Characterization of upper thoracic spinal neurons receiving noxious cardiac and/or somatic inputs in diabetic rats

• Published in: Autonomic neuroscience 2011-12, Vol.165 (2), p.168-177
• Main Authors: Ghorbani, Marie Louise M, Qin, Chao, Wu, Mingyuan, Farber, Jay P, Sheykhzade, Majid, Fjalland, Bjarne, Nyborg, Niels C.B, Foreman, Robert D
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Angina; Animals; Autonomic Nervous System - physiopathology; Autonomic neuropathy; Biological and medical sciences; Diabetes; Diabetes Mellitus, Experimental - physiopathology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Extracellular recording; Fundamental and applied biological sciences. Psychology; Heart - innervation; Male; Medical Education; Medical sciences; Neurons, Afferent - physiology; Peripheral nervous system. Autonomic nervous system. Neuromuscular transmission. Ganglionic transmission. Electric organ; Rats; Rats, Sprague-Dawley; Spinal Cord - physiopathology; Spinal neurons; Streptozotocin; Thoracic spinal cord; Thoracic Vertebrae; Vertebrates: nervous system and sense organs
• ISSN: 1566-0702; 1872-7484
• DOI: 10.1016/j.autneu.2011.07.007

Abstract The aim of the present study was to examine spinal processing of cardiac and somatic nociceptive input in rats with STZ-induced diabetes. Type 1 diabetes was induced with streptozotocin (50 mg/kg) in 14 male Sprague–Dawley rats and citrate buffer was injected in 14 control rats. After 4–11 weeks, the rats were anesthetized with pentobarbital, ventilated and paralyzed. A laminectomy enabled extracellular recording of T3 spinal cord neuronal activity. Intrapericardial administration of a mixture of algogenic chemicals (bradykinin, serotonin, prostaglandin E2 (all at 10 − 5 M), and adenosine (10 − 3 M)) was applied to activate nociceptors of cardiac afferent nerve endings. Furthermore, somatic receptive properties were examined by applying innocuous (brush and light pressure) and noxious (pinch) cutaneous mechanical stimuli. Diabetes-induced increases in spontaneous activity were observed in subsets of neurons exhibiting long-lasting excitatory responses to administration of the algogenic mixture. Algogenic chemicals altered activity of a larger proportion of neurons from diabetic animals (73/111) than control animals (55/115, P < 0.05). Some subtypes of neurons exhibiting long-lasting excitatory responses, elicited prolonged duration and others, had a shortened latency. Some neurons exhibiting short-lasting excitatory responses in diabetic animals elicited a shorter latency and some a decreased excitatory change. The size of the somatic receptive field was increased for cardiosomatic neurons from diabetic animals. Cutaneous somatic mechanical stimulation caused spinal neurons to respond with a mixture of hyper- and hypoexcitability. In conclusion, diabetes induced changes in the spinal processing of cardiac input and these might contribute to cardiovascular autonomic neuropathy in patients with diabetes.