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α 2 ar adra3a  (Novus Biologicals)


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    Novus Biologicals α 2 ar adra3a
    α 2 Ar Adra3a, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bio-Techne corporation α 2 ar agonist uk14304
    (A) Pancreatic NA levels of RD and WD mice after Ex4 injection in the OB (n=2-3/group). (B) Schematic illustration of bilateral OB injections of Ex4 combined with IP administration of <t>UK14304</t> followed by an OGTT in OB-cannulated WD and OB-cannulated RD mice. (C) OGTT tests preceded by an IP injection of UK14304 and an OB injection of Ex4 in OB-cannulated WD after 20 weeks under WD (n=8) (left). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using paired Student’s t-test. (D) Plasma insulin levels of OB-cannulated WD during OGTT tests preceded with OB-injected Ex4 and IP injected UK14304 (RM two-way ANOVA followed by Bonferroni post-hoc test; n=8). (E) Strategy to deliver Ex4 in the OB of OB-cannulated C57BL6 mice. (F) Representative photomicrographs of cFos immunoreactivity and automated cell counting in the MCL using CellProfiler software (left). cFos density in the MCL after Ex4 or saline injection in the OB in WD mice (right). Data are expressed as cFos+ nuclei/mean MCL area of all mice. Data are analyzed using an unpaired Student’s t-test (n=5). (G) cFos density in the LH after Ex4 or saline injection in the OB in WD mice. Data are expressed as cFos+ nuclei/mean LH area of all mice. Data are analyzed using an unpaired Student’s t-test (n=4). (H) Schematic illustration of unilateral Alexa 488-conjugated cholera toxin B subunit (CTB green ) delivery in the LH for retrograde tracing of the primary olfactory cortex. (I) Coronal sections of the LH after unilateral injection of CTB green (left). CTB staining in the primary olfactory cortex (right). LH, lateral hypothalamus; AHP, anterior hypothalamus; VMH, ventromedial hypothalamus; 3V, third ventricle; AON, anterior olfactory nucleus; VTT, ventral tenia tecta; VON, ventral olfactory nucleus; PC, piriform cortex; OT, olfactory tubercle. Structure boundaries were drawn based on Franklin and Paxinos mouse brain atlas. (J) Schematic illustration of viral delivery in the OB and bilateral cannula placement in the PVN of Glp1r -Cre WD mice followed by OGTTs. (K) OGTT tests preceded with an IP injection of CNO in Glp1r OBhM3Dq WD PVN-cannulated mice after 20 weeks under WD (26-week old; n=10) (left). The black square and the green line indicate Bicuculline and CNO delivery, respectively, before the glucose gavage (T0). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using RM one-way ANOVA followed by Bonferroni post-hoc test. (L) Plasma insulin levels of Glp1r OBhM3Dq WD PVN-cannulated mice after CNO IP injection (RM two-way ANOVA followed by Bonferroni post-hoc test, n=10). Data are given as mean ± SEM. *p <0.05; **p < 0.01; ***p < 0.001; ns, not significant.
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    Zenyaku Kogyo Co Ltd α 2 -ar antagonist antisedan
    (A) Pancreatic NA levels of RD and WD mice after Ex4 injection in the OB (n=2-3/group). (B) Schematic illustration of bilateral OB injections of Ex4 combined with IP administration of <t>UK14304</t> followed by an OGTT in OB-cannulated WD and OB-cannulated RD mice. (C) OGTT tests preceded by an IP injection of UK14304 and an OB injection of Ex4 in OB-cannulated WD after 20 weeks under WD (n=8) (left). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using paired Student’s t-test. (D) Plasma insulin levels of OB-cannulated WD during OGTT tests preceded with OB-injected Ex4 and IP injected UK14304 (RM two-way ANOVA followed by Bonferroni post-hoc test; n=8). (E) Strategy to deliver Ex4 in the OB of OB-cannulated C57BL6 mice. (F) Representative photomicrographs of cFos immunoreactivity and automated cell counting in the MCL using CellProfiler software (left). cFos density in the MCL after Ex4 or saline injection in the OB in WD mice (right). Data are expressed as cFos+ nuclei/mean MCL area of all mice. Data are analyzed using an unpaired Student’s t-test (n=5). (G) cFos density in the LH after Ex4 or saline injection in the OB in WD mice. Data are expressed as cFos+ nuclei/mean LH area of all mice. Data are analyzed using an unpaired Student’s t-test (n=4). (H) Schematic illustration of unilateral Alexa 488-conjugated cholera toxin B subunit (CTB green ) delivery in the LH for retrograde tracing of the primary olfactory cortex. (I) Coronal sections of the LH after unilateral injection of CTB green (left). CTB staining in the primary olfactory cortex (right). LH, lateral hypothalamus; AHP, anterior hypothalamus; VMH, ventromedial hypothalamus; 3V, third ventricle; AON, anterior olfactory nucleus; VTT, ventral tenia tecta; VON, ventral olfactory nucleus; PC, piriform cortex; OT, olfactory tubercle. Structure boundaries were drawn based on Franklin and Paxinos mouse brain atlas. (J) Schematic illustration of viral delivery in the OB and bilateral cannula placement in the PVN of Glp1r -Cre WD mice followed by OGTTs. (K) OGTT tests preceded with an IP injection of CNO in Glp1r OBhM3Dq WD PVN-cannulated mice after 20 weeks under WD (26-week old; n=10) (left). The black square and the green line indicate Bicuculline and CNO delivery, respectively, before the glucose gavage (T0). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using RM one-way ANOVA followed by Bonferroni post-hoc test. (L) Plasma insulin levels of Glp1r OBhM3Dq WD PVN-cannulated mice after CNO IP injection (RM two-way ANOVA followed by Bonferroni post-hoc test, n=10). Data are given as mean ± SEM. *p <0.05; **p < 0.01; ***p < 0.001; ns, not significant.
