dendrotoxin  (Alomone Labs)


Bioz Verified Symbol Alomone Labs is a verified supplier
Bioz Manufacturer Symbol Alomone Labs manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93

    Structured Review

    Alomone Labs dendrotoxin
    Dendrotoxin, 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/dendrotoxin/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dendrotoxin - by Bioz Stars, 2022-07
    93/100 stars

    Images

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 93
    Alomone Labs dtx i
    An I D -like current activated from the resting membrane potential is blocked by low doses of 4-AP A , firing response upon injection of a steady inward current (0.1 nA for 800 ms) from a resting membrane potential of -61 mV. Notice the afterhyperpolarisation at the end of the pulse. B , increasing the stimulation intensity (0.2 nA) produced in the same neurone repetitive firing with strong adaptation followed by a prominent afterhyperpolarisation. C , upon membrane hyperpolarisation (-68 mV), the same neurone responded to a current step of 0.2 nA with a reduced number of spikes and with a larger delay in the appearance of the first action potential. Insets in A - C represent the same traces on an expanded time scale. D , mean delay to the appearance of the first spike from the resting membrane potential (control, ctl, -56 ± 1 mV; n = 12) and from a more hyperpolarised membrane potential (hyper, -66 ± 1 mV). E and F , voltage responses to a 0.2 nA current step in control conditions ( E ) and in the presence of 4-AP ( F ) for a different neurone. G , mean delay to the generation of the first spike in control conditions and in the presence of 4-AP ( n = 14). H and I , firing responses to a 0.2 nA current step in control conditions ( H ) and in the presence of <t>DTX-I</t> (DTX, I ; scale bar as in E and F ). J , mean delay to the first spike appearance in control conditions and in the presence of DTX-I ( n = 4). * P
    Dtx I, 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/dtx i/product/Alomone Labs
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    dtx i - by Bioz Stars, 2022-07
    93/100 stars
      Buy from Supplier

    Image Search Results


    An I D -like current activated from the resting membrane potential is blocked by low doses of 4-AP A , firing response upon injection of a steady inward current (0.1 nA for 800 ms) from a resting membrane potential of -61 mV. Notice the afterhyperpolarisation at the end of the pulse. B , increasing the stimulation intensity (0.2 nA) produced in the same neurone repetitive firing with strong adaptation followed by a prominent afterhyperpolarisation. C , upon membrane hyperpolarisation (-68 mV), the same neurone responded to a current step of 0.2 nA with a reduced number of spikes and with a larger delay in the appearance of the first action potential. Insets in A - C represent the same traces on an expanded time scale. D , mean delay to the appearance of the first spike from the resting membrane potential (control, ctl, -56 ± 1 mV; n = 12) and from a more hyperpolarised membrane potential (hyper, -66 ± 1 mV). E and F , voltage responses to a 0.2 nA current step in control conditions ( E ) and in the presence of 4-AP ( F ) for a different neurone. G , mean delay to the generation of the first spike in control conditions and in the presence of 4-AP ( n = 14). H and I , firing responses to a 0.2 nA current step in control conditions ( H ) and in the presence of DTX-I (DTX, I ; scale bar as in E and F ). J , mean delay to the first spike appearance in control conditions and in the presence of DTX-I ( n = 4). * P

    Journal: The Journal of Physiology

    Article Title: An Id-like current that is downregulated by Ca2+ modulates information coding at CA3-CA3 synapses in the rat hippocampus

    doi: 10.1113/jphysiol.2003.051045

    Figure Lengend Snippet: An I D -like current activated from the resting membrane potential is blocked by low doses of 4-AP A , firing response upon injection of a steady inward current (0.1 nA for 800 ms) from a resting membrane potential of -61 mV. Notice the afterhyperpolarisation at the end of the pulse. B , increasing the stimulation intensity (0.2 nA) produced in the same neurone repetitive firing with strong adaptation followed by a prominent afterhyperpolarisation. C , upon membrane hyperpolarisation (-68 mV), the same neurone responded to a current step of 0.2 nA with a reduced number of spikes and with a larger delay in the appearance of the first action potential. Insets in A - C represent the same traces on an expanded time scale. D , mean delay to the appearance of the first spike from the resting membrane potential (control, ctl, -56 ± 1 mV; n = 12) and from a more hyperpolarised membrane potential (hyper, -66 ± 1 mV). E and F , voltage responses to a 0.2 nA current step in control conditions ( E ) and in the presence of 4-AP ( F ) for a different neurone. G , mean delay to the generation of the first spike in control conditions and in the presence of 4-AP ( n = 14). H and I , firing responses to a 0.2 nA current step in control conditions ( H ) and in the presence of DTX-I (DTX, I ; scale bar as in E and F ). J , mean delay to the first spike appearance in control conditions and in the presence of DTX-I ( n = 4). * P

