Transient reduction of spontaneous neuronal network activity by sublethal amyloid beta (1-42) peptide concentrations.
Soluble amyloid beta(1-42) (A beta(1-42)) peptide has recently been assigned a key role in early Alzheimer's disease (AD) pathophysiology accounting for synaptic dysfunction before amyloid plaque formation and neurodegeneration can occur. Following sublethal A beta(1-42) administration, we observed an acute but transient reduction of the spike and burst rate of spontaneously active cortical networks cultured on microelectrode arrays. This simple experimental system appears suitable for future long-term pharmacological and genetic studies of A beta(1-42) signaling, thus providing a valuable new tool in AD research.
Görtz
Philipp
P
Klinik für Psychiatrie und Psychotherapie, Abteilung Experimentelle Gerontopsychiatrie, Heinrich-Heine-Universität, Bergische Landstr. 2, 40629, Düsseldorf, Germany.
Opatz
Jessica
J
Siebler
Mario
M
Funke
Susanne Aileen
SA
Willbold
Dieter
D
Lange-Asschenfeldt
Christian
C
D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology; D016229:Amyloid beta-Peptides / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D018929:Cell Culture Techniques; D002540:Cerebral Cortex / Q000166:cytology*; D004594:Electrophysiology; D008839:Microelectrodes; D009415:Nerve Net / Q000187:drug effects* / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D010446:Peptide Fragments / Q000008:administration & dosage / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)