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    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist <t>(clonidine),</t> β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Novus Biologicals α 2 ar adra3a
    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist <t>(clonidine),</t> β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Tocris α 2 ar agonist uk14 304
    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist <t>(clonidine),</t> β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Novus Biologicals α 2 ar
    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist <t>(clonidine),</t> β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist <t>(clonidine),</t> β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.
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    Millipore α 2 -ar antagonist idazoxan
    Involvement of α1-adrenergic receptor (AR) in the analgesic effect of bvPLA2. Antagonists and its vehicles were intrathecally administered 20 min before the intraperitoneal injection of bvPLA2 ( a – d ). For antagonist test, rats were divided into four groups. ( a ) Control group for prazosin pretreatment. Vehicle for prazosin (dimethyl sulfoxide (DMSO) 20%) was used prior to bvPLA2 treatment ( n = 7). ( b ) Prazosin pretreatment group. The α1-AR antagonist prazosin completely blocked the analgesic effect of bvPLA2 treatment ( n = 7). ( c ) Control group for <t>idazoxan</t> pretreatment. Vehicle for idazoxan (PBS solution) was used for pretreatment ( n = 6). ( d ) Idazoxan pretreatment group. The α2-AR antagonist idazoxan could not block the bvPLA2-mediated analgesic effect ( n = 7). ( e , f ) The analgesic effect induced by intrathecal injection of α1-AR agonist phenylephrine. Direct activation of spinal α1-AR by intrathecal phenylephrine injection ameliorated SNL-induced mechanical allodynia one hour after the treatment ( n = 6 for each group). The data are expressed as mean ± SEM. (* p < 0.05, ** p < 0.01; paired t -test).
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    (A) Pancreatic NA levels of RD and WD mice after Ex4 injection in the OB (n=2-3/group). (B) Schematic illustration of bilateral OB injections of Ex4 combined with IP administration of UK14304 followed by an OGTT in OB-cannulated WD and OB-cannulated RD mice. (C) OGTT tests preceded by an IP injection of UK14304 and an OB injection of Ex4 in OB-cannulated WD after 20 weeks under WD (n=8) (left). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using paired Student’s t-test. (D) Plasma insulin levels of OB-cannulated WD during OGTT tests preceded with OB-injected Ex4 and IP injected UK14304 (RM two-way ANOVA followed by Bonferroni post-hoc test; n=8). (E) Strategy to deliver Ex4 in the OB of OB-cannulated C57BL6 mice. (F) Representative photomicrographs of cFos immunoreactivity and automated cell counting in the MCL using CellProfiler software (left). cFos density in the MCL after Ex4 or saline injection in the OB in WD mice (right). Data are expressed as cFos+ nuclei/mean MCL area of all mice. Data are analyzed using an unpaired Student’s t-test (n=5). (G) cFos density in the LH after Ex4 or saline injection in the OB in WD mice. Data are expressed as cFos+ nuclei/mean LH area of all mice. Data are analyzed using an unpaired Student’s t-test (n=4). (H) Schematic illustration of unilateral Alexa 488-conjugated cholera toxin B subunit (CTB green ) delivery in the LH for retrograde tracing of the primary olfactory cortex. (I) Coronal sections of the LH after unilateral injection of CTB green (left). CTB staining in the primary olfactory cortex (right). LH, lateral hypothalamus; AHP, anterior hypothalamus; VMH, ventromedial hypothalamus; 3V, third ventricle; AON, anterior olfactory nucleus; VTT, ventral tenia tecta; VON, ventral olfactory nucleus; PC, piriform cortex; OT, olfactory tubercle. Structure boundaries were drawn based on Franklin and Paxinos mouse brain atlas. (J) Schematic illustration of viral delivery in the OB and bilateral cannula placement in the PVN of Glp1r -Cre WD mice followed by OGTTs. (K) OGTT tests preceded with an IP injection of CNO in Glp1r OBhM3Dq WD PVN-cannulated mice after 20 weeks under WD (26-week old; n=10) (left). The black square and the green line indicate Bicuculline and CNO delivery, respectively, before the glucose gavage (T0). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using RM one-way ANOVA followed by Bonferroni post-hoc test. (L) Plasma insulin levels of Glp1r OBhM3Dq WD PVN-cannulated mice after CNO IP injection (RM two-way ANOVA followed by Bonferroni post-hoc test, n=10). Data are given as mean ± SEM. *p <0.05; **p < 0.01; ***p < 0.001; ns, not significant.

    Journal: bioRxiv

    Article Title: A neuronal circuit driven by GLP-1 in the olfactory bulb regulates insulin secretion

    doi: 10.1101/2023.08.28.555086

    Figure Lengend Snippet: (A) Pancreatic NA levels of RD and WD mice after Ex4 injection in the OB (n=2-3/group). (B) Schematic illustration of bilateral OB injections of Ex4 combined with IP administration of UK14304 followed by an OGTT in OB-cannulated WD and OB-cannulated RD mice. (C) OGTT tests preceded by an IP injection of UK14304 and an OB injection of Ex4 in OB-cannulated WD after 20 weeks under WD (n=8) (left). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using paired Student’s t-test. (D) Plasma insulin levels of OB-cannulated WD during OGTT tests preceded with OB-injected Ex4 and IP injected UK14304 (RM two-way ANOVA followed by Bonferroni post-hoc test; n=8). (E) Strategy to deliver Ex4 in the OB of OB-cannulated C57BL6 mice. (F) Representative photomicrographs of cFos immunoreactivity and automated cell counting in the MCL using CellProfiler software (left). cFos density in the MCL after Ex4 or saline injection in the OB in WD mice (right). Data are expressed as cFos+ nuclei/mean MCL area of all mice. Data are analyzed using an unpaired Student’s t-test (n=5). (G) cFos density in the LH after Ex4 or saline injection in the OB in WD mice. Data are expressed as cFos+ nuclei/mean LH area of all mice. Data are analyzed using an unpaired Student’s t-test (n=4). (H) Schematic illustration of unilateral Alexa 488-conjugated cholera toxin B subunit (CTB green ) delivery in the LH for retrograde tracing of the primary olfactory cortex. (I) Coronal sections of the LH after unilateral injection of CTB green (left). CTB staining in the primary olfactory cortex (right). LH, lateral hypothalamus; AHP, anterior hypothalamus; VMH, ventromedial hypothalamus; 3V, third ventricle; AON, anterior olfactory nucleus; VTT, ventral tenia tecta; VON, ventral olfactory nucleus; PC, piriform cortex; OT, olfactory tubercle. Structure boundaries were drawn based on Franklin and Paxinos mouse brain atlas. (J) Schematic illustration of viral delivery in the OB and bilateral cannula placement in the PVN of Glp1r -Cre WD mice followed by OGTTs. (K) OGTT tests preceded with an IP injection of CNO in Glp1r OBhM3Dq WD PVN-cannulated mice after 20 weeks under WD (26-week old; n=10) (left). The black square and the green line indicate Bicuculline and CNO delivery, respectively, before the glucose gavage (T0). AUC of glycaemia (right). OGTT data are analyzed using RM two-way ANOVA followed by Bonferroni post-hoc test and AUCs by using RM one-way ANOVA followed by Bonferroni post-hoc test. (L) Plasma insulin levels of Glp1r OBhM3Dq WD PVN-cannulated mice after CNO IP injection (RM two-way ANOVA followed by Bonferroni post-hoc test, n=10). Data are given as mean ± SEM. *p <0.05; **p < 0.01; ***p < 0.001; ns, not significant.

    Article Snippet: Three experimental groups underwent OGTTs: i) WD and RD cannulated mice OB-infused with GLP-1, Ex4 or Ex9 [combined with IP injections of either Ex4 (3 µg/kg) or the α 2 -AR agonist UK14304 (Bio-Techne; 1μg/kg) when stated]; ii) Vagotomized WD mice OB-infused with Ex4; iii) Glp1r OBKORD RD and Glp1r OBhM3Dq WD mice in which OB Glp1r -expressing neurons were chemogenetically activated by IP injections of Salvinorin B (SALB; Sigma-Aldrich; 10mg/kg) or Clozapine N-oxide (CNO; Sigma-Aldrich; 3 mg/kg) respectively (combined with acute PVN injections of Bicuculline Methiodide 3 min prior to CNO administration when stated).

