Abstract
We investigated the effects of beta-amyloid (Abeta) peptides on cholinergic synaptosomes isolated from the electric organ of the Japanese marine ray Narke japonica. Fresh and pre-incubated solutions of Abeta(1-42) inhibited acetylcholine (ACh) release from the synaptosomes evoked by high [K+] depolarization when incubated with synaptosomes for 10 min before the depolarizing stimulus. A freshly prepared solution of Abeta(1-40) did not inhibit the evoked ACh release, but prolonged pre-incubation of Abeta(1-40) solution caused the inhibition. Abeta(1-15) neither in fresh nor pre-incubated solution inhibited. These results have demonstrated that Abeta peptides can acutely inhibit the depolarization-evoked release of ACh by acting directly on cholinergic presynaptic nerve endings. The electrophoresis analysis showed a strong correlation between Abeta aggregation and its inhibition for ACh release.
MeSH terms
-
Acetylcholine / metabolism*
-
Alzheimer Disease / metabolism
-
Alzheimer Disease / pathology
-
Alzheimer Disease / physiopathology
-
Amyloid beta-Peptides / metabolism
-
Amyloid beta-Peptides / pharmacology*
-
Animals
-
Basal Nucleus of Meynert / metabolism
-
Basal Nucleus of Meynert / pathology
-
Basal Nucleus of Meynert / physiopathology
-
Cholinergic Fibers / drug effects*
-
Cholinergic Fibers / metabolism
-
Cholinergic Fibers / pathology
-
Electric Organ / drug effects
-
Electric Organ / metabolism
-
Electric Organ / pathology
-
Peptide Fragments / metabolism
-
Peptide Fragments / pharmacology*
-
Presynaptic Terminals / drug effects*
-
Presynaptic Terminals / metabolism
-
Presynaptic Terminals / pathology
-
Skates, Fish / anatomy & histology
-
Skates, Fish / metabolism
-
Synaptosomes / drug effects
-
Synaptosomes / metabolism
-
Synaptosomes / pathology
Substances
-
Amyloid beta-Peptides
-
Peptide Fragments
-
amyloid beta-protein (1-40)
-
amyloid beta-protein (1-42)
-
Acetylcholine