title: Anatomical architecture and responses to acidosis of a novel respiratory neuron group in the high cervical spinal cord (HCRG) of the neonatal rat.
abstract: It has been postulated that there exists a neuronal mechanism that generates respiratory rhythm and modulates respiratory output pattern in the high cervical spinal cord. Recently, we have found a novel respiratory neuron group in the ventral portion of the high cervical spinal cord, and named it the high cervical spinal cord respiratory group (HCRG). In the present study, we analyzed the detailed anatomical architecture of the HCRG region by double immunostaining of the region using a neuron-specific marker (NeuN) and a marker for motoneurons (ChAT) in the neonatal rat. We found a large number of small NeuN-positive cells without ChAT-immunoreactivity, which were considered interneurons. We also found two and three clusters of motoneurons in the ventral portion of the ventral horn at C1 and C2 levels, respectively. Next, we examined responses of HCRG neurons to respiratory and metabolic acidosis in vitro by voltage-imaging together with cross correlation techniques, i.e., by correlation coefficient imaging, in order to understand the functional role of HCRG neurons. Both respiratory and metabolic acidosis caused the same pattern of changes in their spatiotemporal activation profiles, and the respiratory-related area was enlarged in the HCRG region. After acidosis was introduced, preinspiratory phase-dominant activity was recruited in a number of pixels, and more remarkably inspiratory phase-dominant activity was recruited in a large number of pixels. We suggest that the HCRG composes a local respiratory neuronal network consisting of interneurons and motoneurons and plays an important role in respiratory augmentation in response to acidosis.
authors.affiliation: Department of Medicine, Keio University Tsukigase Rehabilitation Center, Izu, Japan. yasumasaokada@1979.jukuin.keio.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Yokota
authors.forename: Y
authors.initials: Y
authors.lastname: Shinozaki
authors.forename: R
authors.initials: R
authors.lastname: Aoyama
authors.forename: Y
authors.initials: Y
authors.lastname: Yasui
authors.forename: M
authors.initials: M
authors.lastname: Ishiguro
authors.forename: Y
authors.initials: Y
authors.lastname: Oku
mesh_terms: D000142:Acidosis, Respiratory / Q000503:physiopathology*; D000818:Animals; D000831:Animals, Newborn; D002584:Cervix Uteri; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004268:DNA-Binding Proteins; D005260:Female; D051379:Mice; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism; D051381:Rats; D012119:Respiration; D013116:Spinal Cord / Q000166:cytology*; D013194:Staining and Labeling
chemical_list: D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C492380:NeuN protein, mouse; D009687:Nuclear Proteins; D002795:Choline O-Acetyltransferase