Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments
- PMID: 9351645
- DOI: 10.1097/00001756-199710200-00006
Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments
Abstract
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.
Similar articles
-
Use-dependent effects of amyloidogenic fragments of (beta)-amyloid precursor protein on synaptic plasticity in rat hippocampus in vivo.J Neurosci. 2001 Feb 15;21(4):1327-33. doi: 10.1523/JNEUROSCI.21-04-01327.2001. J Neurosci. 2001. PMID: 11160403 Free PMC article.
-
Blockade of long-term potentiation by beta-amyloid peptides in the CA1 region of the rat hippocampus in vivo.J Neurophysiol. 2001 Feb;85(2):708-13. doi: 10.1152/jn.2001.85.2.708. J Neurophysiol. 2001. PMID: 11160505
-
[Involvement of protein tyrosine kinases in β-amyloid protein-induced suppression of long-term potentiation in the rat hippocampal CA1 region in vivo].Sheng Li Xue Bao. 2009 Jun 25;61(3):263-71. Sheng Li Xue Bao. 2009. PMID: 19536439 Chinese.
-
GLP-1 agonists facilitate hippocampal LTP and reverse the impairment of LTP induced by beta-amyloid.Eur J Pharmacol. 2008 Jun 10;587(1-3):112-7. doi: 10.1016/j.ejphar.2008.03.025. Epub 2008 Mar 29. Eur J Pharmacol. 2008. PMID: 18466898
-
Amyloid beta-protein fragment 31-35 suppresses long-term potentiation in hippocampal CA1 region of rats in vivo.Synapse. 2006 Sep 15;60(4):307-13. doi: 10.1002/syn.20302. Synapse. 2006. PMID: 16786537
Cited by
-
The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model.Front Mol Neurosci. 2021 Apr 12;14:576038. doi: 10.3389/fnmol.2021.576038. eCollection 2021. Front Mol Neurosci. 2021. PMID: 33912008 Free PMC article.
-
Calcium-regulated signaling pathways: role in amyloid beta-induced synaptic dysfunction.Neuromolecular Med. 2004;6(1):53-64. doi: 10.1385/NMM:6:1:053. Neuromolecular Med. 2004. PMID: 15781976 Review.
-
AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.Neuron. 2006 Dec 7;52(5):831-43. doi: 10.1016/j.neuron.2006.10.035. Neuron. 2006. PMID: 17145504 Free PMC article.
-
Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment.J Clin Invest. 2004 Dec;114(11):1624-34. doi: 10.1172/JCI22831. J Clin Invest. 2004. PMID: 15578094 Free PMC article.
-
Presenilins and APP in neuritic and synaptic plasticity: implications for the pathogenesis of Alzheimer's disease.Neuromolecular Med. 2002;2(2):167-96. doi: 10.1385/NMM:2:2:167. Neuromolecular Med. 2002. PMID: 12428810 Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous