ro 25-6981 maleate Search Results


glun2a subunit  (Alomone Labs)
94
Alomone Labs glun2a subunit
AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits <t>(GluN2A</t> and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)
Glun2a Subunit, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ro+25-6981+maleate/Ro+25-6981+maleate/pmc08487422-121-20-31
Average 94 stars, based on 1 article reviews
glun2a subunit - by Bioz Stars, 2026-09
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ro 25-6981 maleate  (MuseChem Chemicals)
N/A
Ro 25-6981 maleate（Cat No.:I009118）is a selective antagonist of the NMDA (N-methyl-D-aspartate) receptor, specifically targeting the NR2B subunit. It is primarily used in preclinical research to investigate the role of NMDA receptors in synaptic plasticity, neurodegenerative
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ro25 6981 maleate  (Tocris)
93
Tocris ro25 6981 maleate
AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits <t>(GluN2A</t> and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)
Ro25 6981 Maleate, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 1 article reviews
ro25 6981 maleate - by Bioz Stars, 2026-09
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βs α  (Tocris)
93
Tocris βs α
AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits <t>(GluN2A</t> and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)
βs α, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ro+25-6981+maleate/Ro+25-6981+maleate/pmc02774397-54-20-41
Average 93 stars, based on 1 article reviews
βs α - by Bioz Stars, 2026-09
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ro 25 6981  (Santa Cruz Biotechnology)
88
Santa Cruz Biotechnology ro 25 6981
AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits <t>(GluN2A</t> and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)
Ro 25 6981, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/ro+25-6981+maleate/Ro+25-6981+maleate/pmc06295532-35-58-59
Average 88 stars, based on 1 article reviews
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ro 25-6981 maleate  (Toronto Research Chemicals)
N/A
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ro 25-6981 maleate  (TargetMol)
N/A
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ro 25-6981 maleate  (BOC Sciences)
N/A
The Maleate salt form of Ro 25-6981 which is a NMDA receptors blocker and has been found to exhibit neuroprotectant activity in vitro and in vivo. IC50: 9 nM.
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ro 25-6981 maleate  (Biosynth Carbosynth)
N/A
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ro 25-6981 maleate  (Aladdin Scientific Corporation)
N/A
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AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)

Journal: Molecular Neurobiology

Article Title: Chronic AdipoRon Treatment Mimics the Effects of Physical Exercise on Restoring Hippocampal Neuroplasticity in Diabetic Mice

doi: 10.1007/s12035-021-02441-7

Figure Lengend Snippet: AdipoRon treatment restored NMDA receptor-dependent LTP deficit in diabetic mice depending on PGC-1α signalling. A LTP induction using HFS protocol to examine the effect of AdipoRon on synaptic plasticity in the hippocampal dentate gyrus. B Effect of AdipoRon on field excitatory postsynaptic potential (fEPSP) in control and diabetic brain slices. C The averaged fEPSP slope change of the last 5 min. Brain slice from diabetic mice showed deficit in LTP formation, which was rescued by 0.5 μM AdipoRon (Control: n = 8 slices; Control-AdipoRon: n = 11 slices; STZ: n = 12 slices; STZ-AdipoRon: n = 13 slices; Tukey’s post hoc test: * P < 0.005 Vehicle vs. AdipoRon; ** P < 0.005 between Vehicle vs. AdipoRon; ## P < 0.005 Control vs. STZ). D Experimental protocol of PGC-1α inhibition. E , F : E Effect of PGC-1α inhibition on AdipoRon-elicited field excitatory postsynaptic potential. F The average fEPSP slope change of the last 5 min where inhibition of PGC-1α significantly impaired LTP formation (Tukey’s post hoc test: ** P < 0.005 between Vehicle vs. SR-18292 under STZ condition). n = 7 slice per control group and n = 8 slices per STZ-diabetic group. G Experimental protocol for investigating the involvements of NMDA receptor subunits (GluN2A and GluN2B) in AdipoRon-induced LTP in diabetic slices. H , I : H Inhibition of GluN2A or GluN2B diminished AdipoRon-restored field excitatory postsynaptic potential in diabetic brain slices. I The average fEPSP slope change of the last 5 min where inhibition of GluN2A or GluN2B diminished LTP formation ( n = 10 slices per treatment group; Tukey’s post hoc test: * P < 0.05 NVP-AAM077 or Ro-25-6981 vs. Vehicle)

Article Snippet: In pharmacological intervention, brain slices were acutely perfused in PEAQX tetrasodium hydrate (0.1 μM; NVP-AAM077) (Sigma-Aldrich, MO, USA) to inhibit GluN2A subunit ( ) or in Ro 25-6981 maleate (0.5 μM) (Alomone Labs, Israel) to inhibit GluN2B subunit ( ) for 30 min before HFS.

Techniques: Control, Slice Preparation, Inhibition