h89 tocris Search Results


h89 dihydrochloride  (Tocris)
95
Tocris h89 dihydrochloride
(A) Left, Diagram illustrating the recording configuration. MC and MPP EPSCs were recorded from the same GC and evoked with stimulation electrodes placed in the inner and middle molecular layer, respectively. Right, Current clamp recording showing GC theta-burst firing (GC TBF). LTP induction protocol (GC TBF) was composed of 10 bursts at 5 Hz of 5 action potentials at 50 Hz, repeated 4 times every 5 s. (B) Left, Representative traces before (1) and after (2) GC TBF delivery. Right, Time-course plot showing that GC TBF induced LTP at MC-GC but not at MPP-GC synapses. (C) GC TBF-induced LTP was associated with significant reduction in PPR and CV (n = 13 cells). ** p < 0.01, *** p < 0.001. (D) LTP was abolished when TrkB was conditionally knocked out from from GCs (Post TrkB cKO, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.Cre.GFP). LTP was unaffected in control animals (Control, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.eGFP). (E) LTP was normally induced when loading PKI6-22 (2.5 μM) in GCs via the recording pipette but completely blocked when the cell-permeable PKA inhibitor PKI14-22 myristoylated (1 μM) was bath applied. (F) Summary bar graph showing the magnitude of GC TBF-induced LTP in the presence of DGC-IV (1 μM), when TrkB was conditionally knocked out from MCs (Pre TrkB cKO), when loading the PKI6-22 (2.5 μM) in GCs, and in the presence of D-APV (50 μM). LTP was abolished in the presence of the TrkB antagonist ANA-12 (15 μM), when Botox (0.5 μM) was loaded postsynaptically, in postsynaptic BDNF and TrkB cKO mice, and during bath application of the PKA inhibitors <t>H89</t> (10 μM) or myristoylated PKI14-22 μM). Time-course summary plots are shown in Figure S1. ** p < 0.01, *** p < 0.001. (G) Scheme illustrating the emerging model for the mechanism underlying GC TBF-LTP. GC TBF triggers postsynaptic BDNF release and subsequent TrkB activation in GCs (1). Presynaptic PKA is then engaged downstream of postsynaptic BDNF/TrkB signaling (2), suggesting the requirement of a retrograde signal. Lastly, presynaptic PKA activation resulted in a long-lasting increase in glutamate release (3). Numbers in parentheses indicate the number of cells. Data are presented as mean ± SEM.
H89 Dihydrochloride, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/h89+tocris/pmc11286346-22-0-3?v=Tocris
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h89 dihydrochloride - by Bioz Stars, 2026-08
95/100 stars
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h 89 dihydrochloride  (Bio-Techne corporation)
95
Bio-Techne corporation h 89 dihydrochloride
(A) Left, Diagram illustrating the recording configuration. MC and MPP EPSCs were recorded from the same GC and evoked with stimulation electrodes placed in the inner and middle molecular layer, respectively. Right, Current clamp recording showing GC theta-burst firing (GC TBF). LTP induction protocol (GC TBF) was composed of 10 bursts at 5 Hz of 5 action potentials at 50 Hz, repeated 4 times every 5 s. (B) Left, Representative traces before (1) and after (2) GC TBF delivery. Right, Time-course plot showing that GC TBF induced LTP at MC-GC but not at MPP-GC synapses. (C) GC TBF-induced LTP was associated with significant reduction in PPR and CV (n = 13 cells). ** p < 0.01, *** p < 0.001. (D) LTP was abolished when TrkB was conditionally knocked out from from GCs (Post TrkB cKO, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.Cre.GFP). LTP was unaffected in control animals (Control, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.eGFP). (E) LTP was normally induced when loading PKI6-22 (2.5 μM) in GCs via the recording pipette but completely blocked when the cell-permeable PKA inhibitor PKI14-22 myristoylated (1 μM) was bath applied. (F) Summary bar graph showing the magnitude of GC TBF-induced LTP in the presence of DGC-IV (1 μM), when TrkB was conditionally knocked out from MCs (Pre TrkB cKO), when loading the PKI6-22 (2.5 μM) in GCs, and in the presence of D-APV (50 μM). LTP was abolished in the presence of the TrkB antagonist ANA-12 (15 μM), when Botox (0.5 μM) was loaded postsynaptically, in postsynaptic BDNF and TrkB cKO mice, and during bath application of the PKA inhibitors <t>H89</t> (10 μM) or myristoylated PKI14-22 μM). Time-course summary plots are shown in Figure S1. ** p < 0.01, *** p < 0.001. (G) Scheme illustrating the emerging model for the mechanism underlying GC TBF-LTP. GC TBF triggers postsynaptic BDNF release and subsequent TrkB activation in GCs (1). Presynaptic PKA is then engaged downstream of postsynaptic BDNF/TrkB signaling (2), suggesting the requirement of a retrograde signal. Lastly, presynaptic PKA activation resulted in a long-lasting increase in glutamate release (3). Numbers in parentheses indicate the number of cells. Data are presented as mean ± SEM.
H 89 Dihydrochloride, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/h89+tocris/bio-techne+corporation___2910?v=Bio-Techne+corporation
Average 95 stars, based on 1 article reviews
h 89 dihydrochloride - by Bioz Stars, 2026-08
95/100 stars
  Buy from Supplier

Image Search Results


(A) Left, Diagram illustrating the recording configuration. MC and MPP EPSCs were recorded from the same GC and evoked with stimulation electrodes placed in the inner and middle molecular layer, respectively. Right, Current clamp recording showing GC theta-burst firing (GC TBF). LTP induction protocol (GC TBF) was composed of 10 bursts at 5 Hz of 5 action potentials at 50 Hz, repeated 4 times every 5 s. (B) Left, Representative traces before (1) and after (2) GC TBF delivery. Right, Time-course plot showing that GC TBF induced LTP at MC-GC but not at MPP-GC synapses. (C) GC TBF-induced LTP was associated with significant reduction in PPR and CV (n = 13 cells). ** p < 0.01, *** p < 0.001. (D) LTP was abolished when TrkB was conditionally knocked out from from GCs (Post TrkB cKO, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.Cre.GFP). LTP was unaffected in control animals (Control, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.eGFP). (E) LTP was normally induced when loading PKI6-22 (2.5 μM) in GCs via the recording pipette but completely blocked when the cell-permeable PKA inhibitor PKI14-22 myristoylated (1 μM) was bath applied. (F) Summary bar graph showing the magnitude of GC TBF-induced LTP in the presence of DGC-IV (1 μM), when TrkB was conditionally knocked out from MCs (Pre TrkB cKO), when loading the PKI6-22 (2.5 μM) in GCs, and in the presence of D-APV (50 μM). LTP was abolished in the presence of the TrkB antagonist ANA-12 (15 μM), when Botox (0.5 μM) was loaded postsynaptically, in postsynaptic BDNF and TrkB cKO mice, and during bath application of the PKA inhibitors H89 (10 μM) or myristoylated PKI14-22 μM). Time-course summary plots are shown in Figure S1. ** p < 0.01, *** p < 0.001. (G) Scheme illustrating the emerging model for the mechanism underlying GC TBF-LTP. GC TBF triggers postsynaptic BDNF release and subsequent TrkB activation in GCs (1). Presynaptic PKA is then engaged downstream of postsynaptic BDNF/TrkB signaling (2), suggesting the requirement of a retrograde signal. Lastly, presynaptic PKA activation resulted in a long-lasting increase in glutamate release (3). Numbers in parentheses indicate the number of cells. Data are presented as mean ± SEM.

Journal: Cell reports

Article Title: Retrograde adenosine/A 2A receptor signaling facilitates excitatory synaptic transmission and seizures

doi: 10.1016/j.celrep.2024.114382

Figure Lengend Snippet: (A) Left, Diagram illustrating the recording configuration. MC and MPP EPSCs were recorded from the same GC and evoked with stimulation electrodes placed in the inner and middle molecular layer, respectively. Right, Current clamp recording showing GC theta-burst firing (GC TBF). LTP induction protocol (GC TBF) was composed of 10 bursts at 5 Hz of 5 action potentials at 50 Hz, repeated 4 times every 5 s. (B) Left, Representative traces before (1) and after (2) GC TBF delivery. Right, Time-course plot showing that GC TBF induced LTP at MC-GC but not at MPP-GC synapses. (C) GC TBF-induced LTP was associated with significant reduction in PPR and CV (n = 13 cells). ** p < 0.01, *** p < 0.001. (D) LTP was abolished when TrkB was conditionally knocked out from from GCs (Post TrkB cKO, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.Cre.GFP). LTP was unaffected in control animals (Control, TrkBfl/fl mice injected in the dorsal blade with AAV5.CaMKII.eGFP). (E) LTP was normally induced when loading PKI6-22 (2.5 μM) in GCs via the recording pipette but completely blocked when the cell-permeable PKA inhibitor PKI14-22 myristoylated (1 μM) was bath applied. (F) Summary bar graph showing the magnitude of GC TBF-induced LTP in the presence of DGC-IV (1 μM), when TrkB was conditionally knocked out from MCs (Pre TrkB cKO), when loading the PKI6-22 (2.5 μM) in GCs, and in the presence of D-APV (50 μM). LTP was abolished in the presence of the TrkB antagonist ANA-12 (15 μM), when Botox (0.5 μM) was loaded postsynaptically, in postsynaptic BDNF and TrkB cKO mice, and during bath application of the PKA inhibitors H89 (10 μM) or myristoylated PKI14-22 μM). Time-course summary plots are shown in Figure S1. ** p < 0.01, *** p < 0.001. (G) Scheme illustrating the emerging model for the mechanism underlying GC TBF-LTP. GC TBF triggers postsynaptic BDNF release and subsequent TrkB activation in GCs (1). Presynaptic PKA is then engaged downstream of postsynaptic BDNF/TrkB signaling (2), suggesting the requirement of a retrograde signal. Lastly, presynaptic PKA activation resulted in a long-lasting increase in glutamate release (3). Numbers in parentheses indicate the number of cells. Data are presented as mean ± SEM.

Article Snippet: H89 dihydrochloride , Tocris Bioscience , Cat#2910.

Techniques: Injection, Control, Transferring, Activation Assay

KEY RESOURCES TABLE

Journal: Cell reports

Article Title: Retrograde adenosine/A 2A receptor signaling facilitates excitatory synaptic transmission and seizures

doi: 10.1016/j.celrep.2024.114382

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: H89 dihydrochloride , Tocris Bioscience , Cat#2910.

Techniques: Virus, Plasmid Preparation, Recombinant, Software