Intracardiac nerves and ganglia in diabetic Goto Kakizaki rats

Abstract

Diabetes impacts the ultrastructure, cytochemistry and function of nerves and neurons in various divisions of the nervous system. Recently, a reduced number of the central and autonomic neurons has been reported in type 2 diabetic patients and animal models of the type 2 diabetes. We performed this study to investigate the structure of the cardiac autonomic nervous system in Goto Kakizaki (GK) rats, a model of the type 2 diabetes. Twelve GK rats (276 ± 17 days of age, 443 ± 5 g in weight; mean ± SEM) and 13 metabolic healthy Wistar rats (262 ± 5 days of age, 512 ± 10 g in weight) as controls were used for this study. Blood glucose was determined using test stripes, plasma insulin by RIA. The total hearts were prepared and stained for acetylcholinesterase to visualise the intrinsic nerves and ganglia. The intracardiac neural structures were observed with a stereomicroscope. The area of the intracardiac ganglia and the density of the left atrial epicardial nerves were measured using image analysing software. The GK rats exhibited significantly increased blood glucose levels compared to the control ones (11.0 ± 0.6 vs. 5.9 ± 0.1 mmol/l, P < 0.001), but the concentration of plasma insulin did not differ significantly between GK- and Wistar rats (83.9 ± 9.3 vs. 67.4 ± 10.8 pmol/l, P = 0.27). The total area of the intracardiac ganglia in control rats was 2.23 ± 0.10 mm2. It was significantly decreased to 1.38 ± 0.06 mm2 (P < 0.001) in GK rats. The disposition of the cardiac ganglia and nerves on the cardiac surface was not altered. The calculated density of the epicardiac nerves did not differ significantly between controls and GK rats. Results of the present study imply a 38% decrease of the total area of the intracardiac ganglia in GKcompared to Wistar rats. We conclude that the marked decrease of the area of the intracardiac ganglia in GK rats reflects a loss of the intrinsic neurons due to diabetic metabolic disorders. It seems likely that type.