    Techniques: Injection, Cell Counting, Software, Saline, Retrograde Tracing, Staining

    Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist (clonidine), β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.

    Journal: Viruses

    Article Title: Stress Hormones Epinephrine and Corticosterone Selectively Reactivate HSV-1 and HSV-2 in Sympathetic and Sensory Neurons

    doi: 10.3390/v14051115

    Figure Lengend Snippet: Multiple adrenergic receptors are required for EPI-induced HSV-1 reactivation in sympathetic neurons. ( A ) Reactivation of HSV-1 with EPI in primary adult murine sympathetic SCG cultures either alone, with nonspecific α-AR antagonist (phentolamine), or nonspecific β-AR antagonist (timolol). ( B ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI, α-1 agonist (phenylephrine), α-2 agonist (clonidine), β-1 agonist (dobutamine), or β-2 agonist (terbutaline). ( C ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of two adrenergic agonists utilized in ( B ). ( D ) Reactivation of HSV-1 in primary adult murine SCG cultures with either EPI or a combination of three adrenergic agonists utilized in ( B ). Reactivation was quantified in ( A – D ) by viral DNA collected 24 h posttreatment measured by qPCR. ( E ) Data summary: activation of α2 and any other AR induces HSV-1 reactivation in adult sympathetic SCG neurons. Alternatively, activation of β1 and β2 simultaneously can also induce reactivation. Data are means ± SEM, n > 6; results were compared to untreated cultures by ANOVA and post hoc Tukey’s HSD; * p < 0.05; ** p < 0.01; *** p < 0.001.

    Article Snippet: Adrenergic receptor (AR) agonists included phenylephrine (α-1 AR agonist), clonidine (α-2 AR agonist), dobutamine (β-1 AR agonist), or terbutaline (β-2 AR agonist) (Sigma).

    Techniques: Activation Assay

    Involvement of α1-adrenergic receptor (AR) in the analgesic effect of bvPLA2. Antagonists and its vehicles were intrathecally administered 20 min before the intraperitoneal injection of bvPLA2 ( a – d ). For antagonist test, rats were divided into four groups. ( a ) Control group for prazosin pretreatment. Vehicle for prazosin (dimethyl sulfoxide (DMSO) 20%) was used prior to bvPLA2 treatment ( n = 7). ( b ) Prazosin pretreatment group. The α1-AR antagonist prazosin completely blocked the analgesic effect of bvPLA2 treatment ( n = 7). ( c ) Control group for idazoxan pretreatment. Vehicle for idazoxan (PBS solution) was used for pretreatment ( n = 6). ( d ) Idazoxan pretreatment group. The α2-AR antagonist idazoxan could not block the bvPLA2-mediated analgesic effect ( n = 7). ( e , f ) The analgesic effect induced by intrathecal injection of α1-AR agonist phenylephrine. Direct activation of spinal α1-AR by intrathecal phenylephrine injection ameliorated SNL-induced mechanical allodynia one hour after the treatment ( n = 6 for each group). The data are expressed as mean ± SEM. (* p < 0.05, ** p < 0.01; paired t -test).

    Journal: Toxins

    Article Title: Suppressive Effects of Bee Venom-Derived Phospholipase A2 on Mechanical Allodynia in a Rat Model of Neuropathic Pain

    doi: 10.3390/toxins11080477

    Figure Lengend Snippet: Involvement of α1-adrenergic receptor (AR) in the analgesic effect of bvPLA2. Antagonists and its vehicles were intrathecally administered 20 min before the intraperitoneal injection of bvPLA2 ( a – d ). For antagonist test, rats were divided into four groups. ( a ) Control group for prazosin pretreatment. Vehicle for prazosin (dimethyl sulfoxide (DMSO) 20%) was used prior to bvPLA2 treatment ( n = 7). ( b ) Prazosin pretreatment group. The α1-AR antagonist prazosin completely blocked the analgesic effect of bvPLA2 treatment ( n = 7). ( c ) Control group for idazoxan pretreatment. Vehicle for idazoxan (PBS solution) was used for pretreatment ( n = 6). ( d ) Idazoxan pretreatment group. The α2-AR antagonist idazoxan could not block the bvPLA2-mediated analgesic effect ( n = 7). ( e , f ) The analgesic effect induced by intrathecal injection of α1-AR agonist phenylephrine. Direct activation of spinal α1-AR by intrathecal phenylephrine injection ameliorated SNL-induced mechanical allodynia one hour after the treatment ( n = 6 for each group). The data are expressed as mean ± SEM. (* p < 0.05, ** p < 0.01; paired t -test).

    Article Snippet: PBS was used to dissolve α 2 -AR antagonist idazoxan (Sigma, St. Louis, MO, USA; 50 μg).

    Techniques: Injection, Blocking Assay, Activation Assay