Electrophysiological effects of 25-35 amyloid-beta-protein on guinea-pig lateral septal neurons.
The amyloid-beta-protein (A beta P) is the major component of the amyloid deposition which characterizes Alzheimer's disease. We have investigated the effects of 25-35 A beta P, the biologically active part of A beta P, on 35 lateral septal neurons in slices of guinea-pig brain during intracellular recording. Bath application of 25-35 A beta P (10(-6) M) caused transient or long-lasting membrane depolarizations in 15 neurons. These effects were not obtained with a 25-35 A beta P peptide synthetized at random. In 7 other neurons, in control medium or in presence of tetrodotoxin, 25-35 A beta P increased the amplitude of excitatory responses produced by local iontophoretic applications of glutamate and NMDA. The data demonstrate for the first time the excitatory effects of 25-35 A beta P on central neurons, effects which may be involved in the mechanisms of neuronal death in Alzheimer's disease.
Carette
B
B
INSERM U 156, Lille, France.
Poulain
P
P
Delacourte
A
A
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000166:cytology* / Q000502:physiology; D004594:Electrophysiology; D005260:Female; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D010446:Peptide Fragments / Q000494:pharmacology*; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); D013779:Tetrodotoxin