dpdpe Search Results


dpdpe  (MedChemExpress)
94
MedChemExpress dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Dpdpe, supplied by MedChemExpress, 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/dpdpe/DPDPE/bio_rxiv__64898__2026__05__31__729044-155-22-23
Average 94 stars, based on 1 article reviews
dpdpe - by Bioz Stars, 2026-10
94/100 stars
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d pen2 d pen5 enkephalin dpdpe  (Tocris)
94
Tocris d pen2 d pen5 enkephalin dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
D Pen2 D Pen5 Enkephalin Dpdpe, supplied by Tocris, 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/dpdpe/DPDPE/pm31937563-37-0-6
Average 94 stars, based on 1 article reviews
d pen2 d pen5 enkephalin dpdpe - by Bioz Stars, 2026-10
94/100 stars
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d pen2 5 enkephalin dpdpe  (Tocris)
94
Tocris d pen2 5 enkephalin dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
D Pen2 5 Enkephalin Dpdpe, supplied by Tocris, 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/dpdpe/DPDPE/bio_rxiv__2025__11__14__688475-33-3-6
Average 94 stars, based on 1 article reviews
d pen2 5 enkephalin dpdpe - by Bioz Stars, 2026-10
94/100 stars
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optimem 1  (Thermo Fisher)
88
Thermo Fisher optimem 1
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Optimem 1, supplied by Thermo Fisher, 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/dpdpe/DPDPE/pm16539674-54-16-18
Average 88 stars, based on 1 article reviews
optimem 1 - by Bioz Stars, 2026-10
88/100 stars
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dpdpe  (Thermo Fisher)
90
Thermo Fisher dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Dpdpe, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/DPDPE/pm21098639-94-29-63
Average 90 stars, based on 1 article reviews
dpdpe - by Bioz Stars, 2026-10
90/100 stars
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dpdpe  (Bachem)
90
Bachem dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Dpdpe, supplied by Bachem, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/dpdpe/pmc01574073-81-3-30
Average 90 stars, based on 1 article reviews
dpdpe - by Bioz Stars, 2026-10
90/100 stars
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3h]pcl-phe4-dpdpe 47.0 ci/mmol  (DuPont de Nemours)
90
DuPont de Nemours 3h]pcl-phe4-dpdpe 47.0 ci/mmol
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
3h]Pcl Phe4 Dpdpe 47.0 Ci/Mmol, supplied by DuPont de Nemours, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/3h+pcl+phe4+dpdpe+47+0+ci+mmol/pm10854288-56-0-15
Average 90 stars, based on 1 article reviews
3h]pcl-phe4-dpdpe 47.0 ci/mmol - by Bioz Stars, 2026-10
90/100 stars
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3h]dpdpe  (NEN Life Science)
90
NEN Life Science 3h]dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
3h]Dpdpe, supplied by NEN Life Science, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/3h+dpdpe/pm12420793-29-3-15
Average 90 stars, based on 1 article reviews
3h]dpdpe - by Bioz Stars, 2026-10
90/100 stars
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d-pen 2,5-enkephalin (dpdpe)  (AnaSpec)
90
AnaSpec d-pen 2,5-enkephalin (dpdpe)
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
D Pen 2,5 Enkephalin (Dpdpe), supplied by AnaSpec, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/d+pen+2+5++enkephalin++dpdpe/pmc03241219-117-1-6
Average 90 stars, based on 1 article reviews
d-pen 2,5-enkephalin (dpdpe) - by Bioz Stars, 2026-10
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selective delta receptor agonists dpdpe  (Microm International GmbH)
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Microm International GmbH selective delta receptor agonists dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Selective Delta Receptor Agonists Dpdpe, supplied by Microm International GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/selective+delta+receptor+agonists+dpdpe/pmc06578260-2-2-11
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dpdpe ([ 3 h][ d -pen 2 , d -pen 5 ]enkephalin)  (DuPont de Nemours)
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DuPont de Nemours dpdpe ([ 3 h][ d -pen 2 , d -pen 5 ]enkephalin)
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
Dpdpe ([ 3 H][ D Pen 2 , D Pen 5 ]Enkephalin), supplied by DuPont de Nemours, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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3h]dpdpe  (DuPont de Nemours)
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DuPont de Nemours 3h]dpdpe
a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application <t>of</t> <t>HNK</t> further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , <t>DPDPE,</t> a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).
3h]Dpdpe, supplied by DuPont de Nemours, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/dpdpe/3h+dpdpe/us06916905-599-5-8
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a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application of HNK further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , DPDPE, a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).

Journal: bioRxiv

Article Title: (2R,6R)-Hydroxynorketamine elicits rapid antidepressant effects by promoting astrocytic µ-δ opioid receptor heterodimerization

doi: 10.64898/2026.05.31.729044

Figure Lengend Snippet: a, Schematic of hippocampal slice recording: Stimulating electrode in Schaffer collaterals, recording electrode in CA1 stratum radiatum. b, Ketamine increased the rising slope of SC-CA1 fEPSPs elicited at CA1 stratum radiatum in acutely prepared hippocampal slices. When ketamine-induced potentiation reached a plateau, subsequent bath application of HNK further enhanced SC-CA1 fEPSPs. Left: time course of SC-CA1 fEPSPs changes; Right, representative fEPSP traces before, after ketamine treatment, and following subsequent HNK application. c, Increasing ketamine concentration to 30 μM did not further potentiate SC-CA1 fEPSPs after 10 μM ketamine-induced effects plateaued. d, MK-801, a selective and non-competitive NMDA receptor antagonist, mimicked ketamine’s potentiation of SC-CA1 fEPSPs and did not occlude the effect of HNK. e, DAMGO, a selective MOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DAMGO. f, The selective MOR antagonist CTOP reduced SC-CA1 fEPSP slope and blocked the effect of HNK but not ketamine. g , DPDPE, a selective DOR agonist, increased the rising slope of SC-CA1 fEPSPs and occluded the effect of HNK on SC-CA1 fEPSPs, whereas ketamine further potentiated SC-CA1 fEPSPs on top of DPDPE. h , The selective DOR antagonist ICI blocked the effect of HNK but not ketamine. i , Experimental timeline for assessing the effect of MOR or DOR activation, blockade, or deletion on the antidepressant effect of HNK. j–l, DAMGO (10 mg·kg -1 , i.p.) mimicked and CTOP (3 μg·kg -1 , i.c.v.) blocked the antidepressant actions of HNK (10 mg·kg -1 , i.p.) in FST (j), SPT (k), and three-chamber test (l). m–p, MOR knockout mice exhibited depression-like behaviors in FST (m) and SPT (n) and abolished the antidepressant-like effects of HNK in the two assays (FST, o; SPT, p). q–r, DPDPE (0.5 μg·kg -1 , i.c.v.) mimicked and ICI (3 mg·kg -1 , i.v.) blocked the antidepressant actions of HNK in FST (q) and SPT (r). s–v, Western blot analysis revealed that DAMGO and DPDPE mimicked and occluded the HNK-induced increase in GluA1 levels (s, u), whereas CTOP and ICI blocked this effect (t, v). Scale bar: 5 ms, 0.2 mV in b–d. Data are presented as mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001. ns, not significant (statistical analyses and n values are provided in Supplementary Table 1).

Article Snippet: (R,S)-ketamine provided by Dr. Sungchil Yang of City University of Hong Kong, (2R,6R)-HNK (Tocris), DAMGO (Tocris), CTOP (Tocris), MK-801 (MCE), D-APV (MCE), DPDPE (MCE), ICI174864 (MCE), Picrotoxin (MCE), CYM51010 (MCE), CGP52432 (Millipore), and MOR-DOR heterodimer allosteric inhibitor peptide (PEP; amino acid sequence: VTACTPSDGPGGGAAAYGRKKRRQRRR) (QYAOBIO, Shanghai, China) were dissolved in 0.9% saline to make a stock solution.

Techniques: Concentration Assay, Activation Assay, Knock-Out, Western Blot