ska Search Results


93
Tocris sk ik channel opener ska 31
Sk Ik Channel Opener Ska 31, 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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Shanghai Korain Biotech Co Ltd slug
Slug, supplied by Shanghai Korain Biotech Co Ltd, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Alomone Labs ska
(A) Effect of 3 μM LPI on endothelial hyperpolarization to 2 μM Ach (n = 4). (B) Effect of 10 μM LPI on endothelial hyperpolarization to two consecutive administrations of 2 μM Ach (n = 3). The hyperpolarization to <t>SKA-31</t> (10 μM) remained unaffected by LPI pre-exposure (n = 4). (C) Representative membrane potential recording from in situ mice aortic endothelium showing a failure of LPI (10 μM) to inhibit the hyperpolarization evoked by 10 μM SKA-31 (n = 3).
Ska, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress ska 31
(A) Effect of 3 μM LPI on endothelial hyperpolarization to 2 μM Ach (n = 4). (B) Effect of 10 μM LPI on endothelial hyperpolarization to two consecutive administrations of 2 μM Ach (n = 3). The hyperpolarization to <t>SKA-31</t> (10 μM) remained unaffected by LPI pre-exposure (n = 4). (C) Representative membrane potential recording from in situ mice aortic endothelium showing a failure of LPI (10 μM) to inhibit the hyperpolarization evoked by 10 μM SKA-31 (n = 3).
Ska 31, supplied by MedChemExpress, 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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93
MedChemExpress ska121
Effects of K Ca 3.1 activation and LRRC8A inhibition on CCL2 expression and secretion in M 2 -MACs. ( A , B ): Real-time PCR examination of CCL22 ( A ) and CCL2 ( B ) expression in native THP-1 cells (native) and M 2 -MACs (M 2 ) ( n = 4). Data are normalized to ACTB. ( C , D , F , G ): Real-time PCR examination of CCL22 ( C , F ) and CCL2 ( D , G ) expression following treatment with vehicle, 10 μM <t>SKA121</t> (SKA) ( C , D ), or 10 μM endovion (EDV) ( F , G ) for 12 h in M 2 -MACs ( n = 4). Expression levels are normalized to ACTB and shown relative to vehicle control (set as 1.0). ( E , H ): ELISA quantification of CCL2 secretion after 24 h treatment with SKA ( E ) or EDV ( H ) in M 2 -MACs ( n = 4). Secretion levels are shown relative to vehicle control (set as 1.0). **: p < 0.01 vs. native THP-1 or vehicle control.
Ska121, supplied by MedChemExpress, 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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OriGene mr227370

Mr227370, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Syntech GmbH ska-42, cas 352214-93-8

Ska 42, Cas 352214 93 8, supplied by Syntech GmbH, 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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Jackson Laboratory nrg3 ska mice
Nicotine effects on OFC neuroplasticity rely on <t>NRG3/ErbB4</t> signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.
Nrg3 Ska Mice, supplied by Jackson Laboratory, 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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Janssen gravitational wave astronomy with the ska
Nicotine effects on OFC neuroplasticity rely on <t>NRG3/ErbB4</t> signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.
Gravitational Wave Astronomy With The Ska, supplied by Janssen, 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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Oakwood Chemical ska-255
Nicotine effects on OFC neuroplasticity rely on <t>NRG3/ErbB4</t> signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.
Ska 255, supplied by Oakwood Chemical, 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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Oakwood Chemical ska-41 active
Nicotine effects on OFC neuroplasticity rely on <t>NRG3/ErbB4</t> signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.
Ska 41 Active, supplied by Oakwood Chemical, 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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Hagleitner Hygiene International GmbH challenges in exascale radio astronomy: can the ska ride the wave?
Nicotine effects on OFC neuroplasticity rely on <t>NRG3/ErbB4</t> signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.
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Image Search Results


(A) Effect of 3 μM LPI on endothelial hyperpolarization to 2 μM Ach (n = 4). (B) Effect of 10 μM LPI on endothelial hyperpolarization to two consecutive administrations of 2 μM Ach (n = 3). The hyperpolarization to SKA-31 (10 μM) remained unaffected by LPI pre-exposure (n = 4). (C) Representative membrane potential recording from in situ mice aortic endothelium showing a failure of LPI (10 μM) to inhibit the hyperpolarization evoked by 10 μM SKA-31 (n = 3).

Journal: Vascular pharmacology

Article Title: GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of Na + -Ca 2+ exchanger and endoplasmic reticulum Ca 2+ refilling

doi: 10.1016/j.vph.2017.01.002

Figure Lengend Snippet: (A) Effect of 3 μM LPI on endothelial hyperpolarization to 2 μM Ach (n = 4). (B) Effect of 10 μM LPI on endothelial hyperpolarization to two consecutive administrations of 2 μM Ach (n = 3). The hyperpolarization to SKA-31 (10 μM) remained unaffected by LPI pre-exposure (n = 4). (C) Representative membrane potential recording from in situ mice aortic endothelium showing a failure of LPI (10 μM) to inhibit the hyperpolarization evoked by 10 μM SKA-31 (n = 3).

