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    Millipore fk888 hydrate
    Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, <t>FK888,</t> and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).
    Fk888 Hydrate, supplied by Millipore, 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/fk888+hydrate/fk888+hydrate/pmc08217616-60-76-80
    Average 90 stars, based on 1 article reviews
    fk888 hydrate - by Bioz Stars, 2026-09
    90/100 stars

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    1) Product Images from "Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons"

    Article Title: Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2021.674399

    Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, FK888, and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).
    Figure Legend Snippet: Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, FK888, and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).

    Techniques Used: Injection, Expressing, Produced

    Related Articles

    Injection:

    Article Title: Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons
    Article Snippet: drugs were applied through perfusion or local injection. .. Drugs used in the slice recordings were as follows: tetrodotoxin (TTX, 1 μM, Tocris Bioscience, Bristol, United Kingdom), a voltage-gated sodium channel blocker; picrotoxin (50 μM, Sigma-Aldrich, St. Louis, MO, United States), a blocker of GABA A receptors; 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 μM, Sigma-Aldrich, St. Louis, MO, United States), an AMPA-type glutamate receptor blocker; 2-amino-5-phosphonovalerate (APV, 50 μM, Sigma-Aldrich, St. Louis, MO, United States), an NMDA-type glutamate receptor blocker; SR140333 (10 μM, Tocris Bioscience, Bristol, United Kingdom); FK888 hydrate (10 μM, Sigma-Aldrich, St. Louis, MO, United States) and L-703606 oxalate salt hydrate (100 nM, Sigma-Aldrich, St. Louis, MO, United States), NK1R blockers; carbenoxolone disodium (CBX, 200 μM, Tocris Bioscience, Bristol, United Kingdom) and quinine (200 μM, Sigma-Aldrich, St. Louis, MO, United States), gap junctions blockers; [Sar 9 , Met(O 2 ) 11 ]-substance P (1 μM, Tocris Bioscience, Bristol, United Kingdom), a selective NK1R agonist; and substance P (5 μM, Tocris Bioscience, Bristol, United Kingdom).

    Expressing:

    Article Title: Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons
    Article Snippet: drugs were applied through perfusion or local injection. .. Drugs used in the slice recordings were as follows: tetrodotoxin (TTX, 1 μM, Tocris Bioscience, Bristol, United Kingdom), a voltage-gated sodium channel blocker; picrotoxin (50 μM, Sigma-Aldrich, St. Louis, MO, United States), a blocker of GABA A receptors; 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 μM, Sigma-Aldrich, St. Louis, MO, United States), an AMPA-type glutamate receptor blocker; 2-amino-5-phosphonovalerate (APV, 50 μM, Sigma-Aldrich, St. Louis, MO, United States), an NMDA-type glutamate receptor blocker; SR140333 (10 μM, Tocris Bioscience, Bristol, United Kingdom); FK888 hydrate (10 μM, Sigma-Aldrich, St. Louis, MO, United States) and L-703606 oxalate salt hydrate (100 nM, Sigma-Aldrich, St. Louis, MO, United States), NK1R blockers; carbenoxolone disodium (CBX, 200 μM, Tocris Bioscience, Bristol, United Kingdom) and quinine (200 μM, Sigma-Aldrich, St. Louis, MO, United States), gap junctions blockers; [Sar 9 , Met(O 2 ) 11 ]-substance P (1 μM, Tocris Bioscience, Bristol, United Kingdom), a selective NK1R agonist; and substance P (5 μM, Tocris Bioscience, Bristol, United Kingdom).

    Produced:

    Article Title: Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons
    Article Snippet: drugs were applied through perfusion or local injection. .. Drugs used in the slice recordings were as follows: tetrodotoxin (TTX, 1 μM, Tocris Bioscience, Bristol, United Kingdom), a voltage-gated sodium channel blocker; picrotoxin (50 μM, Sigma-Aldrich, St. Louis, MO, United States), a blocker of GABA A receptors; 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 μM, Sigma-Aldrich, St. Louis, MO, United States), an AMPA-type glutamate receptor blocker; 2-amino-5-phosphonovalerate (APV, 50 μM, Sigma-Aldrich, St. Louis, MO, United States), an NMDA-type glutamate receptor blocker; SR140333 (10 μM, Tocris Bioscience, Bristol, United Kingdom); FK888 hydrate (10 μM, Sigma-Aldrich, St. Louis, MO, United States) and L-703606 oxalate salt hydrate (100 nM, Sigma-Aldrich, St. Louis, MO, United States), NK1R blockers; carbenoxolone disodium (CBX, 200 μM, Tocris Bioscience, Bristol, United Kingdom) and quinine (200 μM, Sigma-Aldrich, St. Louis, MO, United States), gap junctions blockers; [Sar 9 , Met(O 2 ) 11 ]-substance P (1 μM, Tocris Bioscience, Bristol, United Kingdom), a selective NK1R agonist; and substance P (5 μM, Tocris Bioscience, Bristol, United Kingdom).



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    fk888 hydrate  (Millipore)
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    Millipore fk888 hydrate
    Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, <t>FK888,</t> and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).
    Fk888 Hydrate, supplied by Millipore, 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/fk888+hydrate/fk888+hydrate/pmc08217616-60-76-80
    Average 90 stars, based on 1 article reviews
    fk888 hydrate - by Bioz Stars, 2026-09
    90/100 stars
    		  Buy from Supplier

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    Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, FK888, and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).

    Journal: Frontiers in Cellular Neuroscience

    Article Title: Gap Junctions Between Striatal D1 Neurons and Cholinergic Interneurons

    doi: 10.3389/fncel.2021.674399

    Figure Lengend Snippet: Tetanic photostimulation of D1 neurons induces an inward current in ChI that could not be inhibited by SP blockers. (A) Schematic representation showing the injection of AAV2/2-retro-hSyn-Flpo into the substantia nigra pars reticulata (SNR) and of AAV-fDIO-ChR2-EYFP and AAV-DIO-mCherry into the striatum of a ChAT-Cre mouse. (B) Images showing the expression of virus in the striatum (left panel), scale bar = 500 μm. The zoom-in view of the dashed rectangular area, showing the specific expression of ChR2 in D1 neurons and the specific expression of mCherry in ChIs (right panel). Green: D1 neurons with ChR2-EYFP; magenta: ChIs with mCherry. Scale bars = 50 μm. (C) A schematic diagram showing the method of whole-cell recording of the ChR2-expressing D1 neuron by 470 nm stimulation. Trains of brief laser pulse at 5, 10, 20, and 50 Hz (5 ms duration, 5 mW) produced precise firing of action potentials ( n = 7 cells tested). (D) A schematic diagram and example traces (left) show brief optogenetic stimulation of ChR2-expressing D1 neurons produced a fast IPSC in ChI and the IPSC was inhibited by picrotoxin. The right panel shows group data. * p < 0.05 (paired t -test; n = 7 cells; ctrl: 231.6 ± 68.6 pA; mean ± SEM; picrotoxin: 25.2 ± 11.0 pA; recorded at −10 mV). (E) Images showing the specific expression of NK1R and ChAT in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 100 μm. (F) A schematic diagram and example traces show that puffing 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P evoked inward currents from ChIs ( n = 9 cells; peak amplitude: −75.1 ± 14.5 pA). (G) The group data show the effect of the SP blockers cocktail on the response of ChIs to the puffing of 5 μM substance P. * p < 0.05 (paired t -test; n = 7 cells; ctrl: −118.7 ± 31.5 pA; SP blockers: −41.4 ± 11.4 pA). (H) Example traces (left and middle) show the effects of picrotoxin and the SP blockers cocktail of L703606, FK888, and SR14033 on (left panel) the currents evoked by tetanic stimulation (20 Hz, 5 ms pulses, 5 s duration) of D1 neurons and recorded in a ChI. Summary data (right panel) show that the effects of SP blockers lack statistical significance. n.s., non-significant, p > 0.05 (paired t -test; n = 12 cells; ctrl: −102.5 ± 12.7 pA; SP blockers: −97.0 ± 18.6 pA at −65 mV). (I) Images show the expression of NK1R and SST in the striatum. White solid arrowheads indicated colocalized neurons. Scale bar = 200 μm. (J) A schematic diagram and example trace show the response of an SST neuron to the puffing of 1 μM [Sar 9 , Met(O 2 ) 11 ]-substance P ( n = 5 cells; peak amplitude: −12.5 ± 3.2 pA). (K) A schematic diagram and example trace show the lack of response of an SST neuron in response to 5 s continuous optogenetic stimulation of D1 cells in TTX solution ( n = 5 cells; peak amplitude: 4.8 ± 5.1 pA at −65 mV).

    Article Snippet: Drugs used in the slice recordings were as follows: tetrodotoxin (TTX, 1 μM, Tocris Bioscience, Bristol, United Kingdom), a voltage-gated sodium channel blocker; picrotoxin (50 μM, Sigma-Aldrich, St. Louis, MO, United States), a blocker of GABA A receptors; 6,7-dinitroquinoxaline-2,3-dione (DNQX, 10 μM, Sigma-Aldrich, St. Louis, MO, United States), an AMPA-type glutamate receptor blocker; 2-amino-5-phosphonovalerate (APV, 50 μM, Sigma-Aldrich, St. Louis, MO, United States), an NMDA-type glutamate receptor blocker; SR140333 (10 μM, Tocris Bioscience, Bristol, United Kingdom); FK888 hydrate (10 μM, Sigma-Aldrich, St. Louis, MO, United States) and L-703606 oxalate salt hydrate (100 nM, Sigma-Aldrich, St. Louis, MO, United States), NK1R blockers; carbenoxolone disodium (CBX, 200 μM, Tocris Bioscience, Bristol, United Kingdom) and quinine (200 μM, Sigma-Aldrich, St. Louis, MO, United States), gap junctions blockers; [Sar 9 , Met(O 2 ) 11 ]-substance P (1 μM, Tocris Bioscience, Bristol, United Kingdom), a selective NK1R agonist; and substance P (5 μM, Tocris Bioscience, Bristol, United Kingdom).

    Techniques: Injection, Expressing, Produced