Abstract
[3H]Vesamicol binding was characterized in human brain post mortem. The number of binding sites was then determined in parallel with choline acetyltransferase activity in the temporal cortex of patients with Alzheimer's disease, demented and non-demented patients with Parkinson's disease, and in the cerebral cortex of rats with quisqualic acid lesions of the nucleus basalis magnocellularis. Whereas choline acetyltransferase activity decreased in patients with Alzheimer's or Parkinson's disease indicating loss of cholinergic innervation, the number of binding sites for [3H]vesamicol was the same as or higher than in controls. Similar results were obtained with the lesioned rats. It is suggested that the increase in binding sites may reflect compensatory regulation of the spared neurons at the level of the synaptic vesicle.
MeSH terms
-
Aged
-
Aged, 80 and over
-
Alzheimer Disease / metabolism*
-
Alzheimer Disease / physiopathology
-
Animals
-
Brain Injuries / chemically induced
-
Brain Injuries / metabolism*
-
Choline O-Acetyltransferase / metabolism*
-
Female
-
Humans
-
Hydroxydopamines
-
Kinetics
-
Male
-
Neuromuscular Depolarizing Agents / metabolism
-
Oxadiazoles
-
Oxidopamine
-
Parkinson Disease / metabolism*
-
Phencyclidine / analogs & derivatives*
-
Phencyclidine / metabolism
-
Piperidines*
-
Quisqualic Acid
-
Rats
-
Rats, Inbred Strains
-
Receptors, Neurotransmitter / metabolism*
-
Receptors, Phencyclidine
-
Reference Values
-
Substantia Nigra / metabolism
-
Temporal Lobe / metabolism*
Substances
-
Hydroxydopamines
-
Neuromuscular Depolarizing Agents
-
Oxadiazoles
-
Piperidines
-
Receptors, Neurotransmitter
-
Receptors, Phencyclidine
-
vesamicol
-
Oxidopamine
-
Quisqualic Acid
-
Choline O-Acetyltransferase
-
Phencyclidine