1MeTIQ provides protection against Aβ-induced reduction of surface expression of synaptic proteins and inhibits H2O2-induced oxidative stress in primary hippocampal neurons

Neurotoxicity Research

Volumn 25, Issue 4, 2014, Pages 348-357

  Kuszczyk, Magdalena A ^a,b   Sadowski, Martin J ^a   Antkiewicz Michaluk, Lucyna ^c   Lazarewicz, Jerzy W ^b  

^a NEW YORK UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b MOSSAKOWSKI MEDICAL RESEARCH CENTRE   (Poland)

^c INSTITUTE OF PHARMACOLOGY   (Poland)

Author keywords

1MeTIQ; Neuronal culture; NMDA receptor antagonist; ROS production; Synaptic protein; Amyloid

Indexed keywords

1 METHYL 1,2,3,4 TETRAHYDROISOQUINOLINE; AMYLOID BETA PROTEIN; DIZOCILPINE; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; NEUROPROTECTIVE AGENT; POSTSYNAPTIC DENSITY PROTEIN 95; REACTIVE OXYGEN METABOLITE; SYNAPTOPHYSIN; UNCLASSIFIED DRUG; 1-METHYL-1,2,3,4-TETRAHYDROISOQUINOLINE; AMINO ACID RECEPTOR BLOCKING AGENT; AMYLOID BETA PROTEIN[1-40]; DIZOCILPINE MALEATE; DLGH4 PROTEIN, MOUSE; GUANYLATE KINASE; HYDROGEN PEROXIDE; MEMBRANE PROTEIN; NR1 NMDA RECEPTOR; PEPTIDE FRAGMENT; SYP PROTEIN, MOUSE; TETRAHYDROISOQUINOLINE DERIVATIVE;

ANIMAL CELL; ARTICLE; BRAIN NERVE CELL; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; DOWN REGULATION; DRUG EFFECT; DRUG EXPOSURE; HIPPOCAMPAL NEURONAL CULTURE; MOUSE; NEUROPROTECTION; NONHUMAN; OXIDATIVE STRESS; PRIMARY CELL CULTURE; PRIORITY JOURNAL; PROTEIN DEPLETION; PROTEIN EXPRESSION; RAT; ANIMAL; C57BL MOUSE; CELL CULTURE; CELL SURVIVAL; DRUG EFFECTS; HIPPOCAMPUS; METABOLISM; NERVE CELL; SYNAPSE; TOXICITY;

AMYLOID BETA-PEPTIDES; ANIMALS; CELL SURVIVAL; CELLS, CULTURED; DIZOCILPINE MALEATE; EXCITATORY AMINO ACID ANTAGONISTS; GUANYLATE KINASE; HIPPOCAMPUS; HYDROGEN PEROXIDE; MEMBRANE PROTEINS; MICE; MICE, INBRED C57BL; NEURONS; NEUROPROTECTIVE AGENTS; OXIDATIVE STRESS; PEPTIDE FRAGMENTS; REACTIVE OXYGEN SPECIES; RECEPTORS, N-METHYL-D-ASPARTATE; SYNAPSES; SYNAPTOPHYSIN; TETRAHYDROISOQUINOLINES;

EID: 84898813652     PISSN: 10298428     EISSN: 14763524     Source Type: Journal    
DOI: 10.1007/s12640-013-9440-1     Document Type: Article

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