Administration of aggregated beta-amyloid peptide (25-35) induces changes in long-term potentiation in the hippocampus in vivo.
Intracereroventricular administration of aggregated beta-amyloid protein fragment (25-35) (7.5 nmol/ventricle) was followed one month later by significant changes in the dynamics of long-term potentiation in the hippocampus in vivo, expressed as powerful and stable increases in the amplitude of evoked potentials. This phenomenon may be associated with oxidative stress in the hippocampus, which has previously been demonstrated in this model, and, thus, with disturbances in ion homeostasis.
Trubetskaya
V V
VV
Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
Stepanichev
M Yu
MY
Onufriev
M V
MV
Lazareva
N A
NA
Markevich
V A
VA
Gulyaeva
N V
NV
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35)