Methods for exploring the morpho-functional relations of the aortic depressor nerve in experimental diabetes

Abstract

The present study investigated morpho-functional relations of the aortic depressor nerve (ADN) 5, 15 and 120 days after the onset of streptozotocin-induced diabetes in rats. Time control animals received vehicle. Under pentobarbital anesthesia, ADN activity was recorded simultaneously with arterial pressure. After the recordings, nerves were prepared for light microscopy study and morphometry. ADN function was accessed by means of pressure-nerve activity curve (fitted by sigmoidal regression) and cross-spectral analysis between mean arterial pressure (MAP) and ADN activity. The relation between morphological (myelinated fibers number and density, total myelin area, total fiber area and percentage of occupancy) and functional (gain, signal/noise relation, frequency) parameters were accessed by linear regression analysis and correlation coefficient calculations. Functional parameters obtained by means of the sigmoidal regression curve as well as by cross-spectral analysis were similar in diabetic and control rats. Morphometric parameters of the ADN were similar between groups 5 days after the onset of diabetes. Average myelin area and myelinated fiber area were significantly smaller on diabetic rats 15 and 120 days after the onset of diabetes, being the myelinated fiber and respective axons area and diameter also smaller on 120 days group. Nevertheless, G ratio (ratio between axon and fiber diameter) was nearly 0.6 and not different between groups or experimental times. No significant relationship between morphological and functional parameters was detected in all experimental groups. The present study suggests that ADN diabetic neuropathy was time-dependent, with damage to myelinated fibers to be the primary event, not evidenced by physiological methods.

Angiotensin II-NADPH oxidase-derived superoxide mediates diabetes-attenuated cell excitability of aortic baroreceptor neurons

“…In contrast to our study, diabetes doesn't change the AB function during the elevation of arterial blood pressure (12,13,19,23) even though some studies have shown the structural changes of AB axons and terminals in diabetic animals (19,27). One possibility for this discrepancy is that their studies employed whole bundle of aortic depressor nerves to test the AB function.…”

Acute Experimental Diabetes and Aortic Depressor Nerve Ultrastructural Morphometry: Effects of Insulin Treatment

“…Functional alterations of the baroreflex in diabetic rats have been demonstrated and our observation of a decrease in the MAP was also described by others [35][36][37][38]. Several hypotheses for this decrease were raised such as reduced cardiac output due to the hypovolemia caused by osmotic diuresis [39], reduced myocardial contractility leading to myocardial dysfunction [40] or the decrease of peripheral resistance [41].…”

Jinmaitong ameliorates diabetic peripheral neuropathy in streptozotocin-induced diabetic rats by modulating gut microbiota and neuregulin 1

“…Axons g ratios did not differ among different groups ( Figure 2E , p > 0.05) [ 24 ], indicating that atrophy of myelinated fibers occurred to the same degree in both axons and myelin sheaths [ 25 ]. The observed g ratio around 0.6 may explain, at least in part, the preservation of baroreceptor function in the DPN rats [ 26 ].…”