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Mcs GmbH mea2100 system
Mea2100 System, supplied by Mcs GmbH, 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/mea2100/mea2100+system/pm40490012-121-6-12
Average 90 stars, based on 1 article reviews
mea2100 system - by Bioz Stars, 2026-10
90/100 stars

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Microelectrode Array:

Article Title: Evaluating In Vitro Neonatal Hypoxic-Ischemic Injury Using Neural Progenitors Derived from Human Embryonic Stem Cells.
Article Snippet: St e m C el ls a n d D ev el o p m en t Ev al u at in g in v it ro n e o n a ta l h yp o xi cis ch em ic in ju ry u si n g n e u ra l p ro g en it o rs d er iv ed f ro m h u m an e m b ry o n ic s te m c el ls ( D O I: 1 0 .1 0 8 9 /s cd .2 0 2 0 .0 0 1 8 ) Th is p a p er h as b ee n p ee r- re vi ew ed a n d a cc e p te d f o r p u b lic at io n , b u t h as y et t o u n d er go c o p ye d it in g a n d p ro o f co rr ec ti o n . T h e fi n al p u b lis h ed v er si o n m ay d if fe r fr o m t h is p ro o f. In hypoxic-ischemic encephalopathy, the Neural Progenitors (NPs) of the developing brain fail to replenish the oligodendrocyte progenitor cells lost during hypoxic-ischemic injury (HII).. Here, we aim to examine the influence of HII on the vulnerability of human NPs derived from human embryonic stem cells (hESCs) with regard to cell survival and oxidative stress, followed by assessment of cellular deregulation through measuring glutathione-levels, basal-calcium, glutamate-release and intracellular-calcium [Ca2+]i response under KCl and ATP stimulation.. NPs were further evaluated for their fundamental-potential of self-renewal & proliferation, neural and glial progenitor pool and migration.

Article Title: Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks
Article Snippet: The intensity of signal for each GluA1 pS831-positive cluster and the total number of puncta were measured using Metamorph software. .. Spontaneous extracellular electrical activity was recorded using an MEA (MEA2100, Multi Channel Systems MCS GmbH, Reutlingen, Germany). ..

Article Title: Impact of monomeric and aggregated wild-type and A30P/A53T double-mutant α-synuclein on antioxidant mechanism and glutamate metabolic profile of cultured astrocytes.
Article Snippet: Funding information This work is supported by a grant obtained from the Department of Biotechnology (DBT), Government of India, New Delhi; contract grant No. BT/PR21526/ MED/122/49/2016.. AR is supported by DST Inspire Ph.D. fellowship Abstract Serving as a source of glutathione and uptaking and metabolizing glutamate are the primary supportive role of astrocytes for the adjacent neurons.. Despite the clear physical association between astrocytes and αsynuclein, the effect of extracellular αsynuclein on these astrocytic functions has not yet been elucidated.

Article Title: Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks
Article Snippet: The intensity of signal for each GluA1 pS831-positive cluster and the total number of puncta were measured using Metamorph software. .. MEA recordings Spontaneous extracellular electrical activity was recorded using an MEA (MEA2100, Multi Channel Systems MCS GmbH, Reutlingen, Germany). ..

Activity Assay:

Article Title: Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks
Article Snippet: The intensity of signal for each GluA1 pS831-positive cluster and the total number of puncta were measured using Metamorph software. .. Spontaneous extracellular electrical activity was recorded using an MEA (MEA2100, Multi Channel Systems MCS GmbH, Reutlingen, Germany). ..

Article Title: Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks
Article Snippet: The intensity of signal for each GluA1 pS831-positive cluster and the total number of puncta were measured using Metamorph software. .. MEA recordings Spontaneous extracellular electrical activity was recorded using an MEA (MEA2100, Multi Channel Systems MCS GmbH, Reutlingen, Germany). ..

other:

Article Title: µSpikeHunter: An advanced computational tool for the analysis of neuronal communication and action potential propagation in microfluidic platforms
Article Snippet: The computational tool μSpikeHunter runs on both Microsoft Windows and Apple’s macOS operating systems, and is composed of two graphical user interfaces (GUIs): the main GUI, in which the data are imported and analyzed at the single-spike level, and the spike sorting GUI, in which the user can sort spikes into source clusters associated to different neurites. μSpikeHunter was developed to be compatible with recordings obtained using custom setups or commercial recording systems (MEA2100 from MultiChannel Systems MCS GmbH, Germany) for 60-, 120-, and 252-electrode MEAs.

Slice Preparation:

Article Title: Impact of monomeric and aggregated wild-type and A30P/A53T double-mutant α-synuclein on antioxidant mechanism and glutamate metabolic profile of cultured astrocytes.
Article Snippet: Funding information This work is supported by a grant obtained from the Department of Biotechnology (DBT), Government of India, New Delhi; contract grant No. BT/PR21526/ MED/122/49/2016.. AR is supported by DST Inspire Ph.D. fellowship Abstract Serving as a source of glutathione and uptaking and metabolizing glutamate are the primary supportive role of astrocytes for the adjacent neurons.. Despite the clear physical association between astrocytes and αsynuclein, the effect of extracellular αsynuclein on these astrocytic functions has not yet been elucidated.

Incubation:

Article Title: Impact of monomeric and aggregated wild-type and A30P/A53T double-mutant α-synuclein on antioxidant mechanism and glutamate metabolic profile of cultured astrocytes.
Article Snippet: Funding information This work is supported by a grant obtained from the Department of Biotechnology (DBT), Government of India, New Delhi; contract grant No. BT/PR21526/ MED/122/49/2016.. AR is supported by DST Inspire Ph.D. fellowship Abstract Serving as a source of glutathione and uptaking and metabolizing glutamate are the primary supportive role of astrocytes for the adjacent neurons.. Despite the clear physical association between astrocytes and αsynuclein, the effect of extracellular αsynuclein on these astrocytic functions has not yet been elucidated.



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Pharmacologically Mimicking the Reduced ERK1/2 Kinase Activity and Protein Expression found at 24 h post-TBI has a Significant Influence on Spontaneous and <t>Evoked</t> <t>Cortical</t> Excitability. A (i) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the ipsilateral cortical hemisphere. (ii) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the contralateral cortical hemisphere. B Representative blots for cortical ERK1/2 expression from (i) 4 h, (ii) 24 h and (iii) 72 h post-TBI, with GAPDH housekeeper protein for normalisation. C Temporal profile of the fluctuating ERK1/2 protein expression relative to sham from 4 to 72 h post-TBI showing a correlation of ERK1/2 expression with its respective activity at matching timepoints. Grey bars show the standard error of mean of the sham hemispheres (n = 6–18). D . (i) Exemplary placement of the coronal ex vivo brain slice on the <t>MEA</t> chip with the recording electrodes correlating to cortical layers 1–4 outlined in red. (ii) Representative five-minute traces of the spontaneous spiking activity from the control group (black) and the ERK-inhibited group (pink). (iii) Analysis of the spontaneous activity via mean spiking frequency between the control group (black) and the ERK-inhibited group (pink). (iv) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV lateral to the stimulation (0.5–5 V) electrode. Below, the correlating Input/Output Curve analysis from all recordings. (v) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. (vi) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 400 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. n = 11 (control) and n = 14 (ERKi). Statistical analysis for Western Blot was carried out using one-way ANOVA with post hoc Tukey’s multiple comparison test. Statistical analysis for mean spike frequency was carried out using unpaired t-test. Statistical analysis for input–output curves was carried out using two-way ANOVA with post hoc Šídák’s multiple comparisons test. p < 0.05
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Pharmacologically Mimicking the Reduced ERK1/2 Kinase Activity and Protein Expression found at 24 h post-TBI has a Significant Influence on Spontaneous and <t>Evoked</t> <t>Cortical</t> Excitability. A (i) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the ipsilateral cortical hemisphere. (ii) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the contralateral cortical hemisphere. B Representative blots for cortical ERK1/2 expression from (i) 4 h, (ii) 24 h and (iii) 72 h post-TBI, with GAPDH housekeeper protein for normalisation. C Temporal profile of the fluctuating ERK1/2 protein expression relative to sham from 4 to 72 h post-TBI showing a correlation of ERK1/2 expression with its respective activity at matching timepoints. Grey bars show the standard error of mean of the sham hemispheres (n = 6–18). D . (i) Exemplary placement of the coronal ex vivo brain slice on the <t>MEA</t> chip with the recording electrodes correlating to cortical layers 1–4 outlined in red. (ii) Representative five-minute traces of the spontaneous spiking activity from the control group (black) and the ERK-inhibited group (pink). (iii) Analysis of the spontaneous activity via mean spiking frequency between the control group (black) and the ERK-inhibited group (pink). (iv) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV lateral to the stimulation (0.5–5 V) electrode. Below, the correlating Input/Output Curve analysis from all recordings. (v) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. (vi) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 400 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. n = 11 (control) and n = 14 (ERKi). Statistical analysis for Western Blot was carried out using one-way ANOVA with post hoc Tukey’s multiple comparison test. Statistical analysis for mean spike frequency was carried out using unpaired t-test. Statistical analysis for input–output curves was carried out using two-way ANOVA with post hoc Šídák’s multiple comparisons test. p < 0.05
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Pharmacologically Mimicking the Reduced ERK1/2 Kinase Activity and Protein Expression found at 24 h post-TBI has a Significant Influence on Spontaneous and <t>Evoked</t> <t>Cortical</t> Excitability. A (i) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the ipsilateral cortical hemisphere. (ii) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the contralateral cortical hemisphere. B Representative blots for cortical ERK1/2 expression from (i) 4 h, (ii) 24 h and (iii) 72 h post-TBI, with GAPDH housekeeper protein for normalisation. C Temporal profile of the fluctuating ERK1/2 protein expression relative to sham from 4 to 72 h post-TBI showing a correlation of ERK1/2 expression with its respective activity at matching timepoints. Grey bars show the standard error of mean of the sham hemispheres (n = 6–18). D . (i) Exemplary placement of the coronal ex vivo brain slice on the <t>MEA</t> chip with the recording electrodes correlating to cortical layers 1–4 outlined in red. (ii) Representative five-minute traces of the spontaneous spiking activity from the control group (black) and the ERK-inhibited group (pink). (iii) Analysis of the spontaneous activity via mean spiking frequency between the control group (black) and the ERK-inhibited group (pink). (iv) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV lateral to the stimulation (0.5–5 V) electrode. Below, the correlating Input/Output Curve analysis from all recordings. (v) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. (vi) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 400 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. n = 11 (control) and n = 14 (ERKi). Statistical analysis for Western Blot was carried out using one-way ANOVA with post hoc Tukey’s multiple comparison test. Statistical analysis for mean spike frequency was carried out using unpaired t-test. Statistical analysis for input–output curves was carried out using two-way ANOVA with post hoc Šídák’s multiple comparisons test. p < 0.05
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Pharmacologically Mimicking the Reduced ERK1/2 Kinase Activity and Protein Expression found at 24 h post-TBI has a Significant Influence on Spontaneous and Evoked Cortical Excitability. A (i) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the ipsilateral cortical hemisphere. (ii) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the contralateral cortical hemisphere. B Representative blots for cortical ERK1/2 expression from (i) 4 h, (ii) 24 h and (iii) 72 h post-TBI, with GAPDH housekeeper protein for normalisation. C Temporal profile of the fluctuating ERK1/2 protein expression relative to sham from 4 to 72 h post-TBI showing a correlation of ERK1/2 expression with its respective activity at matching timepoints. Grey bars show the standard error of mean of the sham hemispheres (n = 6–18). D . (i) Exemplary placement of the coronal ex vivo brain slice on the MEA chip with the recording electrodes correlating to cortical layers 1–4 outlined in red. (ii) Representative five-minute traces of the spontaneous spiking activity from the control group (black) and the ERK-inhibited group (pink). (iii) Analysis of the spontaneous activity via mean spiking frequency between the control group (black) and the ERK-inhibited group (pink). (iv) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV lateral to the stimulation (0.5–5 V) electrode. Below, the correlating Input/Output Curve analysis from all recordings. (v) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. (vi) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 400 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. n = 11 (control) and n = 14 (ERKi). Statistical analysis for Western Blot was carried out using one-way ANOVA with post hoc Tukey’s multiple comparison test. Statistical analysis for mean spike frequency was carried out using unpaired t-test. Statistical analysis for input–output curves was carried out using two-way ANOVA with post hoc Šídák’s multiple comparisons test. p < 0.05

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex

doi: 10.1007/s00018-025-05638-4

Figure Lengend Snippet: Pharmacologically Mimicking the Reduced ERK1/2 Kinase Activity and Protein Expression found at 24 h post-TBI has a Significant Influence on Spontaneous and Evoked Cortical Excitability. A (i) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the ipsilateral cortical hemisphere. (ii) Temporal profile of ERK1/2 activity from 4 to 72 h post-TBI in the contralateral cortical hemisphere. B Representative blots for cortical ERK1/2 expression from (i) 4 h, (ii) 24 h and (iii) 72 h post-TBI, with GAPDH housekeeper protein for normalisation. C Temporal profile of the fluctuating ERK1/2 protein expression relative to sham from 4 to 72 h post-TBI showing a correlation of ERK1/2 expression with its respective activity at matching timepoints. Grey bars show the standard error of mean of the sham hemispheres (n = 6–18). D . (i) Exemplary placement of the coronal ex vivo brain slice on the MEA chip with the recording electrodes correlating to cortical layers 1–4 outlined in red. (ii) Representative five-minute traces of the spontaneous spiking activity from the control group (black) and the ERK-inhibited group (pink). (iii) Analysis of the spontaneous activity via mean spiking frequency between the control group (black) and the ERK-inhibited group (pink). (iv) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV lateral to the stimulation (0.5–5 V) electrode. Below, the correlating Input/Output Curve analysis from all recordings. (v) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 200 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. (vi) Overlaid representative LFPs of control (black) and ERK-inhibited (pink) slices from 400 μV above the stimulation (0.5–5 V) electrode in the direction of the dorsal cortical surface. Below, the correlating Input/Output Curve analysis from all recordings. n = 11 (control) and n = 14 (ERKi). Statistical analysis for Western Blot was carried out using one-way ANOVA with post hoc Tukey’s multiple comparison test. Statistical analysis for mean spike frequency was carried out using unpaired t-test. Statistical analysis for input–output curves was carried out using two-way ANOVA with post hoc Šídák’s multiple comparisons test. p < 0.05

Article Snippet: Extracellular recordings of the spontaneous neuronal activity and amplitude responses from an input/output curve protocol were acquired in the acute cortical brain slices with a two- chamber MEA system (MEA2100 System, Multi Channel Systems MCS GmbH).

Techniques: Activity Assay, Expressing, Ex Vivo, Slice Preparation, Control, Western Blot, Comparison

Inhibition of PKC Activity Rescues the Increased Spontaneous Activity of the 24-h post-TBI Contralateral Cortical Network back to Sham Level. A Representative slices from the ipsilateral (top) and contralateral (bottom) hemispheres on the MEA chip, with the recording electrodes outlined by the turquoise and purple rectangle, respectively. B (i) Mean spike frequency of the sham cortical hemisphere at the beginning and end of the MEA recording duration. (ii) Mean spike frequency of the post-TBI ipsilateral hemisphere before and after the 25-min chelerythrine wash-in period. (iii) Mean spike frequency of the post-TBI contralateral hemisphere before and after the 25-min chelerythrine wash-in period. C (i) Sham, ipsilateral and contralateral hemisphere mean spike frequency before the wash-in of chelerythrine. (ii) Sham, ipsilateral and contralateral hemisphere mean spike frequency after the wash-in of chelerythrine to the post-TBI slices. (iii) Representative five-minute traces of the spontaneous spiking activity from the same electrode before (light purple) and after (dark purple) the wash-in of chelerythrine to the 24-h post-TBI contralateral hemisphere. Statistical analysis of each hemisphere group before and after chelerythrine application/25-min recording duration was carried out using paired t-test. Statistical analysis comparing the three groups before and the three groups after the chelerythrine wash-in to post-TBI slices was carried out using one-way ANOVA and post hoc Tukey multiple comparison test. p < 0.05

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex

doi: 10.1007/s00018-025-05638-4

Figure Lengend Snippet: Inhibition of PKC Activity Rescues the Increased Spontaneous Activity of the 24-h post-TBI Contralateral Cortical Network back to Sham Level. A Representative slices from the ipsilateral (top) and contralateral (bottom) hemispheres on the MEA chip, with the recording electrodes outlined by the turquoise and purple rectangle, respectively. B (i) Mean spike frequency of the sham cortical hemisphere at the beginning and end of the MEA recording duration. (ii) Mean spike frequency of the post-TBI ipsilateral hemisphere before and after the 25-min chelerythrine wash-in period. (iii) Mean spike frequency of the post-TBI contralateral hemisphere before and after the 25-min chelerythrine wash-in period. C (i) Sham, ipsilateral and contralateral hemisphere mean spike frequency before the wash-in of chelerythrine. (ii) Sham, ipsilateral and contralateral hemisphere mean spike frequency after the wash-in of chelerythrine to the post-TBI slices. (iii) Representative five-minute traces of the spontaneous spiking activity from the same electrode before (light purple) and after (dark purple) the wash-in of chelerythrine to the 24-h post-TBI contralateral hemisphere. Statistical analysis of each hemisphere group before and after chelerythrine application/25-min recording duration was carried out using paired t-test. Statistical analysis comparing the three groups before and the three groups after the chelerythrine wash-in to post-TBI slices was carried out using one-way ANOVA and post hoc Tukey multiple comparison test. p < 0.05

Article Snippet: Extracellular recordings of the spontaneous neuronal activity and amplitude responses from an input/output curve protocol were acquired in the acute cortical brain slices with a two- chamber MEA system (MEA2100 System, Multi Channel Systems MCS GmbH).

Techniques: Inhibition, Activity Assay, Comparison