Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments.
The effects of beta-amyloid precursor protein (beta-APP) fragments on plasticity of glutamtatergic synaptic transmission were examined in the hippocampus of urethane anaesthetized rats. I.c.v. injection of beta-amyloid (A beta) 1-40 and 1-42 and the C-terminal fragment CT105 greatly shortened the duration of high frequency stimulation-induced long-term potentiation (LTP) of field excitatory postsynaptic potentials in the CA1 area. Whereas in vehicle injected animals LTP was stable over a 5 h recording period, doses of these peptides (A beta 1-40, 0.4 and 3.5 nmol; A beta1-42, 0.01 nmol; CT105, 0.05 nmol) which did not affect baseline synaptic transmission abolished LTP within 3-5 h. The reduced duration of this form of synaptic plasticity may contribute to the cognitive deficits in Alzheimer's disease.
Cullen
W K
WK
Department of Pharmacology and Therapeutics, Trinity College, Dublin, Ireland.
Suh
Y H
YH
Anwyl
R
R
Rowan
M J
MJ
D016564:Amyloid beta-Protein Precursor / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D006624:Hippocampus / Q000187:drug effects*; D007276:Injections, Intraventricular; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D010446:Peptide Fragments / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D009435:Synaptic Transmission / Q000187:drug effects
D016564:Amyloid beta-Protein Precursor; D010446:Peptide Fragments