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Respiratory Rhythm Generation (respiratory + rhythm_generation)
Selected AbstractsDevelopmental changes in the modulation of respiratory rhythm generation by extracellular K+ in the isolated bullfrog brainstemDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2003Rachel E. Winmill Abstract This study tested the hypothesis that voltage-dependent, respiratory-related activity in vitro, inferred from changes in [K+]o, changes during development in the amphibian brainstem. Respiratory-related neural activity was recorded from cranial nerve roots in isolated brainstem,spinal cord preparations from 7 premetamorphic tadpoles and 10 adults. Changes in fictive gill/lung activity in tadpoles and buccal/lung activity in adults were examined during superfusion with artificial CSF (aCSF) with [K+]o ranging from 1 to 12 mM (4 mM control). In tadpoles, both fictive gill burst frequency (fgill) and lung burst frequency (flung) were significantly dependent upon [K+]o (r2 > 0.75; p < 0.001) from 1 to 10 mM K+, and there was a strong correlation between fgill and flung (r2 = 0.65; p < 0.001). When [K+]o was raised to 12 mM, there was a reversible abolition of fictive breathing. In adults, fictive buccal frequency (fbuccal), was significantly dependent on [K+]o (r2 = 0.47; p < 0.001), but [K+]o had no effect on flung (p > 0.2), and there was no significant correlation between fbuccal and flung. These data suggest that the neural networks driving gill and lung burst activity in tadpoles may be strongly voltage modulated. In adults, buccal activity, the proposed remnant of gill ventilation in adults, also appears to be voltage dependent, but is not correlated with lung burst activity. These results suggest that lung burst activity in amphibians may shift from a "voltage-dependent" state to a "voltage-independent" state during development. This is consistent with the hypothesis that the fundamental mechanisms generating respiratory rhythm in the amphibian brainstem change during development. We hypothesize that lung respiratory rhythm generation in amphibians undergoes a developmental change from a pacemaker to network-driven process. © 2003 Wiley Periodicals, Inc. J Neurobiol 55: 278,287, 2003 [source] AMPA and metabotropic glutamate receptors cooperatively generate inspiratory-like depolarization in mouse respiratory neurons in vitroEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2008Ryland W. Pace Abstract Excitatory transmission mediated by AMPA receptors is critical for respiratory rhythm generation. However, the role of AMPA receptors has not been fully explored. Here we tested the functional role of AMPA receptors in inspiratory neurons of the neonatal mouse preBötzinger complex (preBötC) using an in vitro slice model that retains active respiratory function. Immediately before and during inspiration, preBötC neurons displayed envelopes of depolarization, dubbed inspiratory drive potentials, that required AMPA receptors but largely depended on the Ca2+ -activated non-specific cation current (ICAN). We showed that AMPA receptor-mediated depolarization opened voltage-gated Ca2+ channels to directly evoke ICAN. Inositol 1,4,5-trisphosphate receptor-mediated intracellular Ca2+ release also evoked ICAN. Inositol 1,4,5-trisphosphate receptors acted downstream of group I metabotropic glutamate receptor activity but, here too, AMPA receptor-mediated Ca2+ influx was essential to trigger the metabotropic glutamate receptor contribution to inspiratory drive potential generation. This study helps to elucidate the role of excitatory transmission in respiratory rhythm generation in vitro. AMPA receptors in preBötC neurons initiate convergent signaling pathways that evoke post-synaptic ICAN, which underlies inspiratory drive potentials. The coupling of AMPA receptors with ICAN suggests that latent burst-generating intrinsic conductances are recruited by excitatory synaptic interactions among preBötC neurons in the context of respiratory network activity in vitro, exemplifying a rhythmogenic mechanism based on emergent properties of the network. [source] To breathe or not to breathe?EXPERIMENTAL PHYSIOLOGY, Issue 1 2009That is the question Our understanding of the role of the brain in respiratory rhythm generation and regulation began the early nineteenth century. Over the next 150 years the neuronal groups in the medulla oblongata and pons that were involved in eupnoea and in gasping were identified by techniques involving the lesioning of areas of the lower brainstem, several transections across the brainstem and focal electrical stimulation. An incomplete picture emerged that stressed the importance of the ventral medulla. Subsequent electrophysiological studies in in vivo, in situ and in vitro preparations have revealed the importance of restricted groups of neurones in this area, within the Bötzinger and pre-Bötzinger nuclei, that are the essential kernel for rhythm generation. The outputs to the spinal motoneurones responsible for the patterning of inspiratory and expiratory discharge are shaped by inputs from these neurones and others within the respiratory complex that determine the activity of respiratory bulbospinal neurones. It is clear that the developmental stage of the preparation is often critical for the pattern of respiratory activity that is generated and that these patterns have important physiological consequences. The models that are currently considered to explain rhythmogenesis are critically evaluated. The respiratory network is subject to regulation from peripheral and central chemoreceptors, amongst other afferent inputs, which act to ensure respiratory homeostasis. The roles of peripheral chemoreceptors as primarily O2 sensors are considered, and the evolution of ideas surrounding their roles is described. New insights into the transduction mechanisms of chemoreception in the carotid body and chemosensitive areas of the ventral medullary surface, specifically in monitoring CO2 levels, are reviewed. As new experimental tools, both genetic and cellular, are emerging, it can be expected that the detailed network architecture and synaptic interactions that pattern respiratory activity in relation to behavioural activity will be revealed over the next years. [source] Functional neuroanatomy of the human pre-Bötzinger complex with particular reference to sudden unexplained perinatal and infant deathNEUROPATHOLOGY, Issue 1 2008Anna M. Lavezzi The authors are the first to identify in man the pre-Bötzinger complex, a structure of the brainstem critical for respiratory rhythmogenesis, previously investigated only in rats. The evaluation of the neurokinin 1 receptors and somatostatin immunoreactivity in a total of 63 brains from 25 fetuses, nine newborns and 29 infants, allowed to delineate the anatomic structure and the boundaries of this human neural center in a restricted area of the ventrolateral medulla at the obex level, ventral to the semicompact ambiguus nucleus. The neurons of the pre-Bötzinger complex were roundish in fetuses before 30 gestational weeks and lengthened after birth, embedded in a dendritic system belonging to the reticular formation. Besides, structural and/or functional alterations of the pre-Bötzinger complex were present in a high percentage of sudden deaths (47%), prevalent in late fetal deaths. In particular, different developmental defects (hypoplasia with a decreased neuronal number and/or dendritic hypodevelopment of the reticular formation, abnormal neuronal morphology, immunonegativity of neurotransmitters, and agenesis) were found. The authors suggest that the pre-Bötzinger complex contains a variety of neurons not only involved in respiratory rhythm generation, but more extensively, essential to the control of all vital functions. Sudden death and in particular sudden unexpected fetal death could therefore be ascribed to a selective process when developmental alterations of the pre-Bötzinger complex arise. [source] A ,group pacemaker' mechanism for respiratory rhythm generationTHE JOURNAL OF PHYSIOLOGY, Issue 9 2008Christopher A. Del Negro No abstract is available for this article. [source] | ||||||||||||||||||||||