title: Electrotonic transmission within pericyte-containing retinal microvessels.
abstract: OBJECTIVE
  Little is known about the electrotonic architecture of the pericyte-containing retinal microvasculature. Here, the authors focus on the cell-to-cell transmission of hyperpolarization, which can induce abluminal pericytes to relax and lumens to dilate.
  
  
  METHODS
  With perforated-patch pipettes, the authors monitored the membrane potentials and ionic currents of pairs of pericytes located on freshly isolated rat retinal microvessels. Voltage changes were induced by administering electrical stimuli into pericytes, miniperfusing the KATP channel opener pinacidil, or using oxotremorine to activate chloride channels.
  
  
  RESULTS
  Suggestive of extensive cell-to-cell communication, spontaneous voltage changes were strikingly similar in widely separated pericytes. In addition, injection of current into one of a pair of sampled pericytes always elicited a voltage response in the other sampled pericyte; the gap junction uncoupler, heptanol, blocked this transmission. In the dual recordings, hyperpolarization spreading from a current-injected pericyte decayed approximately 40% within 100 microm. In contrast, pinacidil-induced hyperpolarizations diminished by only approximately 2% in 100 microm. Depolarizations also appeared to spread with similar transmission efficacies.
  
  
  CONCLUSIONS
  Based on the experiments, the authors propose that key features of the electrotonic architecture of retinal microvessels include highly efficient cell-to-cell communication within the endothelium and relatively inefficient transmission at pericyte/endothelial junctions. Thus, the endothelium is likely to provide an efficient pathway that functionally links contractile pericytes and thereby, serves to coordinate the vasomotor response of a retinal capillary.
authors.affiliation: Department of Ophthalmology & Visual Sciences, University of Michigan, Ann Arbor, Michigan 48105, USA.
authors.forename: David M
authors.initials: DM
authors.lastname: Wu
authors.forename: Masahiro
authors.initials: M
authors.lastname: Minami
authors.forename: Hajime
authors.initials: H
authors.lastname: Kawamura
authors.forename: Donald G
authors.initials: DG
authors.lastname: Puro
mesh_terms: D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D018118:Chloride Channels / Q000187:drug effects / Q000378:metabolism; D004558:Electric Stimulation; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D007365:Intercellular Junctions / Q000187:drug effects / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D008833:Microcirculation / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D008954:Models, Biological; D010095:Oxotremorine / Q000494:pharmacology; D020286:Pericytes / Q000187:drug effects / Q000502:physiology*; D020110:Pinacidil / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D020318:Rats, Long-Evans; D012171:Retinal Vessels / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D018118:Chloride Channels; D015221:Potassium Channels; C117780:mitochondrial K(ATP) channel; D010095:Oxotremorine; D020110:Pinacidil