title: Responses of Nucleus Tractus Solitarius (NTS) early and late neurons to blood pressure changes in anesthetized F344 rats.
abstract: Previously, many different types of NTS barosensitive neurons were identified. However, the time course of NTS barosensitive neuronal activity (NA) in response to arterial pressure (AP) changes, and the relationship of NA-AP changes, have not yet been fully quantified. In this study, we made extracellular recordings of single NTS neurons firing in response to AP elevation induced by occlusion of the descending aorta in anesthetized rats. Our findings were that: 1) Thirty-five neurons (from 46 neurons) increased firing, whereas others neurons either decreased firing upon AP elevation, or were biphasic: first decreased firing upon AP elevation and then increased firing during AP decrease. 2) Fourteen neurons with excitatory responses were activated and rapidly increased their firing during the early phase of AP increase (early neurons); whereas 21 neurons did not increase firing until the mean arterial pressure changes (ΔMAP) reached near/after the peak (late neurons). 3) The early neurons had a significantly higher firing rate than late neurons during AP elevation at a similar rate. 4) Early neuron NA-ΔMAP relationship could be well fitted and characterized by the sigmoid logistic function with the maximal gain of 29.3. 5) The increase of early NA correlated linearly with the initial heart rate (HR) reduction. 6) The late neurons did not contribute to the initial HR reduction. However, the late NA could be well correlated with HR reduction during the late phase. Altogether, our study demonstrated that the NTS excitatory neurons could be grouped into early and late neurons based on their firing patterns. The early neurons could be characterized by the sigmoid logistic function, and different neurons may differently contribute to HR regulation. Importantly, the grouping and quantitative methods used in this study may provide a useful tool for future assessment of functional changes of early and late neurons in disease models.
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: Jenya
authors.initials: J
authors.lastname: Kolpakova
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: Liang
authors.initials: L
authors.lastname: Li
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: Jeffrey T
authors.initials: JT
authors.lastname: Hatcher
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: He
authors.initials: H
authors.lastname: Gu
authors.affiliation: Department of Neurology, Henry Ford Hospital, Detroit, Michigan, United States of America.
authors.forename: Xueguo
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: Jin
authors.initials: J
authors.lastname: Chen
authors.affiliation: Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando FL, United States of America.
authors.forename: Zixi Jack
authors.initials: ZJ
authors.lastname: Cheng
mesh_terms: D000200:Action Potentials; D000818:Animals; D001794:Blood Pressure; D008297:Male; D009474:Neurons / Q000502:physiology*; D051381:Rats; D011916:Rats, Inbred F344; D017552:Solitary Nucleus / Q000166:cytology / Q000502:physiology*