drugs dizocilpine  (Alomone Labs)

Journal: Pharmaceuticals

Article Title: Administration of Bacterial Lipopolysaccharide during Early Postnatal Ontogenesis Induces Transient Impairment of Long-Term Synaptic Plasticity Associated with Behavioral Abnormalities in Young Rats

doi: 10.3390/ph13030048

Figure Lengend Snippet: LTP properties are not disturbed in adolescent rats administered with LPS during the first postnatal week (1wLPS_a) or third postnatal week (3wLPS_a). ( A ) Diagram showing the normalized slope of fEPSP in the control (ctrl) and experimental groups (1wLPS_a and 3wLPS_a) before and after TBS. ( B ) Diagram illustrating average LTP values in these groups. One-way ANOVA: F 2;48 = 0.27; p = 0.77. ( C ) Diagram showing the PPRs of fEPSPs before (baseline) and after (LTP) TBS in different groups. ( D ) Diagram illustrating the effect of MK-801 (10 μM) on LTP magnitude in the control (ctrl) and experimental (1wLPS_a; 3wLPS_a) groups * p

Article Snippet: Drugs Dizocilpine (MK-801, Alomone Labs, Israel, cat # M-230, 10 µM), a non-competitive antagonist of NMDAR, 4-[1-(2-fluoropyridin-3-yl)-5-methyltriazol-4-yl]-N-methylN-propan-2-yl-3,6dihydro-2H-pyridine-1-carboxamide (FTIDC, Alomone Labs, cat # F-190, 5 µM), a potent and selective antagonist of mGlu1Rs, and 4-[2-(4-Benzylpiperidin-1-yl)-1-hydroxypropyl]phenol (ifenprodil, Alomone Labs, cat # I-105, 3 µM), a NMDAR antagonist that selectively inhibits receptors containing the NR2B subunit, were used for the electrophysiology experiments and were diluted in distilled water and then bath-applied.

Techniques:

Journal: Pharmaceuticals

Article Title: Administration of Bacterial Lipopolysaccharide during Early Postnatal Ontogenesis Induces Transient Impairment of Long-Term Synaptic Plasticity Associated with Behavioral Abnormalities in Young Rats

doi: 10.3390/ph13030048

Figure Lengend Snippet: The NMDA receptor (NMDAR)-dependent mechanism of LTP induction is disrupted in the CA1 hippocampus of juvenile animals treated with LPS during the third postnatal week. ( A – C ) The normalized fEPSP slope in the control and experimental groups in the presence of the NMDAR blocker Dizocilpine (MK-801) (10 μM) before and after TBS. ( D – F ) The relative fEPSP slope in the control and experimental groups in the presence of ifenprodil (If, 3 μM), a selective GluN2B-containing NMDAR antagonist, before and after TBS. ( G – H ) Diagrams illustrating the magnitude of plasticity in the control and experimental groups in the presence of MK-801 or ifenprodil. Two-way ANOVA following Tukey post hoc tests were used. * p

Article Snippet: Drugs Dizocilpine (MK-801, Alomone Labs, Israel, cat # M-230, 10 µM), a non-competitive antagonist of NMDAR, 4-[1-(2-fluoropyridin-3-yl)-5-methyltriazol-4-yl]-N-methylN-propan-2-yl-3,6dihydro-2H-pyridine-1-carboxamide (FTIDC, Alomone Labs, cat # F-190, 5 µM), a potent and selective antagonist of mGlu1Rs, and 4-[2-(4-Benzylpiperidin-1-yl)-1-hydroxypropyl]phenol (ifenprodil, Alomone Labs, cat # I-105, 3 µM), a NMDAR antagonist that selectively inhibits receptors containing the NR2B subunit, were used for the electrophysiology experiments and were diluted in distilled water and then bath-applied.

Techniques:

Journal: eLife

Article Title: Two de novo GluN2B mutations affect multiple NMDAR-functions and instigate severe pediatric encephalopathy

doi: 10.7554/eLife.67555

Figure Lengend Snippet: hGluN2B-G689S, but not hGluN2B-G689C, shows reduced apparent open probability (P o ). ( a ) Representative deactivation traces of oocytes co-expressing hGluN1a with hGluN2B wt (black), hGluN2B-G689C (cyan) or hGluN2B-G689S (red). Following opening of channels by 3 mM glutamate, oocytes were washed with glutamate and 1 μM MK-801 (activity-dependent blocker; indicated by black bar above traces). ( b, c ) Summary of deactivation kinetics. t 10-90% inhibition ( b ) and τ off ( c ) (see Materials and methods) are shown (bars are color coded as representative currents). ( d ) Summary of the the expression of GluN2B wt -β-lac ( wt -β, 1 μg DNA) in HEK293T cells, co-transfected with 1 μg GluN1a, when also co-transfected with increasing DNA amounts (0.1, 0.5, and 1 μg) of Kv4.2 (N = two independent experiments). *, p

Article Snippet: Apparent open probability MK-801 (activity-dependent pore blocker of GluNRs) was purchased from Alomone labs (cat.# M-230).

Techniques: Expressing, Activity Assay, Inhibition, Transfection

Journal: Frontiers in Cellular Neuroscience

Article Title: Seizure-Induced Potentiation of AMPA Receptor-Mediated Synaptic Transmission in the Entorhinal Cortex

doi: 10.3389/fncel.2018.00486

Figure Lengend Snippet: Changes in AMPAR, NMDAR, and GABAaR components of the synaptic response during epileptiform activity in ERC with a partial block of NMDA-receptors by intracellular MK-801. Top and bottom-left panels represent the estimates of AMPAR-, NMDAR-, and GABAaR-mediated components of the response to the extracellular stimulus under control conditions (black traces) and during epileptiform activity (red traces). Note the substantial block of NMDAR-mediated conductance by intracellular MK-801 (compare with Figure 2 ). Bar charts (bottom-right) represent the peak AMPAR-mediated conductance and the area under the plot: despite the partial block by intracellular MK-801, the response significantly increased (paired Student’s t -test, P = 0.03, asterisk (*) indicates significant difference); however, no changes in the area under the plot were detected (paired Student’s t -test, P = 0.27).

Article Snippet: In an attempt to avoid the alteration of epileptiform activity by adding the NMDAR antagonists to the perfusing solution, the recordings were performed with MK-801 (3 mM) added to the pipette solution.

Techniques: Activity Assay, Blocking Assay