Description: Transient reduction of spontaneous neuronal network activity by sublethal amyloid ß (1-42) peptide concentrations

This title appears in the Scientific Report : 2009

Transient reduction of spontaneous neuronal network activity by sublethal amyloid ß (1-42) peptide concentrations

Soluble amyloid beta(1-42) (A beta(1-42)) peptide has recently been assigned a key role in early Alzheimer's disease (AD) pathophysiology accounting for synaptic dysfunction before amyloid plaque formation and neurodegeneration can occur. Following sublethal A beta(1-42) administration, we obse...

Personal Name(s):	Görtz, P.
	Opatz, J. / Siebler, M. / Funke, S. A. / Willbold, D. / Lange-Asschenfeldt, C.
Contributing Institute:	Strukturbiochemie; ISB-3 JARA - HPC; JARA-HPC
Published in:	Journal of neural transmission / Parkinson's disease and dementia section, 116 (2009) S. 351 - 355
Imprint:	Wien [u.a.] Springer 2009
Physical Description:	351 - 355
DOI:	10.1007/s00702-009-0188-y
PubMed ID:	19214376
Document Type:	Journal Article
Research Program:	Funktion und Dysfunktion des Nervensystems
Series Title:	Journal of Neural Transmission 116
Subject (ZB):	Action Potentials: drug effects Action Potentials: physiology Amyloid beta-Peptides: administration & dosage Amyloid beta-Peptides: metabolism Amyloid beta-Peptides: pharmacology Animals Cell Culture Techniques Cerebral Cortex: cytology Electrophysiology Microelectrodes Nerve Net: drug effects Nerve Net: physiology Neurons: drug effects Neurons: physiology Peptide Fragments: administration & dosage Peptide Fragments: metabolism Peptide Fragments: pharmacology Rats Amyloid beta-Peptides Peptide Fragments amyloid beta-protein (1-42) J Alzheimer's disease A beta(1-42) Cortical neurons Neuronal network activity Microelectrode array
	Publikationsportal JuSER

Please use the identifier: http://dx.doi.org/10.1007/s00702-009-0188-y in citations.

Soluble amyloid beta(1-42) (A beta(1-42)) peptide has recently been assigned a key role in early Alzheimer's disease (AD) pathophysiology accounting for synaptic dysfunction before amyloid plaque formation and neurodegeneration can occur. Following sublethal A beta(1-42) administration, we observed an acute but transient reduction of the spike and burst rate of spontaneously active cortical networks cultured on microelectrode arrays. This simple experimental system appears suitable for future long-term pharmacological and genetic studies of A beta(1-42) signaling, thus providing a valuable new tool in AD research.