title: Remodelling of the intracardiac ganglia in diabetic Goto-Kakizaki rats: an anatomical study.
abstract: BACKGROUND
  Although cardiac autonomic neuropathy is one of major complications of diabetes mellitus (DM), anatomical data on cardiac innervation of diabetic animal models is scant and controversial. We performed this study to check whether long-term diabetic state impacts the anatomy of intracardiac ganglia in Goto-Kakizaki (GK) rats, a genetic model of type 2 DM.
  
  
  METHODS
  Twelve GK rats (276 ± 17 days of age; mean ± standard error) and 13 metabolically healthy Wistar rats (262 ± 5 days of age) as controls were used for this study. Blood glucose was determined using test strips, plasma insulin by radioimmunoassay. Intrinsic ganglia and nerves were visualized by acetylcholinesterase histochemistry on whole hearts. Ganglion area was measured, and the neuronal number was assessed according to ganglion area.
  
  
  RESULTS
  The GK rats had significantly elevated blood glucose level compared to controls (11.0 ± 0.6 vs. 5.9 ± 0.1 mmol/l, p < 0.001), but concentration of plasma insulin did not differ significantly between the two groups (84.0 ± 9.8 vs. 67.4 ± 10.9 pmol/l, p = 0.17). The GK rats contained significantly fewer intracardiac ganglia, decreased total area of intracardiac ganglia (1.4 ± 0.1 vs. 2.2 ± 0.1 mm2, p < 0.001) and smaller somata of ganglionic neurons. Mean total number of intracardiac neurons in GK rats was 1461 ± 62, while this number in control rats was higher by 39% and reached 2395 ± 110 (p < 0.001).
  
  
  CONCLUSIONS
  Results of our study demonstrate the decreased number of intracardiac neurons in GK rats compared to metabolically healthy Wistar rats of similar age. It is likely that the observed structural remodelling of intracardiac ganglia in GK rats is caused by a long-term diabetic state.
authors.forename: Darius
authors.initials: D
authors.lastname: Batulevicius
authors.forename: Thomas
authors.initials: T
authors.lastname: Frese
authors.forename: Elmar
authors.initials: E
authors.lastname: Peschke
authors.forename: Dainius H
authors.initials: DH
authors.lastname: Pauza
authors.forename: Vaida
authors.initials: V
authors.lastname: Batuleviciene
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000235:genetics / Q000473:pathology*; D003929:Diabetic Neuropathies / Q000097:blood / Q000235:genetics / Q000473:pathology*; D004195:Disease Models, Animal; D058851:GPI-Linked Proteins / Q000378:metabolism; D005725:Ganglia, Autonomic / Q000201:enzymology / Q000473:pathology*; D006321:Heart / Q000294:innervation*; D007328:Insulin / Q000097:blood; D008297:Male; D017208:Rats, Wistar
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D058851:GPI-Linked Proteins; D007328:Insulin; D000110:Acetylcholinesterase; C548246:Ache protein, rat