title: Long pulse gastric electrical stimulation induces regeneration of myenteric plexus synaptic vesicles in diabetic rats.
abstract: BACKGROUND
  Gastric electrical stimulation (GES) may improve delayed gastric emptying in diabetic gastroparesis, but whether enteric nervous system (ENS) is directly involved in its mechanism of improvement in gastric motility is unclear. The aims were to investigate the correlation between the changes in ENS and effects of long pulse GES on them in diabetic rats induced by streptozotocin (STZ).
  
  
  METHODS
  Electron microscopy, immunohistochemistry, RT-PCR and western blot were used to evaluate changes of myenteric plexus neurons and synaptic vesicles in different stages of the diabetic rats. The effects of GES were detected by same methods after pacing wires were implanted and then diabetes was induced and followed by long pulse GES.
  
  
  RESULTS
  Since 6 weeks after STZ injection, the nerve fibres were incompact and synaptic vesicles in myenteric neurons reduced. Furthermore, the myenteric neurons showed severe damage such as partial depletion of the axon, swelling of mitochondria and seriously decreased synaptic vesicles in 12 weeks after STZ injection. The synaptophysin and PGP9.5-positive area and expressions of synaptophysin mRNA and protein decreased with the duration of diabetes. Long pulse GES could induce increase of myenteric neuronal synaptic vesicles, synaptophysin and PGP9.5-positive area and in myenteric plexus. The synaptophysin mRNA and protein expression rose after GES, whatever GES beginning early or late, short-term or long-term.
  
  
  CONCLUSIONS
  The longer duration of diabetes, the more significant damages to myenteric neurons and synaptic vesicles of diabetic rats; long pulse GES could induce regeneration of myenteric plexus synaptic vesicles, thereby reform gastric motility.
authors.affiliation: Division of Gastroenterology, Union Hospital of Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: S
authors.initials: S
authors.lastname: Liu
authors.forename: Y
authors.initials: Y
authors.lastname: Guan
authors.forename: W
authors.initials: W
authors.lastname: Qian
authors.forename: F
authors.initials: F
authors.lastname: du
authors.forename: X
authors.initials: X
authors.lastname: Hou
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism / Q000503:physiopathology*; D004558:Electric Stimulation / Q000379:methods*; D007150:Immunohistochemistry; D008297:Male; D046529:Microscopy, Electron, Transmission; D009197:Myenteric Plexus / Q000502:physiology*; D009416:Nerve Regeneration / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013270:Stomach / Q000294:innervation / Q000502:physiology; D013572:Synaptic Vesicles / Q000502:physiology*; D016708:Synaptophysin / Q000378:metabolism; D043222:Ubiquitin Thiolesterase / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D016708:Synaptophysin; C489034:UCHL1 protein, rat; D043222:Ubiquitin Thiolesterase