polyclonal rabbit anti trek2 antibody Search Results


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    Alomone Labs rabbit anti trek 1
    <t>TREK-1</t> KO depresses the ratio of paired-pulse facilitation, occludes long-term potentiation and impairs hippocampal-dependent space memory. a TREK-1 KO decreases the ratio of paired-pulse facilitation (PPR) of CA3–CA1 synapses. Left , in a WT and TREK-1 KO neuron as indicated, two consecutive EPSCs were induced by SC stimulation pulses at 40 ms interval. b LTP in the CA1 region was induced by high-frequency stimulation of SC (HFS, arrow). The LTP in TREK-1 KO mice was markedly occluded (n = 10) when compared to WT (n = 12). Left , Representative fEPSP traces CA1 region before (solid traces) and 40 min after HFS of SC afferents (dashed traces) in WT and TREK-1 KO mice. c Quantification of fEPSP slope change reveals a TREK-1 KO induced occlusion of LTP. The quantification was made by averaging normalized fEPSP slope from 36 to 40 min after HFS or low-frequency stimulation, as a short line indicated in the time course of B. d New object recognition. Left , schematic for test protocol. Right , the bar graph shows TREK-1 KO mice (n=11) spent less time on new objects than WT mice (n=10), as the discrimination index decreasing. Student’s t -test was used. * P
    Rabbit Anti Trek 1, 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
    https://www.bioz.com/result/rabbit anti trek 1/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit anti trek 1 - by Bioz Stars, 2022-05
    92/100 stars
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    93
    Alomone Labs anti trek 2
    <t>TREK-1</t> KO depresses the ratio of paired-pulse facilitation, occludes long-term potentiation and impairs hippocampal-dependent space memory. a TREK-1 KO decreases the ratio of paired-pulse facilitation (PPR) of CA3–CA1 synapses. Left , in a WT and TREK-1 KO neuron as indicated, two consecutive EPSCs were induced by SC stimulation pulses at 40 ms interval. b LTP in the CA1 region was induced by high-frequency stimulation of SC (HFS, arrow). The LTP in TREK-1 KO mice was markedly occluded (n = 10) when compared to WT (n = 12). Left , Representative fEPSP traces CA1 region before (solid traces) and 40 min after HFS of SC afferents (dashed traces) in WT and TREK-1 KO mice. c Quantification of fEPSP slope change reveals a TREK-1 KO induced occlusion of LTP. The quantification was made by averaging normalized fEPSP slope from 36 to 40 min after HFS or low-frequency stimulation, as a short line indicated in the time course of B. d New object recognition. Left , schematic for test protocol. Right , the bar graph shows TREK-1 KO mice (n=11) spent less time on new objects than WT mice (n=10), as the discrimination index decreasing. Student’s t -test was used. * P
    Anti Trek 2, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti trek 2/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti trek 2 - by Bioz Stars, 2022-05
    93/100 stars
      Buy from Supplier