    Article Snippet: The following drugs were used: 4-AP (Sigma); DTX-I (Alomone Labs, Jerusalem, Israel); DL-2-amino-5-phosphonopentaoic acid (D-AP5), 6,7-dinitroquinoxaline-2,3-dione (DNQX), bicuculline and CGP 55845 (all purchased from Tocris Cookson, Bristol, UK).

    Techniques: Injection, Mass Spectrometry, Produced, CTL Assay

    Experimental demonstration of postinhibitory facilitation. A : patch-clamp recordings (in vitro gerbil medial superior olive [MSO], P22) of membrane potential for a pair of inhibitory and subthreshold excitatory inputs, G ex = 20 nS, are applied with the dynamic-clamp method with varying preceding times of inhibition, G inh = 100 nS, (see text for experimental details). B : elimination of PIF after application of the I KLT blocker dendrotoxin I (DTXI). Over the same range of δ as in A the inhibitory conductance transient (IPSG) does not facilitate the subthreshold excitatory conductance (EPSG) to generate a spike. C: G ex was increased by 5% relative to B for just-suprathreshold EPSG, which was preceded by an IPSG in the presence of DTXI. In all cases of the δ -range expected to show facilitation the IPSG suppressed spiking–no facilitation. To compensate for membrane conductance changes in B and C , the amplitudes of G ex and G inh were reduced approximately 2-fold from the control conditions.

    Journal: Journal of neurophysiology

    Article Title: Well-Timed, Brief Inhibition Can Promote Spiking: Postinhibitory Facilitation

    doi: 10.1152/jn.00752.2005

    Figure Lengend Snippet: Experimental demonstration of postinhibitory facilitation. A : patch-clamp recordings (in vitro gerbil medial superior olive [MSO], P22) of membrane potential for a pair of inhibitory and subthreshold excitatory inputs, G ex = 20 nS, are applied with the dynamic-clamp method with varying preceding times of inhibition, G inh = 100 nS, (see text for experimental details). B : elimination of PIF after application of the I KLT blocker dendrotoxin I (DTXI). Over the same range of δ as in A the inhibitory conductance transient (IPSG) does not facilitate the subthreshold excitatory conductance (EPSG) to generate a spike. C: G ex was increased by 5% relative to B for just-suprathreshold EPSG, which was preceded by an IPSG in the presence of DTXI. In all cases of the δ -range expected to show facilitation the IPSG suppressed spiking–no facilitation. To compensate for membrane conductance changes in B and C , the amplitudes of G ex and G inh were reduced approximately 2-fold from the control conditions.

    Article Snippet: To block I KLT currents 8 nM of dendrotoxin I (DTXI) (Alomone Labs, Jerusalem, Israel) was added to the bathing solution.

    Techniques: Patch Clamp, In Vitro, Inhibition

    Functional expression of Kv1.1 channel in SGZ neural progenitor cells expressing Fezf2-GFP at postnatal 2 weeks. ( A ) In situ hybridization results showed that Kcna1 mRNA is expressed in Fezf2-GFP-positive neural progenitor cells. Inset is displayed at a higher magnification. ( B ) Kcna1 mRNA was not detected in the Kv1.1KO mouse, which served as a negative control. ( C ) Kv1.1 protein was expressed in the doublecortin (DCX)-expressing late-stage neural progenitor cells (arrows) but not Sox2-positive early-stage neural progenitor cells. Kv1.1 protein was highly expressed in the inhibitory interneurons (yellow arrows). ( D–J ) Pharmacological isolation of Kv1 currents in Fezf2-GFP-positive cells. Kv1.1 currents were elicited by trains of voltage steps from -80 mV to +40 mV in 10 mV increments from the holding potential of -80 mV in the absence ( D and G ) or presence of the Kv1-specific blocker dendrotoxin-k (DTX-K; 100 nM) ( E and H ). The DTX-K-sensitive currents were considered Kv1-mediated potassium currents ( F, I, and J ), which were much reduced in the Kv1.1KO mice. n = 4 cells from each phenotype. Scale bar = 20 μm in ( C ). Data are presented as mean ± SEM.

    Journal: eLife

    Article Title: Kv1.1 channels regulate early postnatal neurogenesis in mouse hippocampus via the TrkB signaling pathway

    doi: 10.7554/eLife.58779

    Figure Lengend Snippet: Functional expression of Kv1.1 channel in SGZ neural progenitor cells expressing Fezf2-GFP at postnatal 2 weeks. ( A ) In situ hybridization results showed that Kcna1 mRNA is expressed in Fezf2-GFP-positive neural progenitor cells. Inset is displayed at a higher magnification. ( B ) Kcna1 mRNA was not detected in the Kv1.1KO mouse, which served as a negative control. ( C ) Kv1.1 protein was expressed in the doublecortin (DCX)-expressing late-stage neural progenitor cells (arrows) but not Sox2-positive early-stage neural progenitor cells. Kv1.1 protein was highly expressed in the inhibitory interneurons (yellow arrows). ( D–J ) Pharmacological isolation of Kv1 currents in Fezf2-GFP-positive cells. Kv1.1 currents were elicited by trains of voltage steps from -80 mV to +40 mV in 10 mV increments from the holding potential of -80 mV in the absence ( D and G ) or presence of the Kv1-specific blocker dendrotoxin-k (DTX-K; 100 nM) ( E and H ). The DTX-K-sensitive currents were considered Kv1-mediated potassium currents ( F, I, and J ), which were much reduced in the Kv1.1KO mice. n = 4 cells from each phenotype. Scale bar = 20 μm in ( C ). Data are presented as mean ± SEM.

    Article Snippet: Dendrotoxin-κ (Alomone Labs, Israel) was used to specifically block the Kv1.1 channel.

    Techniques: Functional Assay, Expressing, In Situ Hybridization, Negative Control, Isolation, Mouse Assay

    GABAergic inputs enhance excitability at E14 but are inhibitory at E18 in NM neurons. A , Neurons held in whole-cell current clamp were stimulated with depolarizing current pulses of variable amplitude. GABAergic synaptic stimulation was performed with a bipolar electrode in the presence of bath-applied DNQX and AP5. B , Under control conditions, GPSPs summated with current pulses in E14 neurons to induce spiking, but shunted current pulses at E18 to prevent spiking (left column; stimulus artifacts reduced for clarity). Addition of DTX-I to the bath (right column) induced summation between GPSP and current pulses in neurons of both ages. C , Rheobase during a GPSP was subtracted from the control condition for E14 ( n = 6) and E18 ( n = 7) neurons. All E14 neurons ( n = 6) exhibit negative changes in rheobase, indicating enhancement of excitability. This effect was significantly enhanced by addition of DTX-I (* p

    Journal: The Journal of Neuroscience

    Article Title: A Developmental Switch to GABAergic Inhibition Dependent on Increases in Kv1-Type K+ Currents

    doi: 10.1523/JNEUROSCI.5266-06.2007

    Figure Lengend Snippet: GABAergic inputs enhance excitability at E14 but are inhibitory at E18 in NM neurons. A , Neurons held in whole-cell current clamp were stimulated with depolarizing current pulses of variable amplitude. GABAergic synaptic stimulation was performed with a bipolar electrode in the presence of bath-applied DNQX and AP5. B , Under control conditions, GPSPs summated with current pulses in E14 neurons to induce spiking, but shunted current pulses at E18 to prevent spiking (left column; stimulus artifacts reduced for clarity). Addition of DTX-I to the bath (right column) induced summation between GPSP and current pulses in neurons of both ages. C , Rheobase during a GPSP was subtracted from the control condition for E14 ( n = 6) and E18 ( n = 7) neurons. All E14 neurons ( n = 6) exhibit negative changes in rheobase, indicating enhancement of excitability. This effect was significantly enhanced by addition of DTX-I (* p

    Article Snippet: TTX and DTX-I were obtained from Alomone Labs (Jerusalem, Israel).

    Techniques: