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A-M Systems eeg emg electrodes
Eeg Emg Electrodes, supplied by A-M Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/eeg+emg+electrodes/eeg+electrodes+emg/pmc12674160-267-7-13
Average 86 stars, based on 1 article reviews
eeg emg electrodes - by Bioz Stars, 2026-09
86/100 stars

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Derivative Assay:

Article Title: VTA dopaminergic neuronal activity during NREM sleep is modulated by learning and facilitates motor memory consolidation
Article Snippet: .. EEG and EMG signals derived from the EEG/EMG electrodes were amplified (model 3500, A-M Systems) and digitized at 1017.3 Hz using Tucker-Davis Technologies (TDT) RZ5 processor and Synapse software. .. For a subset of mice in the chemogenetic manipulation experiments, EEG/EMG signals were amplified (model 3500, A-M Systems) and digitized at 512 Hz using the VitalRecorder software (Kissei Comtec America).

Amplification:

Article Title: VTA dopaminergic neuronal activity during NREM sleep is modulated by learning and facilitates motor memory consolidation
Article Snippet: .. EEG and EMG signals derived from the EEG/EMG electrodes were amplified (model 3500, A-M Systems) and digitized at 1017.3 Hz using Tucker-Davis Technologies (TDT) RZ5 processor and Synapse software. .. For a subset of mice in the chemogenetic manipulation experiments, EEG/EMG signals were amplified (model 3500, A-M Systems) and digitized at 512 Hz using the VitalRecorder software (Kissei Comtec America).

Software:

Article Title: VTA dopaminergic neuronal activity during NREM sleep is modulated by learning and facilitates motor memory consolidation
Article Snippet: .. EEG and EMG signals derived from the EEG/EMG electrodes were amplified (model 3500, A-M Systems) and digitized at 1017.3 Hz using Tucker-Davis Technologies (TDT) RZ5 processor and Synapse software. .. For a subset of mice in the chemogenetic manipulation experiments, EEG/EMG signals were amplified (model 3500, A-M Systems) and digitized at 512 Hz using the VitalRecorder software (Kissei Comtec America).



