced-antinociception was significantly reduced by co-administration of the opioid receptor antagonist naloxone ( F (5, 30) = 384.8; P < 0.001). B Similarly, the antinociception resulting from i.c.v. CRF-R1 agonist stressin I was significantly attenuated by co-administered opioid receptor antagonist naloxone ( F (5, 30) = 400.8; P < 0.001) *indicates significant differences from vehicle treatment); data points ( n = 6) represent means ± SD

Figure Legend Snippet: The antinociceptive effects of i.c.v. CRF and CRF-R1 agonist stressin I and their antagonism by the opioid receptor antagonist naloxone in rats with inflamed hindpaws. The effects of i.c.v. co-administration of the opioid receptor antagonist naloxone with CRF or CRF-R1 agonist stressin I on nociceptive thresholds were measured by algesiometer. A The i.c.v. CRF’s induced-antinociception was significantly reduced by co-administration of the opioid receptor antagonist naloxone ( F (5, 30) = 384.8; P < 0.001). B Similarly, the antinociception resulting from i.c.v. CRF-R1 agonist stressin I was significantly attenuated by co-administered opioid receptor antagonist naloxone ( F (5, 30) = 400.8; P < 0.001) *indicates significant differences from vehicle treatment); data points ( n = 6) represent means ± SD

Techniques Used:

Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F or CRF-R2 G – I ( red fluorescence ) with proopiomelanocortin (POMC) ( green fluorescence ) B, H and vasopressin ( green fluorescence ) E in the paraventricular nucleus (PVN) of the rat hypothalamus. A – C Double-immunofluorescence staining of coronal brain sections of the rat with hind paw inflammation showing that CRF-R1-immunoreactive neurons within PVN overlap with the opioid peptide precursor POMC ( A – C ). Some neurons express CRF-R1 or POMC only. D – F Show CRF-R1-immunoreactive neurons in the paraventricular nucleus (PVN) residing in close vicinity of vasopressin positive cells without any overlap of the two cell groups. G – I Show only few scattered CRF-R2-immunoreactive neurons without POMC overlap in the same region. Bar = 20 μm

Figure Legend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F or CRF-R2 G – I ( red fluorescence ) with proopiomelanocortin (POMC) ( green fluorescence ) B, H and vasopressin ( green fluorescence ) E in the paraventricular nucleus (PVN) of the rat hypothalamus. A – C Double-immunofluorescence staining of coronal brain sections of the rat with hind paw inflammation showing that CRF-R1-immunoreactive neurons within PVN overlap with the opioid peptide precursor POMC ( A – C ). Some neurons express CRF-R1 or POMC only. D – F Show CRF-R1-immunoreactive neurons in the paraventricular nucleus (PVN) residing in close vicinity of vasopressin positive cells without any overlap of the two cell groups. G – I Show only few scattered CRF-R2-immunoreactive neurons without POMC overlap in the same region. Bar = 20 μm

Techniques Used: Double Immunofluorescence Staining, Fluorescence

Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F and POMC ( green fluorescence ) B , C or β-endorphin (END) ( green fluorescence ) E , F in the median eminence of the rat hypothalamus. A – F Show that most of CRF-R1-immunoreactive fibers express POMC ( C ) or END ( F ) in coronal sections of the rat brain of Wistar rats, but few fibers contain CRF-R1, POMC or END only. Bar = 20 µm

Figure Legend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F and POMC ( green fluorescence ) B , C or β-endorphin (END) ( green fluorescence ) E , F in the median eminence of the rat hypothalamus. A – F Show that most of CRF-R1-immunoreactive fibers express POMC ( C ) or END ( F ) in coronal sections of the rat brain of Wistar rats, but few fibers contain CRF-R1, POMC or END only. Bar = 20 µm

Techniques Used: Double Immunofluorescence Staining, Fluorescence

Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G and POMC ( green fluorescence ) B , E , H ( green fluorescence ) E in the thalamus A – C and periaqueductal grey D – I of rat brain. A – C Coronal sections of the rat brain with hindpaw inflammation show that most of CRF-R1-positive neurons in the thalamus region express POMC, but few fibers contain CRF-R1 or POMC only. D – F Coronal sections of the rat brain with hindpaw inflammation show co-localization of CRF-R1 with POMC neurons in the periaqueductal grey, but few fibers contain CRF-R1 or POMC only. Bar = 20 µm, G – I Higher magnification of D – F . Bar = 40 µm

