Development and aging of cholinergic synapses. V. Changes in nicotinic cholinergic receptor binding in ciliary ganglia and irises of the chicken.
In order to study possible age-dependent changes in the number of cholinergic binding sites, we have examined alpha-bungarotoxin (ABTX) binding in the ciliary ganglion and iris of the chicken from 3 months after hatching (a.h.) to 5 years of age and have compared it to acetylcholinesterase (AChE) activity and acetylcholine (AChE) levels. In ciliary ganglia the amount of ABTX binding per ganglion increases 16-fold between 3 and 7 months, after which it returns almost to the 3-month level, at 1.3 years. It then remains virtually unchanged to 5 years. A similar pattern is observed in the amount of binding per protein. ACh levels and AChE activity show a different pattern than ABTX binding. In the iris the amount of ABTX binding remains constant between 3 months and 1.3 years and then it increases 1.6-fold up to 3 years. This period is followed by a decrease to 5 years. The amount of ABTX binding per protein which has increased continuously in the iris from the period following hatching up to 7 months, decreases continuously from 7 months to 5 years. In the iris, both ACh levels and AChE activity per protein follow a pattern which is similar to ABTX binding, decreasing from 3 months to 2 years and then remaining relatvely unvaried between 2 and 6-7 years. Our results suggest that a decrease in receptor number begins during early adulthood in the ganglia, whereas this event occurs at a later stage in the iris. However, the total amount of ABTX binding is still relatively high at late stages. These results support our view that the presynaptic component is more affected by the aging process than the postsynaptic component.[1]References
- Development and aging of cholinergic synapses. V. Changes in nicotinic cholinergic receptor binding in ciliary ganglia and irises of the chicken. Marchi, M., Yurkewicz, L., Giacobini, E., Fredrickson, T. Dev. Neurosci. (1981) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg