rat anti k8 troma  (Alomone Labs)


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    Alomone Labs rat anti k8 troma
    Rat Anti K8 Troma, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rat anti k8 troma/product/Alomone Labs
    Average 93 stars, based on 6 article reviews
    Price from $9.99 to $1999.99
    rat anti k8 troma - by Bioz Stars, 2022-08
    93/100 stars

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    Alomone Labs tertiapin q
    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during <t>tertiapin-Q</t> (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.
    Tertiapin Q, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Alomone Labs nmda treatment
    Subcellular GABA A <t>Rα1</t> receptor distribution on soma and neurites in CTRL and <t>NMDA</t> stimulated hippocampal neurons. ( a ): bar plot showing gold clusters density in CTRL and NMDA stimulated neurons; ( b ): bar plot showing clusters size (number of gold particles/cluster) in CTRL and NMDA stimulated neurons; ( c ): bar plot showing the number of clusters formed respectively by n ≤ 5 and n > 5 gold particles on soma and neurites in CTRL and NMDA stimulated hippocampal neurons. * Indicates significant differences (*p
    Nmda Treatment, 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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    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Journal: Frontiers in Pharmacology

    Article Title: Mu-Opioid Receptor Agonist Induces Kir3 Currents in Mouse Peripheral Sensory Neurons – Effects of Nerve Injury

    doi: 10.3389/fphar.2018.01478

    Figure Lengend Snippet: DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Article Snippet: For tertiapin-Q experiments we applied voltage ramps from a holding potential of -40 mV and measured the induced current at -80 mV, based on previously published protocols ( ; ).

    Techniques: Mouse Assay

    DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Journal: Frontiers in Pharmacology

    Article Title: Mu-Opioid Receptor Agonist Induces Kir3 Currents in Mouse Peripheral Sensory Neurons – Effects of Nerve Injury

    doi: 10.3389/fphar.2018.01478

    Figure Lengend Snippet: DAMGO (10 μM)-induced potassium currents in mouse DRG neurons obtained in the voltage ramp mode. (A) Number of neurons responding and non-responding to DAMGO from naïve and CCI mice. The proportion of DAMGO-responding to DAMGO-non-responding neurons from naïve vs. CCI mice did not differ significantly ( P = 0.596; Fisher’s exact t -test). The neurons were sampled from cultures obtained from DRG of seven naïve and eight CCI mice. (B) Single neuron currents in DAMGO-responders. The data points represent single neuron values, and the red horizontal lines indicate the means. Numbers in brackets indicate the number of neurons. (C–F) Exemplary currents of DRG neurons non-responding (C) and responding (D) to DAMGO from naïve mice, and DRG neurons non-responding (E) and responding (F) to DAMGO from mice on day 2 following CCI. The DAMGO effects are shown before and during tertiapin-Q (100 nM) application. (G,H) Tertiapin-Q (100 nM)-mediated attenuation of DAMGO-induced currents in individual neurons from naïve mice ( n = 8 neurons; ∗ P = 0.0204, paired t -test) (G) and CCI mice ( n = 9 neurons; ∗∗ P = 0.0073, paired t -test) (H) . Only DAMGO-responding neurons are shown. Data points represent DAMGO-induced currents of the same neuron before and after application of tertiapin-Q. Dotted lines represent zero current. In all experiments, the currents were obtained by voltage ramps from a holding potential of –40 mV and measured at –80 mV in high potassium extracellular buffer (45 mM). Neurons were defined as responding to DAMGO if the resulting current was larger than three times the noise range.

    Article Snippet: Discussion In this study, we found that the MOR-selective agonist DAMGO induces potassium currents in DRG neurons of both naïve mice and mice with CCI of the sciatic nerve, which were diminished by barium and tertiapin-Q indicating the involvement of Kir3 channels.

    Techniques: Mouse Assay

    Effects of tertiapin-Q on oxycodone- and morphine-induced K IR 3.1 channel activation in Xenopus oocytes. The data presented are typical recordings of K + channel current by (A) oxycodone and (B) morphine. Representative current responses to oxycodone (100

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced K IR 3.1 channel activation in Xenopus oocytes. The data presented are typical recordings of K + channel current by (A) oxycodone and (B) morphine. Representative current responses to oxycodone (100

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Activation Assay

    Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques:

    Effects of tertiapin-Q on oxycodone- and morphine-induced antinociceptive effects in the (A) FBC and (B) neuropathic pain models. Groups of mice were treated with tertiapin-Q (30 pmol per mouse, i.c.v.) 10 min before the opioids, and either oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced antinociceptive effects in the (A) FBC and (B) neuropathic pain models. Groups of mice were treated with tertiapin-Q (30 pmol per mouse, i.c.v.) 10 min before the opioids, and either oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay

    Dose-dependent antinociceptive effects induced by i.t. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effects induced by i.t. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on the antinociceptive effects of morphine and oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques:

    Dose-dependent antinociceptive effect induced by i.c.v. administration of fentanyl in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before fentanyl. Fentanyl (0.1–1.7

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effect induced by i.c.v. administration of fentanyl in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before fentanyl. Fentanyl (0.1–1.7

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Dose-dependent antinociceptive effects induced by i.c.v. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Dose-dependent antinociceptive effects induced by i.c.v. administration of oxycodone and morphine in the presence of tertiapin-Q in mice tail-flick test. Groups of mice were pretreated with tertiapin-Q (30 pmol per mouse) 10 min before the opioids. The

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Effects of tertiapin-Q on oxycodone- and morphine-induced antinociception after i.c.v. administration in mice tail-flick test. Groups of mice were treated with tertiapin-Q (3–30 mol per mouse, i.c.v.) 10 min before the opioids, either oxycodone

    Journal: British Journal of Pharmacology

    Article Title: G protein-gated inwardly rectifying potassium (KIR3) channels play a primary role in the antinociceptive effect of oxycodone, but not morphine, at supraspinal sites

    doi: 10.1111/bph.12441

    Figure Lengend Snippet: Effects of tertiapin-Q on oxycodone- and morphine-induced antinociception after i.c.v. administration in mice tail-flick test. Groups of mice were treated with tertiapin-Q (3–30 mol per mouse, i.c.v.) 10 min before the opioids, either oxycodone

    Article Snippet: Tertiapin-Q was purchased from Alomone Labs Ltd. (Jerusalem, Israel), and pertussis toxin (PTX) was purchased from Sigma-Aldrich (Tokyo, Japan).

    Techniques: Mouse Assay, Tail Flick Test

    Subcellular GABA A Rα1 receptor distribution on soma and neurites in CTRL and NMDA stimulated hippocampal neurons. ( a ): bar plot showing gold clusters density in CTRL and NMDA stimulated neurons; ( b ): bar plot showing clusters size (number of gold particles/cluster) in CTRL and NMDA stimulated neurons; ( c ): bar plot showing the number of clusters formed respectively by n ≤ 5 and n > 5 gold particles on soma and neurites in CTRL and NMDA stimulated hippocampal neurons. * Indicates significant differences (*p

    Journal: Scientific Reports

    Article Title: Correlating Fluorescence and High-Resolution Scanning Electron Microscopy (HRSEM) for the study of GABAA receptor clustering induced by inhibitory synaptic plasticity

    doi: 10.1038/s41598-017-14210-5

    Figure Lengend Snippet: Subcellular GABA A Rα1 receptor distribution on soma and neurites in CTRL and NMDA stimulated hippocampal neurons. ( a ): bar plot showing gold clusters density in CTRL and NMDA stimulated neurons; ( b ): bar plot showing clusters size (number of gold particles/cluster) in CTRL and NMDA stimulated neurons; ( c ): bar plot showing the number of clusters formed respectively by n ≤ 5 and n > 5 gold particles on soma and neurites in CTRL and NMDA stimulated hippocampal neurons. * Indicates significant differences (*p

    Article Snippet: During the recovery period, 12 minutes after the end of the NMDA treatment, live immunolabelling of GABAA Rα1 subunits was performed, namely cells were incubated 13 minutes in a solution containing primary antibody against GABAA Rα1 (Alomone Labs, Israel) diluted 1:30 in 0.5% bovine serum albumin (BSA), 350 mM sucrose in PBS, followed by 13 minutes incubation with gold-conjugated secondary antibody.

    Techniques:

    Post-synaptic surface and post-synaptic GABA A Rα1 distribution at inhibitory synapses of CTRL and NMDA stimulated hippocampal neurons. ( a ): 3D model of an inhibitory synapse immuno-labelled for the GABA A Rα1 in a hippocampal neuron in control conditions (CTRL). Slice1 and slice2 are two tomographic slices through the dotted lines in a. Arrowheads point to gold clusters; ( b ): 3D model of an inhibitory synapse immunolabelled for the GABA A Rα1 in a hippocampal neuron after the induction of plasticity by NMDA stimulation. Slice1 and slice2 are two tomographic slices through the dotted lines in b. Arrowheads point to gold clusters; note that in NMDA treated samples, more gold clusters are visible. ( c ): bar plot showing the area of the post-synaptic membrane on GABA A Rα1 immunolabelled synapses in both CTRL and NMDA stimulated neurons; ( d ): bar plot showing the number of gold clusters/synapse in CTRL and NMDA stimulated neurons; ( e ): bar plot showing the gold clusters volume normalized over the post-synaptic area in CTRL and NMDA stimulated neurons. Values are mean ± s.e.m. * Indicates significant differences (p

    Journal: Scientific Reports

    Article Title: Correlating Fluorescence and High-Resolution Scanning Electron Microscopy (HRSEM) for the study of GABAA receptor clustering induced by inhibitory synaptic plasticity

    doi: 10.1038/s41598-017-14210-5

    Figure Lengend Snippet: Post-synaptic surface and post-synaptic GABA A Rα1 distribution at inhibitory synapses of CTRL and NMDA stimulated hippocampal neurons. ( a ): 3D model of an inhibitory synapse immuno-labelled for the GABA A Rα1 in a hippocampal neuron in control conditions (CTRL). Slice1 and slice2 are two tomographic slices through the dotted lines in a. Arrowheads point to gold clusters; ( b ): 3D model of an inhibitory synapse immunolabelled for the GABA A Rα1 in a hippocampal neuron after the induction of plasticity by NMDA stimulation. Slice1 and slice2 are two tomographic slices through the dotted lines in b. Arrowheads point to gold clusters; note that in NMDA treated samples, more gold clusters are visible. ( c ): bar plot showing the area of the post-synaptic membrane on GABA A Rα1 immunolabelled synapses in both CTRL and NMDA stimulated neurons; ( d ): bar plot showing the number of gold clusters/synapse in CTRL and NMDA stimulated neurons; ( e ): bar plot showing the gold clusters volume normalized over the post-synaptic area in CTRL and NMDA stimulated neurons. Values are mean ± s.e.m. * Indicates significant differences (p

    Article Snippet: During the recovery period, 12 minutes after the end of the NMDA treatment, live immunolabelling of GABAA Rα1 subunits was performed, namely cells were incubated 13 minutes in a solution containing primary antibody against GABAA Rα1 (Alomone Labs, Israel) diluted 1:30 in 0.5% bovine serum albumin (BSA), 350 mM sucrose in PBS, followed by 13 minutes incubation with gold-conjugated secondary antibody.

    Techniques:

    Correlative light-high resolution scanning electron microscopy (CL-HRSEM) localization of GABA A Rα1 in control (CTRL, a–e) and iLTP (NMDA, f–i) primary hippocampal neurons growing on photo-etched coverslips. The BSE signal (pseudo-coloured in yellow) is superimposed on the grey-scale SE images. ( a ): low magnification HRSEM images of a CTRL neuron immunolabelled for GABA A Rα1. Inset: same neurons imaged by CFM. ( b ): CFM image of part of the neurite bundle boxed in a. Note the presence of GABA A Rα1 clusters (bright spots) along the neurite. The boxed regions are magnified in c (insets) and in d–e. ( c ): HRSEM image showing the same region boxed in a. The yellow spots on the neurite bundle are GABA A Rα1 receptor clusters. The double inset shows higher magnifications of the single neurite boxed in (c) (bottom left) imaged respectively at the CFM (above) and at the HRSEM (below). The arrowheads point to neurites without gold nanoparticles; ( d ): HRSEM image of the bundle of neurites boxed in c (upper right); ( e ): CFM image of the same bundle of neurites imaged in d. The arrow points to a fluorescent spot not observed in d; ( f ): low magnification HRSEM images of a NMDA stimulated neurons immunolabelled for GABA A Rα1. Inset: the same neurons imaged by CFM; ( g ): HRSEM image showing a portion of the cell body of the neuron imaged in f (upper Inset). Left inset: the same region imaged at the CFM. Right Inset: HRSEM higher magnification of the region boxed in g. ( h ): HRSEM image of the region boxed in f (bottom Inset). The arrowheads point to neurites without gold nanoparticles; ( i ), CFM image of the same region imaged in h. The arrow points to a fluorescent spot not observed in h. Circles and brackets point to the same sub-regions. Scale bars are 10 µm in a, a inset, f, f inset; 5 µm in b and g right inset; 1 µm in c–e and g–i; 0.2 µm in g right inset.

    Journal: Scientific Reports

    Article Title: Correlating Fluorescence and High-Resolution Scanning Electron Microscopy (HRSEM) for the study of GABAA receptor clustering induced by inhibitory synaptic plasticity

    doi: 10.1038/s41598-017-14210-5

    Figure Lengend Snippet: Correlative light-high resolution scanning electron microscopy (CL-HRSEM) localization of GABA A Rα1 in control (CTRL, a–e) and iLTP (NMDA, f–i) primary hippocampal neurons growing on photo-etched coverslips. The BSE signal (pseudo-coloured in yellow) is superimposed on the grey-scale SE images. ( a ): low magnification HRSEM images of a CTRL neuron immunolabelled for GABA A Rα1. Inset: same neurons imaged by CFM. ( b ): CFM image of part of the neurite bundle boxed in a. Note the presence of GABA A Rα1 clusters (bright spots) along the neurite. The boxed regions are magnified in c (insets) and in d–e. ( c ): HRSEM image showing the same region boxed in a. The yellow spots on the neurite bundle are GABA A Rα1 receptor clusters. The double inset shows higher magnifications of the single neurite boxed in (c) (bottom left) imaged respectively at the CFM (above) and at the HRSEM (below). The arrowheads point to neurites without gold nanoparticles; ( d ): HRSEM image of the bundle of neurites boxed in c (upper right); ( e ): CFM image of the same bundle of neurites imaged in d. The arrow points to a fluorescent spot not observed in d; ( f ): low magnification HRSEM images of a NMDA stimulated neurons immunolabelled for GABA A Rα1. Inset: the same neurons imaged by CFM; ( g ): HRSEM image showing a portion of the cell body of the neuron imaged in f (upper Inset). Left inset: the same region imaged at the CFM. Right Inset: HRSEM higher magnification of the region boxed in g. ( h ): HRSEM image of the region boxed in f (bottom Inset). The arrowheads point to neurites without gold nanoparticles; ( i ), CFM image of the same region imaged in h. The arrow points to a fluorescent spot not observed in h. Circles and brackets point to the same sub-regions. Scale bars are 10 µm in a, a inset, f, f inset; 5 µm in b and g right inset; 1 µm in c–e and g–i; 0.2 µm in g right inset.

    Article Snippet: During the recovery period, 12 minutes after the end of the NMDA treatment, live immunolabelling of GABAA Rα1 subunits was performed, namely cells were incubated 13 minutes in a solution containing primary antibody against GABAA Rα1 (Alomone Labs, Israel) diluted 1:30 in 0.5% bovine serum albumin (BSA), 350 mM sucrose in PBS, followed by 13 minutes incubation with gold-conjugated secondary antibody.

    Techniques: Electron Microscopy