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Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

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Physiological carotid body denervation during aging.

C Di Giulio¹, J Antosiewicz, M Walski

¹Department of Basics and Applied Medical Sciences, University of Chieti, Chieti, Italy. digiulio@unich.it

Advances in Experimental Medicine and Biology

|June 19, 2009

Summary

Aging reduces carotid body (CB) synaptic connections, leading to decreased homeostatic capacity. This "physiological denervation" may protect cells from oxidative stress during aging.

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Area of Science:

Physiology
Cell Biology
Gerontology

Background:

Aging is associated with diminished homeostatic capacity.
The carotid body (CB) is crucial for maintaining homeostasis, particularly in response to oxygen levels.
The impact of aging on CB synaptic mechanisms remains incompletely understood.

Purpose of the Study:

To investigate whether aging affects oxygen-sensitive mechanisms in CB cells by reducing synaptic junction contact surfaces.
To test the hypothesis that the aging CB undergoes a
physiological denervation
.

Main Methods:

Comparative analysis of young (2-3 months) and senescent (22 months) male Wistar rats.
Transmission electron microscopy to examine CB ultrastructure.
Immunohistochemical analysis to evaluate expressions of HIF-1α, VEGF, and NOS-1.

Main Results:

Senescent CBs exhibited decreased expression of HIF-1α, VEGF, and NOS-1.
Reduced cell volume, fewer mitochondria, and shrunken nuclei were observed in older rats.
A significant reduction in synaptic connections (from 125 in young to 28 in old rats) was the most notable finding.
Accumulation of lipofuscin and increased extracellular matrix were also present in aged CBs.

Conclusions:

The aging carotid body undergoes a
physiological denervation
characterized by a significant loss of synaptic connections.
This reduction in synaptic junctions may contribute to the decreased homeostatic capacity observed in aging.
The age-related synaptic reduction could be a protective mechanism against reactive oxygen species accumulation.