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d-cppene  (Sandoz)

 
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    Sandoz d-cppene
    D Cppene, supplied by Sandoz, 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/d-cppene/d+cppene/pm37474350-26-14-7
    Average 90 stars, based on 1 article reviews
    d-cppene - by Bioz Stars, 2026-10
    90/100 stars

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    other:

    Article Title: Positive Modulatory Interactions of NMDA Receptor GluN1/2B Ligand Binding Domains Attenuate Antagonists Activity.
    Article Snippet: The structural homology of this region with other subunits across the iGluR family has been exploited to develop a large number of competitive antagonists (Selfotel– Novartis, Gavestinel-GlaxoSmithKline, D-CPPene -Sandoz, and GV196771–GlaxoSmithKline) that serve as chemical tools to study NMDA receptor physiology or are considered as drug candidates for the treatment of neurological disorders and for preventing death and long term disability after stroke and traumatic brain injury in human beings, as extensively reviewed in (Muir, 2006) and (Traynelis et al., 2010).

    Article Title: The 5-HT2A receptor antagonist M100907 is more effective in counteracting NMDA antagonist- than dopamine agonist-induced hyperactivity in mice.
    Article Snippet: The purpose of the present study was to compare the effectiveness of the selective 5-HT2A antagonist M100907 in different psychosis models.. The classical neuroleptic haloperidol was used as reference compound.. Two hyperdopaminergia and two hypoglutamatergia mouse models were used.

    Article Title: Jeffrey Clifton Watkins FRS - The father of the glutamate receptor.
    Article Snippet: Although his work with Paul Herrling at Sandoz using derivatives of D-AP5, such as D-CPPene, did not ultimately produce a therapeutic agent the concept that targeting the NMDAR for stroke is alive and kicking today.



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    Input to Cheriff-CA1 neurons 3 days after optogenetic STDP. (A) Dodt-contrast image (40x objective) of the CA1 region with overlaid epifluorescence image. Black asterisks: CheRiff-eGFP expressing CA1 pyramidal neurons; white asterisks: NT CA1 pyramidal neurons suitable for recording. Scale bar 25 μm. (B) Yellow light (1 ms, 594 nm) on ChrimsonR-CA3 neurons EPSCs in CA1 neurons of a control (no oSTDP pairing) slice. EPSCs are recorded sequentially from CheRiff-CA1 pyramidal neurons (green, average of 10 gray individual EPSCs) and at least 3 NT CA1 neurons (black average of 10 gray individual EPSCs). (C) Automatically detected EPSC peak (red x) and slope (dashed red line, 20–60% peak) from individual CheRiff-CA1 neurons and the average of NT neurons. (D–F) Red and violet ticks indicate pre- (red) <t>and</t> <t>post-synaptic</t> (violet) light stimulation. (D) Normalized input strength of CheRiff-CA1 neurons recorded from nonpaired control (left: no light stimulation; right: postsynaptic stimulation only) slices and mKate2-CA1 neurons 3 days later. mean ± SEM. n = 12; 7; 10 (left to right). (E) Normalized input strength of CheRiff-CA1 neurons 3 days after 300 pairings of single presynaptic and 3 postsynaptic spikes at 5 Hz. During anticausal pairing the last postsynaptic spike occurred −50 or − 10 ms before the EPSP. During causal pairing the first postsynaptic spike occurred +10 or + 50 ms after the EPSP. n = 10; 24; 25; 10 (left to right). * P < 0.05, *** P < 0.001. (F) Same as (E), but the pairing frequency was reduced to 0.1 Hz (360 pairings in 1 h) or the NMDA receptor antagonist <t>CPPene</t> (1 μM) was in the culture medium (±10 ms pairing 300x at 5 Hz. n = 5; 14; 14; 13, left to right). (G) Mean input strength (data from E) as a function of timing between EPSPs (red) and postsynaptic spike bursts (violet, at mean) at 5 Hz repetition frequency. Two complete cycles are illustrated.
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    Image Search Results


    Input to Cheriff-CA1 neurons 3 days after optogenetic STDP. (A) Dodt-contrast image (40x objective) of the CA1 region with overlaid epifluorescence image. Black asterisks: CheRiff-eGFP expressing CA1 pyramidal neurons; white asterisks: NT CA1 pyramidal neurons suitable for recording. Scale bar 25 μm. (B) Yellow light (1 ms, 594 nm) on ChrimsonR-CA3 neurons EPSCs in CA1 neurons of a control (no oSTDP pairing) slice. EPSCs are recorded sequentially from CheRiff-CA1 pyramidal neurons (green, average of 10 gray individual EPSCs) and at least 3 NT CA1 neurons (black average of 10 gray individual EPSCs). (C) Automatically detected EPSC peak (red x) and slope (dashed red line, 20–60% peak) from individual CheRiff-CA1 neurons and the average of NT neurons. (D–F) Red and violet ticks indicate pre- (red) and post-synaptic (violet) light stimulation. (D) Normalized input strength of CheRiff-CA1 neurons recorded from nonpaired control (left: no light stimulation; right: postsynaptic stimulation only) slices and mKate2-CA1 neurons 3 days later. mean ± SEM. n = 12; 7; 10 (left to right). (E) Normalized input strength of CheRiff-CA1 neurons 3 days after 300 pairings of single presynaptic and 3 postsynaptic spikes at 5 Hz. During anticausal pairing the last postsynaptic spike occurred −50 or − 10 ms before the EPSP. During causal pairing the first postsynaptic spike occurred +10 or + 50 ms after the EPSP. n = 10; 24; 25; 10 (left to right). * P < 0.05, *** P < 0.001. (F) Same as (E), but the pairing frequency was reduced to 0.1 Hz (360 pairings in 1 h) or the NMDA receptor antagonist CPPene (1 μM) was in the culture medium (±10 ms pairing 300x at 5 Hz. n = 5; 14; 14; 13, left to right). (G) Mean input strength (data from E) as a function of timing between EPSPs (red) and postsynaptic spike bursts (violet, at mean) at 5 Hz repetition frequency. Two complete cycles are illustrated.

    Journal: Cerebral Cortex (New York, NY)

    Article Title: Spike-timing-dependent plasticity rewards synchrony rather than causality

    doi: 10.1093/cercor/bhac050

    Figure Lengend Snippet: Input to Cheriff-CA1 neurons 3 days after optogenetic STDP. (A) Dodt-contrast image (40x objective) of the CA1 region with overlaid epifluorescence image. Black asterisks: CheRiff-eGFP expressing CA1 pyramidal neurons; white asterisks: NT CA1 pyramidal neurons suitable for recording. Scale bar 25 μm. (B) Yellow light (1 ms, 594 nm) on ChrimsonR-CA3 neurons EPSCs in CA1 neurons of a control (no oSTDP pairing) slice. EPSCs are recorded sequentially from CheRiff-CA1 pyramidal neurons (green, average of 10 gray individual EPSCs) and at least 3 NT CA1 neurons (black average of 10 gray individual EPSCs). (C) Automatically detected EPSC peak (red x) and slope (dashed red line, 20–60% peak) from individual CheRiff-CA1 neurons and the average of NT neurons. (D–F) Red and violet ticks indicate pre- (red) and post-synaptic (violet) light stimulation. (D) Normalized input strength of CheRiff-CA1 neurons recorded from nonpaired control (left: no light stimulation; right: postsynaptic stimulation only) slices and mKate2-CA1 neurons 3 days later. mean ± SEM. n = 12; 7; 10 (left to right). (E) Normalized input strength of CheRiff-CA1 neurons 3 days after 300 pairings of single presynaptic and 3 postsynaptic spikes at 5 Hz. During anticausal pairing the last postsynaptic spike occurred −50 or − 10 ms before the EPSP. During causal pairing the first postsynaptic spike occurred +10 or + 50 ms after the EPSP. n = 10; 24; 25; 10 (left to right). * P < 0.05, *** P < 0.001. (F) Same as (E), but the pairing frequency was reduced to 0.1 Hz (360 pairings in 1 h) or the NMDA receptor antagonist CPPene (1 μM) was in the culture medium (±10 ms pairing 300x at 5 Hz. n = 5; 14; 14; 13, left to right). (G) Mean input strength (data from E) as a function of timing between EPSPs (red) and postsynaptic spike bursts (violet, at mean) at 5 Hz repetition frequency. Two complete cycles are illustrated.

    Article Snippet: Whole cell currents were recorded (see electrophysiology below) with synaptic transmission and action potentials blocked by CPPene (10 μM, Tocris bioscience; 1265), NBQX (10 μM, Tocris bioscience; 1044), picrotoxin (100 μM, Sigma; P1675-1G), and tetrodotoxin (TTX, 1 μM, HelloBio; HB1035).

    Techniques: Expressing, Control