Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
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
Substances
-
Amyloid beta-Peptides
-
Peptide Fragments
-
amyloid beta-protein (1-42)