    Image Search Results


    TREK-1 KO depresses the ratio of paired-pulse facilitation, occludes long-term potentiation and impairs hippocampal-dependent space memory. a TREK-1 KO decreases the ratio of paired-pulse facilitation (PPR) of CA3–CA1 synapses. Left , in a WT and TREK-1 KO neuron as indicated, two consecutive EPSCs were induced by SC stimulation pulses at 40 ms interval. b LTP in the CA1 region was induced by high-frequency stimulation of SC (HFS, arrow). The LTP in TREK-1 KO mice was markedly occluded (n = 10) when compared to WT (n = 12). Left , Representative fEPSP traces CA1 region before (solid traces) and 40 min after HFS of SC afferents (dashed traces) in WT and TREK-1 KO mice. c Quantification of fEPSP slope change reveals a TREK-1 KO induced occlusion of LTP. The quantification was made by averaging normalized fEPSP slope from 36 to 40 min after HFS or low-frequency stimulation, as a short line indicated in the time course of B. d New object recognition. Left , schematic for test protocol. Right , the bar graph shows TREK-1 KO mice (n=11) spent less time on new objects than WT mice (n=10), as the discrimination index decreasing. Student’s t -test was used. * P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO depresses the ratio of paired-pulse facilitation, occludes long-term potentiation and impairs hippocampal-dependent space memory. a TREK-1 KO decreases the ratio of paired-pulse facilitation (PPR) of CA3–CA1 synapses. Left , in a WT and TREK-1 KO neuron as indicated, two consecutive EPSCs were induced by SC stimulation pulses at 40 ms interval. b LTP in the CA1 region was induced by high-frequency stimulation of SC (HFS, arrow). The LTP in TREK-1 KO mice was markedly occluded (n = 10) when compared to WT (n = 12). Left , Representative fEPSP traces CA1 region before (solid traces) and 40 min after HFS of SC afferents (dashed traces) in WT and TREK-1 KO mice. c Quantification of fEPSP slope change reveals a TREK-1 KO induced occlusion of LTP. The quantification was made by averaging normalized fEPSP slope from 36 to 40 min after HFS or low-frequency stimulation, as a short line indicated in the time course of B. d New object recognition. Left , schematic for test protocol. Right , the bar graph shows TREK-1 KO mice (n=11) spent less time on new objects than WT mice (n=10), as the discrimination index decreasing. Student’s t -test was used. * P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Mouse Assay

    TREK-1 KO depolarizes membrane potential and increases input resistance of hippocampal pyramidal neurons. a TREK-1 (left) and neuronal marker NeuN (middle) immunostaining in the hippocampal CA1 region. Areas outlined in the square boxes are shown in higher magnification in the lower panels where TREK-1 and NeuN staining are nicely co-localized in neuronal soma and primary dendritic processes. Scale bar represents 25 μm. b TREK-1 KO depolarizes the membrane potential of CA1 pyramidal neurons. c TREK-1 KO increases the input resistance (R in ) of CA1 pyramidal neurons in K + -based physiological pipette solution ([K + ] p ) but not in Cs + -based pipette solution ([Cs + ] p ). d The membrane capacitance (C M ) is not altered in CA1 pyramidal neurons in TREK-1 KO mice. Numbers of neurons analyzed are shown in bars. Statistical significance was evaluated by Student’s t-test. (* P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO depolarizes membrane potential and increases input resistance of hippocampal pyramidal neurons. a TREK-1 (left) and neuronal marker NeuN (middle) immunostaining in the hippocampal CA1 region. Areas outlined in the square boxes are shown in higher magnification in the lower panels where TREK-1 and NeuN staining are nicely co-localized in neuronal soma and primary dendritic processes. Scale bar represents 25 μm. b TREK-1 KO depolarizes the membrane potential of CA1 pyramidal neurons. c TREK-1 KO increases the input resistance (R in ) of CA1 pyramidal neurons in K + -based physiological pipette solution ([K + ] p ) but not in Cs + -based pipette solution ([Cs + ] p ). d The membrane capacitance (C M ) is not altered in CA1 pyramidal neurons in TREK-1 KO mice. Numbers of neurons analyzed are shown in bars. Statistical significance was evaluated by Student’s t-test. (* P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Marker, Immunostaining, Staining, Transferring, Mouse Assay

    TREK-1 KO increases the excitability of CA1 pyramidal neurons. a Left, a 100 pA/300 ms current step induced 4 and 7 spikes in a WT and TREK-1 KO CA1 pyramidal neuron, respectively. Cells were held at −70 mV. Right, a series of current steps, ranging from 10 pA to 230 pA at 300 ms duration and 20 pA increment, induced a steeper current input-spike output relationship in TREK-1KO (n = 14) than WT neurons (n = 9). b Rheobase current for neuronal firing threshold. The inset shows the current steps from 10 pA −100 pA steps at 10 ms duration and 10 pA increments for detecting of the rheobase current and threshold (dash line) for neuronal firing in a WT and TREK-1 KO neuron, respectively. c TREK-1 KO significantly reduces the rheobase currents. d TREK-1 KO decreases the threshold for neuronal firing. e TREK-1 KO does not affect the amplitude of neuronal firing spikes. Statistical significance was evaluated by Student’s t -test (bar graphs) or two-way ANOVA followed by a post-hoc Tukey HSD test (input-output plots). * P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO increases the excitability of CA1 pyramidal neurons. a Left, a 100 pA/300 ms current step induced 4 and 7 spikes in a WT and TREK-1 KO CA1 pyramidal neuron, respectively. Cells were held at −70 mV. Right, a series of current steps, ranging from 10 pA to 230 pA at 300 ms duration and 20 pA increment, induced a steeper current input-spike output relationship in TREK-1KO (n = 14) than WT neurons (n = 9). b Rheobase current for neuronal firing threshold. The inset shows the current steps from 10 pA −100 pA steps at 10 ms duration and 10 pA increments for detecting of the rheobase current and threshold (dash line) for neuronal firing in a WT and TREK-1 KO neuron, respectively. c TREK-1 KO significantly reduces the rheobase currents. d TREK-1 KO decreases the threshold for neuronal firing. e TREK-1 KO does not affect the amplitude of neuronal firing spikes. Statistical significance was evaluated by Student’s t -test (bar graphs) or two-way ANOVA followed by a post-hoc Tukey HSD test (input-output plots). * P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques:

    TREK-1 KO does not alter astrocyte K + conductance or astrocyte syncytial isopotentiality. a TREK-1 immunostaining signal is negligible in astrocytes. TREK-1 (red), NeuN (blue) double staining in Aldh1l1-eGFP mouse in CA1 region. Scale bar: 25 μm. b TREK-1 OK does not alter the resting V M of hippocampal astrocytes at CA1 region (WT, n=33; TREK-1 KO, n=31). c TREK-1 KO does not alter the passive K + conductance of astrocytes. Astrocyte was held at −80 mV and the membrane currents were induced by command voltages from −180 to +20 mV with 10 mV increment (inset, command voltages). Astrocytes in both genotypes showed a similar linear I-V relationship membrane conductance (passive) and comparable amplitude of passive conductance. d The I-V curves that were constructed from the current amplitudes. The current amplitude at y1 (V +20 mV ) and y2 (V -180 mV ). e Astrocyte syncytial isopotentiality remains intact in TREK-1 KO mice. Left , a schematic illustration of the use of non-physiological [Na + ] p or [Cs + ] p to examine the existence of syncytial isopotentiality in an astrocyte network. Right , representative V M,ss recordings with [K + ] p , [Na + ] p and [Cs + ] p , respectively. Insets show an unchanged V M,ss in TREK-1 KO astrocytes. Student’s t -test was used.

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO does not alter astrocyte K + conductance or astrocyte syncytial isopotentiality. a TREK-1 immunostaining signal is negligible in astrocytes. TREK-1 (red), NeuN (blue) double staining in Aldh1l1-eGFP mouse in CA1 region. Scale bar: 25 μm. b TREK-1 OK does not alter the resting V M of hippocampal astrocytes at CA1 region (WT, n=33; TREK-1 KO, n=31). c TREK-1 KO does not alter the passive K + conductance of astrocytes. Astrocyte was held at −80 mV and the membrane currents were induced by command voltages from −180 to +20 mV with 10 mV increment (inset, command voltages). Astrocytes in both genotypes showed a similar linear I-V relationship membrane conductance (passive) and comparable amplitude of passive conductance. d The I-V curves that were constructed from the current amplitudes. The current amplitude at y1 (V +20 mV ) and y2 (V -180 mV ). e Astrocyte syncytial isopotentiality remains intact in TREK-1 KO mice. Left , a schematic illustration of the use of non-physiological [Na + ] p or [Cs + ] p to examine the existence of syncytial isopotentiality in an astrocyte network. Right , representative V M,ss recordings with [K + ] p , [Na + ] p and [Cs + ] p , respectively. Insets show an unchanged V M,ss in TREK-1 KO astrocytes. Student’s t -test was used.

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Immunostaining, Double Staining, Construct, Mouse Assay

    TREK-1 KO increases excitatory and inhibitory synaptic transmission in CA1 pyramidal neurons. a The frequency but not the amplitude of mEPSCs increases in TREK-1 KO neurons. mEPSCs were recorded in the presence of 0.5 μM TTX and 100 μM PTX. Top , representative mEPSCs traces; Bottom , the cumulative probability of the mEPSC frequency (left) and amplitude (right). b Input-output relationship of EPSCs in CA1 neurons. Input refers to graded electrical stimulation of Schaffer collateral (SC), whereas output refers to SC stimulation-induced whole-cell EPSCs. The neuronal EPSCs outputs show an increase in TREK-1 KO neurons (n=19) compared to wild-type neurons (n=17). c Left , the SC stimulation-induced EPSCs and IPSCs were recorded from the same neuron by varying holding V M from −70 mV to 0 mV, respectively. TREK-1 KO resulted in an enhanced EPSCs and IPSCs compared to wildtype ( P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO increases excitatory and inhibitory synaptic transmission in CA1 pyramidal neurons. a The frequency but not the amplitude of mEPSCs increases in TREK-1 KO neurons. mEPSCs were recorded in the presence of 0.5 μM TTX and 100 μM PTX. Top , representative mEPSCs traces; Bottom , the cumulative probability of the mEPSC frequency (left) and amplitude (right). b Input-output relationship of EPSCs in CA1 neurons. Input refers to graded electrical stimulation of Schaffer collateral (SC), whereas output refers to SC stimulation-induced whole-cell EPSCs. The neuronal EPSCs outputs show an increase in TREK-1 KO neurons (n=19) compared to wild-type neurons (n=17). c Left , the SC stimulation-induced EPSCs and IPSCs were recorded from the same neuron by varying holding V M from −70 mV to 0 mV, respectively. TREK-1 KO resulted in an enhanced EPSCs and IPSCs compared to wildtype ( P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Transmission Assay

    TREK-1 null alters dendritic sprouting and the number of spines. a Representative images of CA1 pyramidal neurons revealed by electrode biocytin-loading followed by Alexa 488-conjugated streptavidin staining. Scale bar: 100 μm. b-d Summary of the total dendritic length (B), branch numbers (C) in both apical and basal dendritic trees, and apical dendritic arborization in terms of the number of intersections (D). e Representative higher resolution 3D confocal dendritic segment images for spine detection, classification, and measurements. Scale bar: 3 μm. f Summary of the dendritic spine densities in WT and TREK-1 KO groups. g Quantification of dendritic spine subtypes. Left , images of the four different spine subtypes. Right , quantification of mature and immature dendritic spine subtypes of CA1 neurons. The numbers of the dendritic segments used for quantification are shown in the bars, and these segments were obtained from 4–7 mice in each group. h Western immunoblots show comparable levels of expression of presynaptic (synaptophysin), and postsynaptic (PSD-95) proteins in WT and TREK-1 KO mice. GAPDH was used as a protein quantity loading control. Data for all bar graphs were analyzed using Student’s t -test. In C , the comparison of the number of intersections between the two groups was analyzed using repeated-measures two-way ANOVA. (* P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 null alters dendritic sprouting and the number of spines. a Representative images of CA1 pyramidal neurons revealed by electrode biocytin-loading followed by Alexa 488-conjugated streptavidin staining. Scale bar: 100 μm. b-d Summary of the total dendritic length (B), branch numbers (C) in both apical and basal dendritic trees, and apical dendritic arborization in terms of the number of intersections (D). e Representative higher resolution 3D confocal dendritic segment images for spine detection, classification, and measurements. Scale bar: 3 μm. f Summary of the dendritic spine densities in WT and TREK-1 KO groups. g Quantification of dendritic spine subtypes. Left , images of the four different spine subtypes. Right , quantification of mature and immature dendritic spine subtypes of CA1 neurons. The numbers of the dendritic segments used for quantification are shown in the bars, and these segments were obtained from 4–7 mice in each group. h Western immunoblots show comparable levels of expression of presynaptic (synaptophysin), and postsynaptic (PSD-95) proteins in WT and TREK-1 KO mice. GAPDH was used as a protein quantity loading control. Data for all bar graphs were analyzed using Student’s t -test. In C , the comparison of the number of intersections between the two groups was analyzed using repeated-measures two-way ANOVA. (* P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Staining, Mouse Assay, Western Blot, Expressing

    TREK-1 KO increases the active/silent ratio of SC-CA1 glutamatergic synapses. a In the presence of PTX, the AMPA-EPSC and NMDA-EPSC in CA1 pyramidal neurons were induced by SC stimulation at the holding V M of −70 and +40 mV, respectively. TREK-1 KO increases the AMPA-EPSC/ NMDA-EPSC ratio. b The amplitudes of SC stimulation-induced NMDA receptor currents are comparable between WT and TREK-1 KO neurons. The NMDA receptor currents were isolated by adding PTX and NBQX for inhibition of GABAa and AMPA receptors, respectively. c Minimal SC stimulation-induced AMPA-EPSC (holding at −70 mV) and NMDA-EPSC (holding at +40 mV) in WT and TREK-1 KO neurons. In each case, 6 consecutive traces are superimposed to show the variation from absence to the presence of SC stimulation-induced EPSCs. The NMDA-EPSCs were recorded in the presence of 10 μM NBQX. d Use of minimal SC stimulation, the induced and failed EPSC events are plotted over a 40 min duration in a WT and TREK-1 KO neuron as indicated. In each case, the AMPA-EPSC events were recorded first by holding the cell at −70 mV, and the NMDA-EPSC events were recorded afterward by switching the holding to +40 mV in the presence of 10 μM NBQX. e Summary of the data from D, a less failure rate without affecting the amplitude of minimal SC stimulation-induced AMPA-EPSCs occurred in TREK-1 KO neurons. f Summary of the data from D, no change in either the failure rate or the amplitude of minimal SC stimulation-induced NMDA-EPSCs in TREK-1 KO neurons. Student’s t -test was used. * P

    Journal: Molecular neurobiology

    Article Title: TREK-1 null impairs neuronal excitability, synaptic plasticity, and cognitive function

    doi: 10.1007/s12035-019-01828-x

    Figure Lengend Snippet: TREK-1 KO increases the active/silent ratio of SC-CA1 glutamatergic synapses. a In the presence of PTX, the AMPA-EPSC and NMDA-EPSC in CA1 pyramidal neurons were induced by SC stimulation at the holding V M of −70 and +40 mV, respectively. TREK-1 KO increases the AMPA-EPSC/ NMDA-EPSC ratio. b The amplitudes of SC stimulation-induced NMDA receptor currents are comparable between WT and TREK-1 KO neurons. The NMDA receptor currents were isolated by adding PTX and NBQX for inhibition of GABAa and AMPA receptors, respectively. c Minimal SC stimulation-induced AMPA-EPSC (holding at −70 mV) and NMDA-EPSC (holding at +40 mV) in WT and TREK-1 KO neurons. In each case, 6 consecutive traces are superimposed to show the variation from absence to the presence of SC stimulation-induced EPSCs. The NMDA-EPSCs were recorded in the presence of 10 μM NBQX. d Use of minimal SC stimulation, the induced and failed EPSC events are plotted over a 40 min duration in a WT and TREK-1 KO neuron as indicated. In each case, the AMPA-EPSC events were recorded first by holding the cell at −70 mV, and the NMDA-EPSC events were recorded afterward by switching the holding to +40 mV in the presence of 10 μM NBQX. e Summary of the data from D, a less failure rate without affecting the amplitude of minimal SC stimulation-induced AMPA-EPSCs occurred in TREK-1 KO neurons. f Summary of the data from D, no change in either the failure rate or the amplitude of minimal SC stimulation-induced NMDA-EPSCs in TREK-1 KO neurons. Student’s t -test was used. * P

    Article Snippet: They were rabbit anti-TREK-1 (1:1000, Alomone Labs, Jerusalem, Israel) and mouse anti-NeuN (1:1000; Abcam, Cambridge, MA, USA).

    Techniques: Isolation, Inhibition