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  • acsf  (Tocris)
    95
    Tocris acsf
    On the indirect pathway A2a and <t>D2</t> receptors cause dyskinesia. A) Inslices representing dyskinesia, inclusion of a D2 antagonist in the <t>aCSF</t> (Sulpiride, 10µM) and application of the positive-timing protocol resulted in an increase in the EPSP
    Acsf, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 296 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 95 stars, based on 296 article reviews
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    93
    Millipore acsf
    α 2 <t>-antiplasmin</t> can prevent kainate-induced neuronal degeneration. Cresyl violet-stained coronal sections through the hippocampus of wild-type mice. The mice were infused with buffer <t>(aCSF)</t> or α 2 -antiplasmin for 2 d, kainate was injected, and then the infusion continued for 5 d more, and the mice were analyzed. Top , Section from a wild-type mouse infused with aCSF showing extensive kainate-induced degeneration. Bottom , Section from a wild-type mouse infused with α 2 -antiplasmin, showing resistance to kainate-induced degeneration. Arrowheads point to the site of injection; arrows indicate the site of infusion.
    Acsf, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 635 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/acsf/product/Millipore
    Average 93 stars, based on 635 article reviews
    Price from $9.99 to $1999.99
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    85
    Millipore acsf components
    Monoamine oxidase (MAO) is not a source of modulatory H 2 O 2 in striatum. Representative [DA] o evoked by pulse-train stimulation (30 pulses, 10 Hz) in <t>ACSF</t> (Control) and in the presence of the MAO inhibitors, <t>clorgyline</t> and pargyline (Clorg-Parg; 10 μM each). ( b ) Average evoked [DA] o normalized to control (100%) for each slice. Evoked [DA] o was unaltered by Clorg-Parg ( p > 0.05; n = 6). ( c ) Representative dopamine release records in the presence of Clorg-Parg and in GYKI-52466 (GYKI; 50 μM) in the continued presence of Clorg-Parg. ( d ) Average evoked [DA] o , with data normalized to peak evoked [DA] o in Clorg-Parg (100%) for each slice. The increase in evoked [DA] o when AMPARs were blocked by GYKI was unaffected by MAO inhibition (*** p
    Acsf Components, supplied by Millipore, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    On the indirect pathway A2a and D2 receptors cause dyskinesia. A) Inslices representing dyskinesia, inclusion of a D2 antagonist in the aCSF (Sulpiride, 10µM) and application of the positive-timing protocol resulted in an increase in the EPSP

    Journal: Neurobiology of disease

    Article Title: Selective loss of bi-directional synaptic plasticity in the direct and indirect striatal output pathways accompanies generation of parkinsonism and l-DOPA induced dyskinesia in mouse models

    doi: 10.1016/j.nbd.2014.08.006

    Figure Lengend Snippet: On the indirect pathway A2a and D2 receptors cause dyskinesia. A) Inslices representing dyskinesia, inclusion of a D2 antagonist in the aCSF (Sulpiride, 10µM) and application of the positive-timing protocol resulted in an increase in the EPSP

    Article Snippet: When indicated, the A2a antagonist (SCH 58261, 100 nM), A2a agonist (CGS 21680, 100 nM), D2 antagonist ((S)-(–)-Sulpiride, 10 µM), and D2 agonist (Quinpirole, 10 µM) were added to the aCSF (all Tocris Biosciences, UK).

    Techniques:

    Pharmacological inhibition of CSF formation by acetazolamide A: CSF outflow at baseline was 1.16 μL/min; infusion of aCSF (1.93 μL/min) yielded a measured outflow rate of 2.98 μL/min, or a calculated rate of CSF formation of 1.05 μL/min, within 10% of baseline (3 rats; 11 weeks of age). B: In two different experiments, CSF outflow at baseline was 0.95±0.23 μL/min (filled circles) or 0.96±0.03 μL/min (empty circles); infusion of acetazolamide (45 mM in aCSF; pH 9.0; 1.93 μL/min) or of mannitol (88.2 mM in aCSF; pH 9.0; 1.93 μL/min) yielded calculated rates of CSF formation 0.48±0.12 μL/min (filled circles) or of 1.12±0.17 μL/min (empty circles); based on these 2 experiments, inhibition by acetazolamide was calculated to be 57%; note that inhibition by acetazolamide was not reversible, with a rate of 0.38±0.10 μL/min observed after stopping infusion (3 rats/experiment; 10 weeks of age).

    Journal: Journal of neuroscience methods

    Article Title: A novel method to study cerebrospinal fluid dynamics in rats

    doi: 10.1016/j.jneumeth.2014.12.015

    Figure Lengend Snippet: Pharmacological inhibition of CSF formation by acetazolamide A: CSF outflow at baseline was 1.16 μL/min; infusion of aCSF (1.93 μL/min) yielded a measured outflow rate of 2.98 μL/min, or a calculated rate of CSF formation of 1.05 μL/min, within 10% of baseline (3 rats; 11 weeks of age). B: In two different experiments, CSF outflow at baseline was 0.95±0.23 μL/min (filled circles) or 0.96±0.03 μL/min (empty circles); infusion of acetazolamide (45 mM in aCSF; pH 9.0; 1.93 μL/min) or of mannitol (88.2 mM in aCSF; pH 9.0; 1.93 μL/min) yielded calculated rates of CSF formation 0.48±0.12 μL/min (filled circles) or of 1.12±0.17 μL/min (empty circles); based on these 2 experiments, inhibition by acetazolamide was calculated to be 57%; note that inhibition by acetazolamide was not reversible, with a rate of 0.38±0.10 μL/min observed after stopping infusion (3 rats/experiment; 10 weeks of age).

    Article Snippet: Intraventricular infusion solutions were made using artificial CSF (aCSF), composed as follows (in mM): Na 150; K 3.0; Ca 1.4; Mg 0.8; P 1.0; Cl 155, pH 7.19 (Tocris, Bristol UK), with a calculated osmolarity of 311.2 mOsmC /L.

    Techniques: Inhibition

    EEG effects of subcortical reverse microdialysis. (A) Schematic drawing (AP = −3.14 from bregma, Paxinos and Watson, 2007 ) showing the position of the bilaterally implanted microdialysis probes (black) with their active membrane shown in red. The dashed areas indicate the zone of diffusion of the drug around the dialysis probes (see text for additional details). (B) Delta waves detected by wavelet transform (top plots) of the EEG signal (bottom traces) show a clear reduction in frequency during TTA-P2 microdialysis in the VB. (C) Delta frequency distribution in one rat (black: aCSF; red: TTA-P2). (D) Density distribution of delta wave frequency (2–4.5 Hz) (black: aCSF n = 13, red: TTA-P2, n = 10; shaded areas represent ±SEM). (E) Average (±SEM) delta frequency during aCSF (black) and TTA-P2 (red) reverse microdialysis. The start of the microdialysis application of TTA-P2 is at time 0.

    Journal: Journal of Neuroscience Methods

    Article Title: Investigating local and long-range neuronal network dynamics by simultaneous optogenetics, reverse microdialysis and silicon probe recordings in vivo

    doi: 10.1016/j.jneumeth.2014.06.031

    Figure Lengend Snippet: EEG effects of subcortical reverse microdialysis. (A) Schematic drawing (AP = −3.14 from bregma, Paxinos and Watson, 2007 ) showing the position of the bilaterally implanted microdialysis probes (black) with their active membrane shown in red. The dashed areas indicate the zone of diffusion of the drug around the dialysis probes (see text for additional details). (B) Delta waves detected by wavelet transform (top plots) of the EEG signal (bottom traces) show a clear reduction in frequency during TTA-P2 microdialysis in the VB. (C) Delta frequency distribution in one rat (black: aCSF; red: TTA-P2). (D) Density distribution of delta wave frequency (2–4.5 Hz) (black: aCSF n = 13, red: TTA-P2, n = 10; shaded areas represent ±SEM). (E) Average (±SEM) delta frequency during aCSF (black) and TTA-P2 (red) reverse microdialysis. The start of the microdialysis application of TTA-P2 is at time 0.

    Article Snippet: The microdialysis pump delivered a constant flow rate of 1 μL/min of artificial cerebrospinal fluid (aCSF) bought from Tocris (ref. 3525) which contains the following Final ion concentrations (in mM): Na 150; K 3.0; Ca 1.4; Mg 0.8; P 1.0; Cl 155.

