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Age-related decrease in omega conotoxin binding to rat cardiac synaptosomes
A M Parikh1, M D Johnson, V Aloyo
1Department of Pharmacology, Medical College of Pennsylvania, Philadelphia 19129.
Abstract:
A cardiac synaptosomal preparation developed by this laboratory was used to study neuronal calcium channels in aging rat heart. Ca2+ channels were quantified by measuring binding of iodinated omega conotoxin, which is reported to specifically block neuronal Ca2+ channels. We determined the binding of [125I]-omega conotoxin GVIA to a synaptosomal preparation from the hearts of 6- and 24-month-old male Fisher 344 rats. The maximum number of binding sites (Bmax +/- SD, fmol/mg protein) is lower in preparations from 24-month (2.2 +/- 0.6) than from 6-month (3.4 +/- 0.7)-old rats. This decrease in number of binding sites suggests an age-related reduction in the number of neuronal calcium channels. Since calcium is essential for exocytotic release of norepinephrine and is made available intracellularly through neuronal calcium channels, the reduction in neuronal calcium channel number may explain, in part, our previous observations of diminished release of norepinephrine in senescent hearts.
Insights
Aging reduces neuronal calcium channels in rat hearts. This age-related decline in calcium channels may explain lower norepinephrine release in older hearts.
Area of Science:
- Cardiovascular Physiology
- Neurobiology
- Aging Research
Background:
- Neuronal calcium channels play a critical role in neurotransmitter release.
- Age-related changes in cardiac function are often linked to altered neuronal signaling.
- Previous studies indicated diminished norepinephrine release in senescent hearts.
Purpose of the Study:
- To investigate age-related changes in neuronal calcium channels within the rat heart.
- To quantify neuronal calcium channel density in young versus aged rats.
- To explore the potential link between reduced calcium channels and norepinephrine release in aging hearts.
Main Methods:
- Utilized a cardiac synaptosomal preparation from Fisher 344 rats of 6 and 24 months of age.
- Quantified neuronal calcium channels by measuring the binding of [125I]-omega conotoxin GVIA.
- Determined the maximum number of binding sites (Bmax) for omega conotoxin.
Main Results:
- The maximum number of neuronal calcium channel binding sites (Bmax) was significantly lower in 24-month-old rats (2.2 +/- 0.6 fmol/mg protein) compared to 6-month-old rats (3.4 +/- 0.7 fmol/mg protein).
- This reduction indicates an age-dependent decrease in the density of neuronal calcium channels in the aging rat heart.
- The findings suggest a correlation between reduced calcium channel numbers and impaired norepinephrine release.
Conclusions:
- There is an age-related reduction in the number of neuronal calcium channels in the rat heart.
- This decrease in neuronal calcium channels may contribute to the diminished release of norepinephrine observed in senescent hearts.
- The study highlights the importance of neuronal calcium channel function in maintaining cardiac neurotransmission during aging.