Figure Legend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G and POMC ( green fluorescence ) B , E , H ( green fluorescence ) E in the thalamus A – C and periaqueductal grey D – I of rat brain. A – C Coronal sections of the rat brain with hindpaw inflammation show that most of CRF-R1-positive neurons in the thalamus region express POMC, but few fibers contain CRF-R1 or POMC only. D – F Coronal sections of the rat brain with hindpaw inflammation show co-localization of CRF-R1 with POMC neurons in the periaqueductal grey, but few fibers contain CRF-R1 or POMC only. Bar = 20 µm, G – I Higher magnification of D – F . Bar = 40 µm

Techniques Used: Double Immunofluorescence Staining, Fluorescence

Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G or CRF-R2 J – l with proopiomelanocortin (POMC) ( B , K ), β-endorphin (END) E and vasopressin H ( green fluorescence ) in the supraoptic area (SOA) of the rat hypothalamus. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing that CRF-R-immunoreactive neurons within SON overlap with the opioid peptide precursor POMC C or ( F ). Some neurons express CRF-R1 or POMC only. G – I Show the majority of CRF-R1-immunoreactive neurons residing in close vicinity, and rarely overlap (as indicated by yellow fluorescence) with vasopressin positive cells. J – L Show few scattered CRF-R2-immunoreactive neurons with only rare overlap with POMC-ir neurons. Bar = 20 μm

Figure Legend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G or CRF-R2 J – l with proopiomelanocortin (POMC) ( B , K ), β-endorphin (END) E and vasopressin H ( green fluorescence ) in the supraoptic area (SOA) of the rat hypothalamus. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing that CRF-R-immunoreactive neurons within SON overlap with the opioid peptide precursor POMC C or ( F ). Some neurons express CRF-R1 or POMC only. G – I Show the majority of CRF-R1-immunoreactive neurons residing in close vicinity, and rarely overlap (as indicated by yellow fluorescence) with vasopressin positive cells. J – L Show few scattered CRF-R2-immunoreactive neurons with only rare overlap with POMC-ir neurons. Bar = 20 μm

Techniques Used: Double Immunofluorescence Staining, Fluorescence

Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D with proopiomelanocortin (POMC) B or β-endorphin (END) E ( green fluorescence ) in the Locus coeruleus (LC) of the rat brain. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing co-expression of CRF-R1 with POMC C or END F within LC. Some neurons express CRF-R1, POMC or END only. Bar = 20 µm for A – C . Bar = 40 μm for ( D – F )

Figure Legend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D with proopiomelanocortin (POMC) B or β-endorphin (END) E ( green fluorescence ) in the Locus coeruleus (LC) of the rat brain. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing co-expression of CRF-R1 with POMC C or END F within LC. Some neurons express CRF-R1, POMC or END only. Bar = 20 µm for A – C . Bar = 40 μm for ( D – F )

Techniques Used: Double Immunofluorescence Staining, Fluorescence, Expressing

CRF-R1 and CRF-R2 mRNA expression in the hypothalamus region of the rat with 4 day FCA-induced hind paw inflammation. A RNA extraction from the rat hypothalamus, implementation of conventional PCR using specific primer pairs for CRF-R1 and CRF-R2, and subsequent visualization on a 2% agarose gel provided specific PCR products for the expression of CRF-R1 (280 bp) and CRF-R2 (230 bp) mRNA. B Shows the DNA melting profiles of the CRF-R1 (right) and CRF-R2 (left) specific primer pairs. C , D Quantification of CRF-R1 and CRF-R2 mRNA using Taqman® Real-Time PCR in the hypothalamus region of the rat brain. C The amplification profiles of the 18S- and CRF-R1- and CRF-R2-specific cDNA of rat hypothalamus. D The column graph representing % CRF-R1 mRNA expression relative to the expression of CRF-R2 mRNA. Note that CRF-R1 expression is more than threefold higher than that of CRF-R2 (experiments were done in duplicate from n = 5 rats, * P < 0.05, two-tailed independent Student t-test)

Figure Legend Snippet: CRF-R1 and CRF-R2 mRNA expression in the hypothalamus region of the rat with 4 day FCA-induced hind paw inflammation. A RNA extraction from the rat hypothalamus, implementation of conventional PCR using specific primer pairs for CRF-R1 and CRF-R2, and subsequent visualization on a 2% agarose gel provided specific PCR products for the expression of CRF-R1 (280 bp) and CRF-R2 (230 bp) mRNA. B Shows the DNA melting profiles of the CRF-R1 (right) and CRF-R2 (left) specific primer pairs. C , D Quantification of CRF-R1 and CRF-R2 mRNA using Taqman® Real-Time PCR in the hypothalamus region of the rat brain. C The amplification profiles of the 18S- and CRF-R1- and CRF-R2-specific cDNA of rat hypothalamus. D The column graph representing % CRF-R1 mRNA expression relative to the expression of CRF-R2 mRNA. Note that CRF-R1 expression is more than threefold higher than that of CRF-R2 (experiments were done in duplicate from n = 5 rats, * P < 0.05, two-tailed independent Student t-test)

Techniques Used: Expressing, RNA Extraction, Agarose Gel Electrophoresis, Real-time Polymerase Chain Reaction, Amplification, Two Tailed Test

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Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Antagonism of antinociceptive effects of i.c.v. administered CRF by CRF-R1 antagonist NBI 27914 and CRF-R2 antagonist K41498. In Wistar rats with 4-day FCA-induced hind paw inflammation, effects of i.c.v. administered CRF on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. application of CRF (0.5, 01.0, 1.5, 2.0 µmol) significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 445; P < 0.001). B Dose-dependent antagonism of i.c.v. CRF’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 502.9; P < 0.001). C In contrast, increasing doses of the i.c.v. CRF-R2 antagonist K41498 only partially antagonized CRF’s antinociception ( F (4, 25) = 315.7; P < 0.001). *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Article Snippet: The following drugs were used: rat/human CRF (Sigma-Aldrich, St. Louis, MO); CRF-R1 agonist stressin I and CRF-R1 antagonist NBI 27914 (Bio-Techne GmbH, Wiesbaden-Nordenstadt, Germany); CRF-R2 agonist urocortin-2 (Ucn-2), CRF-R2 antagonist K41498 (Bio-Techne GmbH, Wiesbaden-Nordenstadt, Germany); naloxone hydrochloride (Sigma-Aldrich, St. Louis, MO).

Techniques:

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Antinociceptive effects of the i.c.v. CRF-R1 agonist stressin I or CRF-R2 agonist Ucn-2 and their antagonism by the respective CRF-R1 (NBI 27914) or CRF-R2 (K41498) selective antagonists. The effects of i.c.v. CRF-R1 (stressin I) or CRF-R2 (Ucn-2) agonists on nociceptive paw pressure thresholds were measured by algesiometry. A i.c.v. administration of the CRF-R1 agonist stressin I significantly increased nociceptive thresholds in a dose-dependent manner ( F (4, 25) = 552.4; P < 0.001). B i.c.v. administration of the CRF-R2 agonist Ucn-2 significantly increased nociceptive thresholds ( F (4, 25) = 389.1; P < 0.001). C Dose-dependent antagonism of i.c.v. CRF-R1 agonist’s antinociception by co-administered CRF-R1 antagonist NBI 27914 ( F (4, 25) = 73.9; P < 0.001, one-way ANOVA and Dunnett’s test). D ) Dose-dependent antagonism of i.c.v. Ucn-2 antinociception by co-administered CRF-R2 antagonist K41498 was significant ( F (5, 30) = 88.4; P < 0.001), *indicates significant differences from vehicle treatment; data points (n = 6) represent means ± SD

Techniques:

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: The antinociceptive effects of i.c.v. CRF and CRF-R1 agonist stressin I and their antagonism by the opioid receptor antagonist naloxone in rats with inflamed hindpaws. The effects of i.c.v. co-administration of the opioid receptor antagonist naloxone with CRF or CRF-R1 agonist stressin I on nociceptive thresholds were measured by algesiometer. A The i.c.v. CRF’s induced-antinociception was significantly reduced by co-administration of the opioid receptor antagonist naloxone ( F (5, 30) = 384.8; P < 0.001). B Similarly, the antinociception resulting from i.c.v. CRF-R1 agonist stressin I was significantly attenuated by co-administered opioid receptor antagonist naloxone ( F (5, 30) = 400.8; P < 0.001) *indicates significant differences from vehicle treatment); data points ( n = 6) represent means ± SD

Techniques:

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F or CRF-R2 G – I ( red fluorescence ) with proopiomelanocortin (POMC) ( green fluorescence ) B, H and vasopressin ( green fluorescence ) E in the paraventricular nucleus (PVN) of the rat hypothalamus. A – C Double-immunofluorescence staining of coronal brain sections of the rat with hind paw inflammation showing that CRF-R1-immunoreactive neurons within PVN overlap with the opioid peptide precursor POMC ( A – C ). Some neurons express CRF-R1 or POMC only. D – F Show CRF-R1-immunoreactive neurons in the paraventricular nucleus (PVN) residing in close vicinity of vasopressin positive cells without any overlap of the two cell groups. G – I Show only few scattered CRF-R2-immunoreactive neurons without POMC overlap in the same region. Bar = 20 μm

Techniques: Double Immunofluorescence Staining, Fluorescence

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A – F and POMC ( green fluorescence ) B , C or β-endorphin (END) ( green fluorescence ) E , F in the median eminence of the rat hypothalamus. A – F Show that most of CRF-R1-immunoreactive fibers express POMC ( C ) or END ( F ) in coronal sections of the rat brain of Wistar rats, but few fibers contain CRF-R1, POMC or END only. Bar = 20 µm

Techniques: Double Immunofluorescence Staining, Fluorescence

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G and POMC ( green fluorescence ) B , E , H ( green fluorescence ) E in the thalamus A – C and periaqueductal grey D – I of rat brain. A – C Coronal sections of the rat brain with hindpaw inflammation show that most of CRF-R1-positive neurons in the thalamus region express POMC, but few fibers contain CRF-R1 or POMC only. D – F Coronal sections of the rat brain with hindpaw inflammation show co-localization of CRF-R1 with POMC neurons in the periaqueductal grey, but few fibers contain CRF-R1 or POMC only. Bar = 20 µm, G – I Higher magnification of D – F . Bar = 40 µm

Techniques: Double Immunofluorescence Staining, Fluorescence

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D , G or CRF-R2 J – l with proopiomelanocortin (POMC) ( B , K ), β-endorphin (END) E and vasopressin H ( green fluorescence ) in the supraoptic area (SOA) of the rat hypothalamus. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing that CRF-R-immunoreactive neurons within SON overlap with the opioid peptide precursor POMC C or ( F ). Some neurons express CRF-R1 or POMC only. G – I Show the majority of CRF-R1-immunoreactive neurons residing in close vicinity, and rarely overlap (as indicated by yellow fluorescence) with vasopressin positive cells. J – L Show few scattered CRF-R2-immunoreactive neurons with only rare overlap with POMC-ir neurons. Bar = 20 μm

Techniques: Double Immunofluorescence Staining, Fluorescence

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: Double-immunofluorescence staining of CRF-R1 ( red fluorescence ) A , D with proopiomelanocortin (POMC) B or β-endorphin (END) E ( green fluorescence ) in the Locus coeruleus (LC) of the rat brain. A – F Double-immunofluorescence staining of coronal sections of the rat brain with hind paw inflammation showing co-expression of CRF-R1 with POMC C or END F within LC. Some neurons express CRF-R1, POMC or END only. Bar = 20 µm for A – C . Bar = 40 μm for ( D – F )

Techniques: Double Immunofluorescence Staining, Fluorescence, Expressing

Journal: Journal of Neuroinflammation

Article Title: Superior control of inflammatory pain by corticotropin-releasing factor receptor 1 via opioid peptides in distinct pain-relevant brain areas

doi: 10.1186/s12974-022-02498-8

Figure Lengend Snippet: CRF-R1 and CRF-R2 mRNA expression in the hypothalamus region of the rat with 4 day FCA-induced hind paw inflammation. A RNA extraction from the rat hypothalamus, implementation of conventional PCR using specific primer pairs for CRF-R1 and CRF-R2, and subsequent visualization on a 2% agarose gel provided specific PCR products for the expression of CRF-R1 (280 bp) and CRF-R2 (230 bp) mRNA. B Shows the DNA melting profiles of the CRF-R1 (right) and CRF-R2 (left) specific primer pairs. C , D Quantification of CRF-R1 and CRF-R2 mRNA using Taqman® Real-Time PCR in the hypothalamus region of the rat brain. C The amplification profiles of the 18S- and CRF-R1- and CRF-R2-specific cDNA of rat hypothalamus. D The column graph representing % CRF-R1 mRNA expression relative to the expression of CRF-R2 mRNA. Note that CRF-R1 expression is more than threefold higher than that of CRF-R2 (experiments were done in duplicate from n = 5 rats, * P < 0.05, two-tailed independent Student t-test)

Techniques: Expressing, RNA Extraction, Agarose Gel Electrophoresis, Real-time Polymerase Chain Reaction, Amplification, Two Tailed Test

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