    Techniques: Diffusion-based Assay

    Combined optogenetics, reverse microdialysis and silicone probe recordings. (A) Schematic drawing (AP = −3.14 from bregma, Paxinos and Watson, 2007 ) showing the position in the VB of the optrode (with the four shanks of the silicone probe in orange and the attached optic fiber in gray) and the microdialysis probes (black) with their active membranes shown in red. (B) Coronal brain section indicating the tracks of the microdialysis probe (DP) and the optrode (SP + OF). (C) Wavelet transform (top) and ipsilateral EEG (bottom) during laser light stimulation in the VB, consisting of 5 trains of 5 (5 ms) pulses at 10 Hz (laser intensity: 40 mW) during reverse microdialysis of aCSF (C1) and TTA-P2 (C2) in an anesthetized rat. Blue lines mark the time of the laser light stimulation. (D) Spindle activity on raw (top) and band-passed signal (low trace) before (D1) and after (D2) TTA-P2 microdialysis. Calibrations in D1 also apply to D2. (E) Raster plots (and superimposed respective EEG traces) showing the activity of 4 VB TC neurons in response to the light pulses during aCSF (E1) and TTA-P2 (E2) microdialysis. Light pulse-triggered spike rates (E3) from 15 stimulation epochs.

    Journal: Journal of Neuroscience Methods

    Article Title: Investigating local and long-range neuronal network dynamics by simultaneous optogenetics, reverse microdialysis and silicon probe recordings in vivo

    doi: 10.1016/j.jneumeth.2014.06.031

    Figure Lengend Snippet: Combined optogenetics, reverse microdialysis and silicone probe recordings. (A) Schematic drawing (AP = −3.14 from bregma, Paxinos and Watson, 2007 ) showing the position in the VB of the optrode (with the four shanks of the silicone probe in orange and the attached optic fiber in gray) and the microdialysis probes (black) with their active membranes shown in red. (B) Coronal brain section indicating the tracks of the microdialysis probe (DP) and the optrode (SP + OF). (C) Wavelet transform (top) and ipsilateral EEG (bottom) during laser light stimulation in the VB, consisting of 5 trains of 5 (5 ms) pulses at 10 Hz (laser intensity: 40 mW) during reverse microdialysis of aCSF (C1) and TTA-P2 (C2) in an anesthetized rat. Blue lines mark the time of the laser light stimulation. (D) Spindle activity on raw (top) and band-passed signal (low trace) before (D1) and after (D2) TTA-P2 microdialysis. Calibrations in D1 also apply to D2. (E) Raster plots (and superimposed respective EEG traces) showing the activity of 4 VB TC neurons in response to the light pulses during aCSF (E1) and TTA-P2 (E2) microdialysis. Light pulse-triggered spike rates (E3) from 15 stimulation epochs.

    Article Snippet: The microdialysis pump delivered a constant flow rate of 1 μL/min of artificial cerebrospinal fluid (aCSF) bought from Tocris (ref. 3525) which contains the following Final ion concentrations (in mM): Na 150; K 3.0; Ca 1.4; Mg 0.8; P 1.0; Cl 155.

    Techniques: Optogenetics, Mass Spectrometry, Activity Assay

    Effects of intrahippocampal delivery of GnRH alone or with an aromatase inhibitor on performance on a hippocampus-dependent spatial memory task. Rats were ovariectomized, and all were implanted with capsules containing cholesterol vehicle. Chronic bilateral intrahippocampal delivery of GnRH, GnRH + the aromatase inhibitor letrozole, or aCSF vehicle was initiated 1 week before and maintained throughout testing. A , Memory performance in a radial-arm maze with delays imposed between the fourth and fifth arm choices. Mean number of errors of the first eight arm choices (±SEM) at each delay. B , Mean number of errors of the first eight arm choices (±SEM) averaged across both delays. * p

    Journal: eNeuro

    Article Title: Circulating Estradiol Regulates Brain-Derived Estradiol via Actions at GnRH Receptors to Impact Memory in Ovariectomized Rats

    doi: 10.1523/ENEURO.0321-16.2016

    Figure Lengend Snippet: Effects of intrahippocampal delivery of GnRH alone or with an aromatase inhibitor on performance on a hippocampus-dependent spatial memory task. Rats were ovariectomized, and all were implanted with capsules containing cholesterol vehicle. Chronic bilateral intrahippocampal delivery of GnRH, GnRH + the aromatase inhibitor letrozole, or aCSF vehicle was initiated 1 week before and maintained throughout testing. A , Memory performance in a radial-arm maze with delays imposed between the fourth and fifth arm choices. Mean number of errors of the first eight arm choices (±SEM) at each delay. B , Mean number of errors of the first eight arm choices (±SEM) averaged across both delays. * p

    Article Snippet: Cannulae were connected to Alzet osmotic minipumps by vinyl tubing that delivered artificial cerebrospinal fluid (aCSF) vehicle (Tocris Bioscience, Ellisville, MO) or letrozole (1.67 μg/μl; Bachem, Torrance, CA), an aromatase inhibitor, dissolved in dimethylsulfoxide and diluted in vehicle at a rate of 0.5 μl/h.

    Techniques:

    Effects of estradiol treatment and inhibition of brain estradiol synthesis on a hippocampus-dependent spatial memory task. Rats were ovariectomized and implanted with capsules containing estradiol (E) or cholesterol vehicle (CH). Chronic intracerebroventricular delivery of the aromatase inhibitor letrozole or aCSF vehicle was initiated 1 week before and maintained throughout testing. A , Working memory performance in a radial-arm maze with delays imposed between the fourth and fifth arm choices. Mean number of errors of the first eight arm choices (±SEM) at each delay. B , Mean number of errors of the first eight arm choices (±SEM) averaged across both delays. * p

    Journal: eNeuro

    Article Title: Circulating Estradiol Regulates Brain-Derived Estradiol via Actions at GnRH Receptors to Impact Memory in Ovariectomized Rats

    doi: 10.1523/ENEURO.0321-16.2016

    Figure Lengend Snippet: Effects of estradiol treatment and inhibition of brain estradiol synthesis on a hippocampus-dependent spatial memory task. Rats were ovariectomized and implanted with capsules containing estradiol (E) or cholesterol vehicle (CH). Chronic intracerebroventricular delivery of the aromatase inhibitor letrozole or aCSF vehicle was initiated 1 week before and maintained throughout testing. A , Working memory performance in a radial-arm maze with delays imposed between the fourth and fifth arm choices. Mean number of errors of the first eight arm choices (±SEM) at each delay. B , Mean number of errors of the first eight arm choices (±SEM) averaged across both delays. * p

    Article Snippet: Cannulae were connected to Alzet osmotic minipumps by vinyl tubing that delivered artificial cerebrospinal fluid (aCSF) vehicle (Tocris Bioscience, Ellisville, MO) or letrozole (1.67 μg/μl; Bachem, Torrance, CA), an aromatase inhibitor, dissolved in dimethylsulfoxide and diluted in vehicle at a rate of 0.5 μl/h.

    Techniques: Inhibition

    α 2 -antiplasmin can prevent kainate-induced neuronal degeneration. Cresyl violet-stained coronal sections through the hippocampus of wild-type mice. The mice were infused with buffer (aCSF) or α 2 -antiplasmin for 2 d, kainate was injected, and then the infusion continued for 5 d more, and the mice were analyzed. Top , Section from a wild-type mouse infused with aCSF showing extensive kainate-induced degeneration. Bottom , Section from a wild-type mouse infused with α 2 -antiplasmin, showing resistance to kainate-induced degeneration. Arrowheads point to the site of injection; arrows indicate the site of infusion.

    Journal: The Journal of Neuroscience

    Article Title: An Extracellular Proteolytic Cascade Promotes Neuronal Degeneration in the Mouse Hippocampus

    doi: 10.1523/JNEUROSCI.17-02-00543.1997

    Figure Lengend Snippet: α 2 -antiplasmin can prevent kainate-induced neuronal degeneration. Cresyl violet-stained coronal sections through the hippocampus of wild-type mice. The mice were infused with buffer (aCSF) or α 2 -antiplasmin for 2 d, kainate was injected, and then the infusion continued for 5 d more, and the mice were analyzed. Top , Section from a wild-type mouse infused with aCSF showing extensive kainate-induced degeneration. Bottom , Section from a wild-type mouse infused with α 2 -antiplasmin, showing resistance to kainate-induced degeneration. Arrowheads point to the site of injection; arrows indicate the site of infusion.

    Article Snippet: Adult wild-type male mice were anesthetized as above and placed in a stereotaxic apparatus, and a micro-osmotic pump containing artificial cerebrospinal fluid (aCSF) (for control animals) or 100 μl of α2 -antiplasmin in aCSF (1 mg/ml; Sigma, St. Louis, MO) was placed subcutaneously in the back of the animals.

    Techniques: Staining, Mouse Assay, Injection

    Monoamine oxidase (MAO) is not a source of modulatory H 2 O 2 in striatum. Representative [DA] o evoked by pulse-train stimulation (30 pulses, 10 Hz) in ACSF (Control) and in the presence of the MAO inhibitors, clorgyline and pargyline (Clorg-Parg; 10 μM each). ( b ) Average evoked [DA] o normalized to control (100%) for each slice. Evoked [DA] o was unaltered by Clorg-Parg ( p > 0.05; n = 6). ( c ) Representative dopamine release records in the presence of Clorg-Parg and in GYKI-52466 (GYKI; 50 μM) in the continued presence of Clorg-Parg. ( d ) Average evoked [DA] o , with data normalized to peak evoked [DA] o in Clorg-Parg (100%) for each slice. The increase in evoked [DA] o when AMPARs were blocked by GYKI was unaffected by MAO inhibition (*** p

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    Article Title: Mitochondria are the source of hydrogen peroxide for dynamic brain-cell signaling

    doi: 10.1523/JNEUROSCI.1706-09.2009

    Figure Lengend Snippet: Monoamine oxidase (MAO) is not a source of modulatory H 2 O 2 in striatum. Representative [DA] o evoked by pulse-train stimulation (30 pulses, 10 Hz) in ACSF (Control) and in the presence of the MAO inhibitors, clorgyline and pargyline (Clorg-Parg; 10 μM each). ( b ) Average evoked [DA] o normalized to control (100%) for each slice. Evoked [DA] o was unaltered by Clorg-Parg ( p > 0.05; n = 6). ( c ) Representative dopamine release records in the presence of Clorg-Parg and in GYKI-52466 (GYKI; 50 μM) in the continued presence of Clorg-Parg. ( d ) Average evoked [DA] o , with data normalized to peak evoked [DA] o in Clorg-Parg (100%) for each slice. The increase in evoked [DA] o when AMPARs were blocked by GYKI was unaffected by MAO inhibition (*** p

    Article Snippet: Disodium succinate, glibenclamide, rotenone, mercaptosuccinic acid, pargyline hydrochloride, clorgyline, phenylarsine oxide (PAO), and all ACSF components were from Sigma (St. Louis, MO, USA); GYKI-52466 was from Tocris (Ellisville, MO, USA) and catalase (bovine liver) was from Calbiochem (La Jolla, CA, USA).

    Techniques: Inhibition

    NADPH oxidase (Nox) is not a source of modulatory H 2 O 2 in striatum. ( a ) Representative [DA] o evoked by pulse-train stimulation (30 pulses, 10 Hz) in ACSF (Control) and in the presence of the Nox inhibitor, phenylarsine oxide (PAO; 10 μM). ( b ) Average evoked [DA] o normalized to control (100%) for each slice. Evoked [DA] o was unaltered by PAO ( p > 0.05; n = 7). ( c ) Representative dopamine release records in the presence of PAO and in GYKI-52466 (GYKI; 50 μM) in the continued presence of PAO. ( d ) Average evoked [DA] o normalized to that in PAO (100%) for each slice. The usual increase in evoked [DA] o release with GYKI persisted in the presence of PAO (*** p

    Journal: The Journal of neuroscience : the official journal of the Society for Neuroscience

    Article Title: Mitochondria are the source of hydrogen peroxide for dynamic brain-cell signaling

    doi: 10.1523/JNEUROSCI.1706-09.2009

    Figure Lengend Snippet: NADPH oxidase (Nox) is not a source of modulatory H 2 O 2 in striatum. ( a ) Representative [DA] o evoked by pulse-train stimulation (30 pulses, 10 Hz) in ACSF (Control) and in the presence of the Nox inhibitor, phenylarsine oxide (PAO; 10 μM). ( b ) Average evoked [DA] o normalized to control (100%) for each slice. Evoked [DA] o was unaltered by PAO ( p > 0.05; n = 7). ( c ) Representative dopamine release records in the presence of PAO and in GYKI-52466 (GYKI; 50 μM) in the continued presence of PAO. ( d ) Average evoked [DA] o normalized to that in PAO (100%) for each slice. The usual increase in evoked [DA] o release with GYKI persisted in the presence of PAO (*** p

    Article Snippet: Disodium succinate, glibenclamide, rotenone, mercaptosuccinic acid, pargyline hydrochloride, clorgyline, phenylarsine oxide (PAO), and all ACSF components were from Sigma (St. Louis, MO, USA); GYKI-52466 was from Tocris (Ellisville, MO, USA) and catalase (bovine liver) was from Calbiochem (La Jolla, CA, USA).

    Techniques: