PMID- 11160403
OWN - NLM
STAT- MEDLINE
DCOM- 20010607
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 21
IP  - 4
DP  - 2001 Feb 15
TI  - Use-dependent effects of amyloidogenic fragments of (beta)-amyloid precursor 
      protein on synaptic plasticity in rat hippocampus in vivo.
PG  - 1327-33
AB  - The Alzheimer's disease-related beta-amyloid precursor protein (beta-APP) is 
      metabolized to a number of potentially amyloidogenic peptides that are believed 
      to be pathogenic. Application of relatively low concentrations of the soluble 
      forms of these peptides has previously been shown to block high-frequency 
      stimulation-induced long-term potentiation (LTP) of glutamatergic transmission in 
      the hippocampus. The present experiments examined how these peptides affect 
      low-frequency stimulation-induced long-term depression (LTD) and the reversal of 
      LTP (depotentiation). We discovered that beta-amyloid peptide (Abeta1-42) and the 
      Abeta-containing C -terminus of beta-APP (CT) facilitate the induction of LTD in 
      the CA1 area of the intact rat hippocampus. The LTD was frequency- and NMDA 
      receptor-dependent. Thus, although low-frequency stimulation alone was 
      ineffective, after intracerebroventricular injection of Abeta1-42, it induced an 
      LTD that was blocked by d-(-)-2-amino-5-phosphonopentanoic acid. Furthermore, an 
      NMDA receptor-dependent depotentiation was induced in a time-dependent manner, 
      being evoked by injection of CT 10 min, but not 1 hr, after LTP induction. These 
      use- and time-dependent effects of the amyloidogenic peptides on synaptic 
      plasticity promote long-lasting reductions in synaptic strength and oppose 
      activity-dependent strengthening of transmission in the hippocampus. This will 
      result in a profound disruption of information processing dependent on 
      hippocampal synaptic plasticity.
FAU - Kim, J H
AU  - Kim JH
AD  - Departments of Pharmacology, Trinity College, Dublin 2, Ireland.
FAU - Anwyl, R
AU  - Anwyl R
FAU - Suh, Y H
AU  - Suh YH
FAU - Djamgoz, M B
AU  - Djamgoz MB
FAU - Rowan, M J
AU  - Rowan MJ
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Amyloid)
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Excitatory Amino Acid Antagonists)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 0 (amyloid beta-protein precursor CT105)
SB  - IM
MH  - Amyloid/biosynthesis
MH  - Amyloid beta-Peptides/administration & dosage
MH  - Amyloid beta-Protein Precursor/administration & dosage/*metabolism
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Electric Stimulation/methods
MH  - Electrodes, Implanted
MH  - Excitatory Amino Acid Antagonists/pharmacology
MH  - Excitatory Postsynaptic Potentials/drug effects
MH  - Hippocampus/*drug effects/*metabolism
MH  - Injections, Intraventricular
MH  - Long-Term Potentiation/drug effects
MH  - Male
MH  - Neural Inhibition/drug effects
MH  - Neuronal Plasticity/*drug effects
MH  - Peptide Fragments/*administration & dosage
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism
PMC - PMC6762223
EDAT- 2001/02/13 11:00
MHDA- 2001/06/08 10:01
PMCR- 2001/08/15
CRDT- 2001/02/13 11:00
PHST- 2001/02/13 11:00 [pubmed]
PHST- 2001/06/08 10:01 [medline]
PHST- 2001/02/13 11:00 [entrez]
PHST- 2001/08/15 00:00 [pmc-release]
AID - 21/4/1327 [pii]
AID - 4977 [pii]
AID - 10.1523/JNEUROSCI.21-04-01327.2001 [doi]
PST - ppublish
SO  - J Neurosci. 2001 Feb 15;21(4):1327-33. doi: 10.1523/JNEUROSCI.21-04-01327.2001.