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a , Bilateral targeting of hippocampal astrocytes of Adora2b flox/flox mice to express iCre recombinase (A2BR-Astro-KD) or reporter protein (tdTomato; control). b , Schematic of the object recognition test. c , Summary data showing the time the animals spent exploring two identical objects (O1 and O2) during training and then one familiar (O1) and a new object (new) during testing. d , Calculated discrimination index as a measure of relative object preference, showing that A2BR deletion in hippocampal astrocytes impaired the recognition memory. e , Generation of mice with conditional deletion of A2BR in astrocytes. f , Summary data showing the discrimination index calculated for Adora2b flox/flox : Aldh1l1 Cre− and Adora2b flox/flox : \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Aldh{1}l{{1}}^{Cre/ERT{{2}}^{+}}$$\end{document} A l d h 1 l 1 C r e / E R T 2 + mice treated with vehicle (oil) or tamoxifen. Deletion of A2BR in astrocytes impaired the recognition memory. g , Schematic of the <t>EEG</t> <t>and</t> <t>EMG</t> recording setup and representative EEG and EMG traces. h , Representative hypnograms obtained by 24 h of EEG recordings showing fragmentation of wake and NREM sleep during the light phase in mice with conditional deletion of A2BR in brain astrocytes. ZT, Zeitgeber time. Schematic in panel g was created using BioRender ( https://biorender.com ). i , A2BR deletion in astrocytes markedly decreased the slow-wave activity (0.5–4.0 Hz) and low-frequency slow-wave activity (0.5–1.5 Hz), indicative of a reduction in sleep pressure. Data are presented as mean ± s.e.m. # P = 0.010; P values indicated signify the differences between genotypes. j , Schematic illustrating the proposed mechanism that controls astrocyte glucose metabolism and provides metabolic support of neuronal activity. Potential sources of activity-dependent adenosine release are illustrated, including transporter-mediated release , , and extracellular breakdown of ATP released at synapses and by astrocytes . β-AR, β-adrenoceptor; G6P, glucose-6-phosphate. In panels c , d , f , i , the numbers in parentheses indicate the numbers of animals per experimental group. P values were determined by one-way ANOVA followed by Sidak’s post-hoc test ( c , d , f ) or two-way ANOVA ( i ).
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a , Bilateral targeting of hippocampal astrocytes of Adora2b flox/flox mice to express iCre recombinase (A2BR-Astro-KD) or reporter protein (tdTomato; control). b , Schematic of the object recognition test. c , Summary data showing the time the animals spent exploring two identical objects (O1 and O2) during training and then one familiar (O1) and a new object (new) during testing. d , Calculated discrimination index as a measure of relative object preference, showing that A2BR deletion in hippocampal astrocytes impaired the recognition memory. e , Generation of mice with conditional deletion of A2BR in astrocytes. f , Summary data showing the discrimination index calculated for Adora2b flox/flox : Aldh1l1 Cre− and Adora2b flox/flox : \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Aldh{1}l{{1}}^{Cre/ERT{{2}}^{+}}$$\end{document} A l d h 1 l 1 C r e / E R T 2 + mice treated with vehicle (oil) or tamoxifen. Deletion of A2BR in astrocytes impaired the recognition memory. g , Schematic of the <t>EEG</t> <t>and</t> <t>EMG</t> recording setup and representative EEG and EMG traces. h , Representative hypnograms obtained by 24 h of EEG recordings showing fragmentation of wake and NREM sleep during the light phase in mice with conditional deletion of A2BR in brain astrocytes. ZT, Zeitgeber time. Schematic in panel g was created using BioRender ( https://biorender.com ). i , A2BR deletion in astrocytes markedly decreased the slow-wave activity (0.5–4.0 Hz) and low-frequency slow-wave activity (0.5–1.5 Hz), indicative of a reduction in sleep pressure. Data are presented as mean ± s.e.m. # P = 0.010; P values indicated signify the differences between genotypes. j , Schematic illustrating the proposed mechanism that controls astrocyte glucose metabolism and provides metabolic support of neuronal activity. Potential sources of activity-dependent adenosine release are illustrated, including transporter-mediated release , , and extracellular breakdown of ATP released at synapses and by astrocytes . β-AR, β-adrenoceptor; G6P, glucose-6-phosphate. In panels c , d , f , i , the numbers in parentheses indicate the numbers of animals per experimental group. P values were determined by one-way ANOVA followed by Sidak’s post-hoc test ( c , d , f ) or two-way ANOVA ( i ).
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Pinnacle Technology Inc eeg electrodes no. 8201: 2 eeg/1 emg mouse headmount
a , Bilateral targeting of hippocampal astrocytes of Adora2b flox/flox mice to express iCre recombinase (A2BR-Astro-KD) or reporter protein (tdTomato; control). b , Schematic of the object recognition test. c , Summary data showing the time the animals spent exploring two identical objects (O1 and O2) during training and then one familiar (O1) and a new object (new) during testing. d , Calculated discrimination index as a measure of relative object preference, showing that A2BR deletion in hippocampal astrocytes impaired the recognition memory. e , Generation of mice with conditional deletion of A2BR in astrocytes. f , Summary data showing the discrimination index calculated for Adora2b flox/flox : Aldh1l1 Cre− and Adora2b flox/flox : \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Aldh{1}l{{1}}^{Cre/ERT{{2}}^{+}}$$\end{document} A l d h 1 l 1 C r e / E R T 2 + mice treated with vehicle (oil) or tamoxifen. Deletion of A2BR in astrocytes impaired the recognition memory. g , Schematic of the <t>EEG</t> <t>and</t> <t>EMG</t> recording setup and representative EEG and EMG traces. h , Representative hypnograms obtained by 24 h of EEG recordings showing fragmentation of wake and NREM sleep during the light phase in mice with conditional deletion of A2BR in brain astrocytes. ZT, Zeitgeber time. Schematic in panel g was created using BioRender ( https://biorender.com ). i , A2BR deletion in astrocytes markedly decreased the slow-wave activity (0.5–4.0 Hz) and low-frequency slow-wave activity (0.5–1.5 Hz), indicative of a reduction in sleep pressure. Data are presented as mean ± s.e.m. # P = 0.010; P values indicated signify the differences between genotypes. j , Schematic illustrating the proposed mechanism that controls astrocyte glucose metabolism and provides metabolic support of neuronal activity. Potential sources of activity-dependent adenosine release are illustrated, including transporter-mediated release , , and extracellular breakdown of ATP released at synapses and by astrocytes . β-AR, β-adrenoceptor; G6P, glucose-6-phosphate. In panels c , d , f , i , the numbers in parentheses indicate the numbers of animals per experimental group. P values were determined by one-way ANOVA followed by Sidak’s post-hoc test ( c , d , f ) or two-way ANOVA ( i ).
Eeg Electrodes No. 8201: 2 Eeg/1 Emg Mouse Headmount, supplied by Pinnacle Technology Inc, 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/eeg+emg+electrodes/eeg+emg+headmounts+8201/pm38225934-170-27-36
Average 90 stars, based on 1 article reviews
eeg electrodes no. 8201: 2 eeg/1 emg mouse headmount - by Bioz Stars, 2026-09
90/100 stars
  Buy from Supplier

Image Search Results


a , Bilateral targeting of hippocampal astrocytes of Adora2b flox/flox mice to express iCre recombinase (A2BR-Astro-KD) or reporter protein (tdTomato; control). b , Schematic of the object recognition test. c , Summary data showing the time the animals spent exploring two identical objects (O1 and O2) during training and then one familiar (O1) and a new object (new) during testing. d , Calculated discrimination index as a measure of relative object preference, showing that A2BR deletion in hippocampal astrocytes impaired the recognition memory. e , Generation of mice with conditional deletion of A2BR in astrocytes. f , Summary data showing the discrimination index calculated for Adora2b flox/flox : Aldh1l1 Cre− and Adora2b flox/flox : \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Aldh{1}l{{1}}^{Cre/ERT{{2}}^{+}}$$\end{document} A l d h 1 l 1 C r e / E R T 2 + mice treated with vehicle (oil) or tamoxifen. Deletion of A2BR in astrocytes impaired the recognition memory. g , Schematic of the EEG and EMG recording setup and representative EEG and EMG traces. h , Representative hypnograms obtained by 24 h of EEG recordings showing fragmentation of wake and NREM sleep during the light phase in mice with conditional deletion of A2BR in brain astrocytes. ZT, Zeitgeber time. Schematic in panel g was created using BioRender ( https://biorender.com ). i , A2BR deletion in astrocytes markedly decreased the slow-wave activity (0.5–4.0 Hz) and low-frequency slow-wave activity (0.5–1.5 Hz), indicative of a reduction in sleep pressure. Data are presented as mean ± s.e.m. # P = 0.010; P values indicated signify the differences between genotypes. j , Schematic illustrating the proposed mechanism that controls astrocyte glucose metabolism and provides metabolic support of neuronal activity. Potential sources of activity-dependent adenosine release are illustrated, including transporter-mediated release , , and extracellular breakdown of ATP released at synapses and by astrocytes . β-AR, β-adrenoceptor; G6P, glucose-6-phosphate. In panels c , d , f , i , the numbers in parentheses indicate the numbers of animals per experimental group. P values were determined by one-way ANOVA followed by Sidak’s post-hoc test ( c , d , f ) or two-way ANOVA ( i ).

Journal: Nature

Article Title: Adenosine signalling to astrocytes coordinates brain metabolism and function

doi: 10.1038/s41586-024-07611-w

Figure Lengend Snippet: a , Bilateral targeting of hippocampal astrocytes of Adora2b flox/flox mice to express iCre recombinase (A2BR-Astro-KD) or reporter protein (tdTomato; control). b , Schematic of the object recognition test. c , Summary data showing the time the animals spent exploring two identical objects (O1 and O2) during training and then one familiar (O1) and a new object (new) during testing. d , Calculated discrimination index as a measure of relative object preference, showing that A2BR deletion in hippocampal astrocytes impaired the recognition memory. e , Generation of mice with conditional deletion of A2BR in astrocytes. f , Summary data showing the discrimination index calculated for Adora2b flox/flox : Aldh1l1 Cre− and Adora2b flox/flox : \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$Aldh{1}l{{1}}^{Cre/ERT{{2}}^{+}}$$\end{document} A l d h 1 l 1 C r e / E R T 2 + mice treated with vehicle (oil) or tamoxifen. Deletion of A2BR in astrocytes impaired the recognition memory. g , Schematic of the EEG and EMG recording setup and representative EEG and EMG traces. h , Representative hypnograms obtained by 24 h of EEG recordings showing fragmentation of wake and NREM sleep during the light phase in mice with conditional deletion of A2BR in brain astrocytes. ZT, Zeitgeber time. Schematic in panel g was created using BioRender ( https://biorender.com ). i , A2BR deletion in astrocytes markedly decreased the slow-wave activity (0.5–4.0 Hz) and low-frequency slow-wave activity (0.5–1.5 Hz), indicative of a reduction in sleep pressure. Data are presented as mean ± s.e.m. # P = 0.010; P values indicated signify the differences between genotypes. j , Schematic illustrating the proposed mechanism that controls astrocyte glucose metabolism and provides metabolic support of neuronal activity. Potential sources of activity-dependent adenosine release are illustrated, including transporter-mediated release , , and extracellular breakdown of ATP released at synapses and by astrocytes . β-AR, β-adrenoceptor; G6P, glucose-6-phosphate. In panels c , d , f , i , the numbers in parentheses indicate the numbers of animals per experimental group. P values were determined by one-way ANOVA followed by Sidak’s post-hoc test ( c , d , f ) or two-way ANOVA ( i ).

Article Snippet: EEG and EMG electrode headmounts (Pinnacle Technology) were secured to the skull using stainless steel screws and silver epoxy was used for optimal electrical connectivity.

Techniques: Control, Activity Assay