Effects of prolonged hypobaric hypoxia on carotid nerve endings and glomus cells. Changes in intercellular coupling.
Carotid bodies were removed from anesthetized rats kept under normobaric (640 Torr) and hypobaric conditions (380 Torr for 2-3 weeks). Slices (100-150 microm) of the organ were viewed under an inverted microscope for simultaneous stimulation and recording of coupled glomus cells and carotid nerve endings. The latter were identified by their more negative Em, high input resistance (Ro) and time-dependent rectification in response to negative current pulses. Also, when nerve endings had an Em more negative than -40 mV showed spontaneous activity in the form of mini-receptor potentials (mrps). Glomus cells had less negative Em and lower Ro. Prolonged hypobaric hypoxia did not change the Em of nerve endings and glomus cells. However, in both structures, Ro increased. Also, the mrps became smaller and occurred less frequently. Intercellular coupling was recognized when currents applied to one cell spread to adjoining ones. In the case of glomus cells (GC/GC coupling), it was mostly resistive and bidirectional. Coupling between nerve endings and glomus cells was more complex, When a glomus cell was stimulated, current spread to the nerve ending (GC/NE coupling) was similar in magnitude (2-3%) to coupling between GCs. However, when NE was stimulated current spread to GC (NE/GC coupling) was minimal (less than 0.1%) and transient (capacitive). Nerve endings were also bidirectionally and capacitively coupled (NE/NE coupling) with a median of 2,8%. Intracellularly injected Lucifer Yellow or Alexa 488 diffused to neighboring structures. Prolonged hypobaric hypoxia significantly tightened coupling modes GC/NE, NE/GC, and NE/NE but reduced GC/GC coupling. Tighter coupling was accompanied by lower coupling resistance, and the opposite occurred when intercellular coupling decreased. Increased GC/NE and reduced GC/GC coupling during hypobaric hypoxia may be partly responsible for the increased reactivity of these receptors under this condition.
Department of Physiology, University of Utah School of Medicine, Research Park, Salt Lake City, UT 84108-1297, USA.
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D000818:Animals; D002344:Carotid Body / Q000166:cytology* / Q000502:physiology* / Q000528:radiation effects; D015687:Cell Hypoxia / Q000502:physiology / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D005455:Fluorescent Antibody Technique / Q000379:methods; D006834:Hydrazines; D066298:In Vitro Techniques; D007365:Intercellular Junctions / Q000502:physiology* / Q000528:radiation effects; D007546:Isoquinolines; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D018613:Microscopy, Confocal / Q000379:methods; D009411:Nerve Endings / Q000502:physiology* / Q000528:radiation effects; D018408:Patch-Clamp Techniques / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
C417561:Alexa 488 hydrazide; D006834:Hydrazines; D007546:Isoquinolines; C017475:lucifer yellow; D014446:Tyrosine 3-Monooxygenase