Abstract
The respiratory physiology of bullfrogs undergoes important modifications during development [1,2,3]. The dramatic changes in the partitioning of gas exchange function between lungs and gills during development require important alterations in the neural mechanisms controlling ventilation [4,5]. Yet, the mechanisms at the basis of these changes in respiratory motor behaviour remain poorly understood. Hilaire and Duron proposed that maturation of the mammalian respiratory network may be defined, at least partly, by serotonergic modulatory processes [6]. To test the hypothesis that serotonergic modulation of respiratory neural activity changes during tadpole development, the effects of serotonin (5-HT) on neural correlates of respiratory activity were assessed using an in vitro brainstemspinal cord preparation. Preparations from tadpoles of developmental stages varying between TK stagesVI and XXV were superfused with mock CSF containing 5-HT concentrations ranging from 0–25 μM. Neural correlates of gill and lung ventilation were recorded extracellularly from cranial nerve rootletsV andX. In younger tadpoles (facultative air breathers; TK stages VI-XV) 5-HT bath application attenuated the frequency and amplitude of respiratory-related motor output (both fictive gill and lung ventilation), an effect most notable at high concentrations. In more mature animals (obligate air breathers; TK stages XVI-XXV), the effects of 5-HT bath application on fictive lung ventilation was bi-phasic. Fictive lung ventilation frequency was enhanced at low 5-HT concentrations (0.5 μ) and was depressed by higher 5-HT concentration. Moreover, 5-HT-induced attenuation of fictive gill ventilation was stronger in obligate air breathers than in preparations from younger tadpoles. These results indicate that serotonergic modulation of respiratory activity changes substantially during tadpole development. Such changes in modulatory influences may contribute to the maturation of the respiratory control system in this species.
Highlights
To be effective, inspiratory muscles on the left and right sides must contract together
We have found that a prominent gap in the column of ventral respiratory group (VRG) The nucleus tractus solitarii (NTS) relays information from primary related parvalbumin cells [2] likely corresponds to the pBc since visceral receptors to the central nervous system and is critically parvalbumin cells are rare in this zone and never co-localize with involved in the reflex control of autonomic functions
The specific protein(s) necessary for longterm facilitation (LTF) is unknown, we recently found that episodic hypoxia and LTF are associated with elevations in ventral spinal concentrations of brain derived neurotrophic factor (BDNF)
Summary
Inspiratory muscles on the left and right sides must contract together. The left and right halves of the diaphragm are synchronised because a bilateral population of medullary premotor neurones [1] simultaneously excites left and right phrenic motoneurones. Transection studies demonstrate that each side of the brainstem is capable of generating respiratory rhythm independently [2], so that left and right medullary inspiratory neurones must themselves be synchronised. The interconnections and common excitation that accomplish such synchronisation are unknown in rats. The respiratory rhythm of hypoglossal (XII) nerve discharge in transverse medullary slice preparations from neonatal rats is thought to originate in the region of the ventral respiratory group (VRG); generated there by a combination of “pacemaker” neurones [1] and their interactions with other respiratory neurones. Our goal was to discover interconnections between left and right VRG neurones as well as their connections to XII motoneurones
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