Article Snippet: Materials LPC16:0 (1-palmitoyl-2-hydroxy- sn - glycero -3-phosphocholine) was purchased from Avanti Polar Lipids, LPI from Sigma Aldrich, paxilline and SKA-31 were purchased from Alomone Labs, KB-R7943 was purchased from TCI Chemicals.

Techniques: In Situ

Effects of K Ca 3.1 activation and LRRC8A inhibition on CCL2 expression and secretion in M 2 -MACs. ( A , B ): Real-time PCR examination of CCL22 ( A ) and CCL2 ( B ) expression in native THP-1 cells (native) and M 2 -MACs (M 2 ) ( n = 4). Data are normalized to ACTB. ( C , D , F , G ): Real-time PCR examination of CCL22 ( C , F ) and CCL2 ( D , G ) expression following treatment with vehicle, 10 μM SKA121 (SKA) ( C , D ), or 10 μM endovion (EDV) ( F , G ) for 12 h in M 2 -MACs ( n = 4). Expression levels are normalized to ACTB and shown relative to vehicle control (set as 1.0). ( E , H ): ELISA quantification of CCL2 secretion after 24 h treatment with SKA ( E ) or EDV ( H ) in M 2 -MACs ( n = 4). Secretion levels are shown relative to vehicle control (set as 1.0). **: p < 0.01 vs. native THP-1 or vehicle control.

Journal: International Journal of Molecular Sciences

Article Title: Transcriptional Repression of CCL2 by K Ca 3.1 K + Channel Activation and LRRC8A Anion Channel Inhibition in THP-1-Differentiated M 2 Macrophages

doi: 10.3390/ijms26157624

Figure Lengend Snippet: Effects of K Ca 3.1 activation and LRRC8A inhibition on CCL2 expression and secretion in M 2 -MACs. ( A , B ): Real-time PCR examination of CCL22 ( A ) and CCL2 ( B ) expression in native THP-1 cells (native) and M 2 -MACs (M 2 ) ( n = 4). Data are normalized to ACTB. ( C , D , F , G ): Real-time PCR examination of CCL22 ( C , F ) and CCL2 ( D , G ) expression following treatment with vehicle, 10 μM SKA121 (SKA) ( C , D ), or 10 μM endovion (EDV) ( F , G ) for 12 h in M 2 -MACs ( n = 4). Expression levels are normalized to ACTB and shown relative to vehicle control (set as 1.0). ( E , H ): ELISA quantification of CCL2 secretion after 24 h treatment with SKA ( E ) or EDV ( H ) in M 2 -MACs ( n = 4). Secretion levels are shown relative to vehicle control (set as 1.0). **: p < 0.01 vs. native THP-1 or vehicle control.

Article Snippet: EDV (HY-105917), SKA121 (HY-107414), SP600125 (HY-12041), and PD169316 (HY-10578) were from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Activation Assay, Inhibition, Expressing, Real-time Polymerase Chain Reaction, Control, Enzyme-linked Immunosorbent Assay

Journal: Cell Metabolism

Article Title: The Polycomb-Dependent Epigenome Controls β Cell Dysfunction, Dedifferentiation, and Diabetes

doi: 10.1016/j.cmet.2018.04.013

Figure Lengend Snippet:

Article Snippet: Twist1 (NM_011658) Mouse Tagged ORF Clone , Origene , MR227370.

Techniques: Immunofluorescence, Recombinant, Enzyme-linked Immunosorbent Assay, Sample Prep, TUNEL Assay, Software

Nicotine effects on OFC neuroplasticity rely on NRG3/ErbB4 signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.

Journal: Neuropsychopharmacology

Article Title: Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition

doi: 10.1038/npp.2017.278

Figure Lengend Snippet: Nicotine effects on OFC neuroplasticity rely on NRG3/ErbB4 signaling. (a) A stimulation protocol, inducing LTP in control (ACSF) conditions results in LTD in the presence of NRG3 (2 nM) or nicotine (1 μM) (ACSF: n=12 slices, 5 mice; NRG3: n=6 slices, 3 mice; nicotine: n=7 slices, 3 mice). (b) DL-AP5 (50 μM) blocks LTP in normal ACSF but not LTD in ACSF supplemented by NRG3 (2 nM) or nicotine (1 μM) (AP5: n=7 slices, 3 mice; Nicotine+AP5: n=6 slices, 3 mice; NRG3+AP5: n=8 slices, 3 mice). (c) ErbB4 inhibitor afatinib (10 μM) attenuated both nicotine- and neuregulin induced LTD (NRG3+afatinib: n=6 slices, 3 mice; nicotine+afatinib: n=7 slices, 3 mice). Nicotine-induced LTD is also attenuated in a strain of NRG3ska mice that express reduced NRG3 levels (Nicotine (NRG3ska): n=7 slices, 3 mice). (d) Nicotine-induced LTD was attenuated by α7 nAChRs antagonist, αBTX (100 μM); α4β2*, antagonist, DHβE (1 μM); ryanodine-sensitive Ca2+ release blocker, ruthenium red (20 μM); or BACE1 inhibitor, LY2811376 (25 μM) (Nicotine+ αBTX: n=7 slices, 3 mice; Nicotine+DHβE: n=6 slices, 3 mice; Nicotine+ruthenium red: n=8 slices, 3 mice; Nicotine+LY2811376: n=9 slices, 4 mice). (e) fEPSP amplitudes in the last 10 min of recordings for treatment groups in a–d. Data are presented as mean±SEM. Data are analyzed by one-way ANOVAs followed by Bonferroni’s post hoc tests, or Student’s t-test. *p<0.05 vs ACSF; &p<0.05 vs NRG3; #p<0.05 vs nicotine.

Article Snippet: Animals and Housing Male B6/129F1 and NRG3 ska (Jackson Laboratories; 6–10 weeks of age; 20–25 g) were used in both the electrophysiology and molecular experiments.

Techniques: Control

Molecular changes in the OFC of NRG3ska mice. (a) NRG3ska mice have reduced expression of NRG3 protein in the OFC compared to wild type controls. (b) ErbB4 mRNA is increased in the OFC of NRG3ska mice. (c) NRG1 and ErbB3 mRNA levels are similar in WT and NRG3ska mice. (d) The expression of nAChRs mRNA is unchanged in the NRG3ska mice. Protein levels of NRG3 or ErbB4 were normalized to GAPDH or β-tubulin, then normalized to WT controls. mRNA levels are normalized to WT controls. Data are presented as mean±SEM. n=8 for both WT and NRG3ska mice. Data are analyzed by Student’s t-tests. *p<0.05 compared to WT.

Journal: Neuropsychopharmacology

Article Title: Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition

doi: 10.1038/npp.2017.278

Figure Lengend Snippet: Molecular changes in the OFC of NRG3ska mice. (a) NRG3ska mice have reduced expression of NRG3 protein in the OFC compared to wild type controls. (b) ErbB4 mRNA is increased in the OFC of NRG3ska mice. (c) NRG1 and ErbB3 mRNA levels are similar in WT and NRG3ska mice. (d) The expression of nAChRs mRNA is unchanged in the NRG3ska mice. Protein levels of NRG3 or ErbB4 were normalized to GAPDH or β-tubulin, then normalized to WT controls. mRNA levels are normalized to WT controls. Data are presented as mean±SEM. n=8 for both WT and NRG3ska mice. Data are analyzed by Student’s t-tests. *p<0.05 compared to WT.

Article Snippet: Animals and Housing Male B6/129F1 and NRG3 ska (Jackson Laboratories; 6–10 weeks of age; 20–25 g) were used in both the electrophysiology and molecular experiments.

Techniques: Expressing

A proposed model for nicotine-induced synaptic plasticity in the OFC. Nicotine activates Ca2+-permeable nAChRs, and Ca2+-sensitive ryanodine receptors (RyR). Increased intracellular Ca2+ enhances the proteolytic activity of BACE1, which directly cleaves NRG3. NRG3 binds to ErbB4 and increases GABA release. Nicotine also increases GABA uptake, presumably via an ErbB4-independent pathway. Increased vesicular GABA coupled with ErbB4-facilitated GABA release decreases excitability of post-synaptic pyramidal neurons and promotes LTD.

Journal: Neuropsychopharmacology

Article Title: Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition

doi: 10.1038/npp.2017.278

Figure Lengend Snippet: A proposed model for nicotine-induced synaptic plasticity in the OFC. Nicotine activates Ca2+-permeable nAChRs, and Ca2+-sensitive ryanodine receptors (RyR). Increased intracellular Ca2+ enhances the proteolytic activity of BACE1, which directly cleaves NRG3. NRG3 binds to ErbB4 and increases GABA release. Nicotine also increases GABA uptake, presumably via an ErbB4-independent pathway. Increased vesicular GABA coupled with ErbB4-facilitated GABA release decreases excitability of post-synaptic pyramidal neurons and promotes LTD.

Article Snippet: Animals and Housing Male B6/129F1 and NRG3 ska (Jackson Laboratories; 6–10 weeks of age; 20–25 g) were used in both the electrophysiology and molecular experiments.

Techniques: Activity Assay