Jean‐Charles Viemari

Institut de Neurosciences de la Timone

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Gérard Hilaire

Aix-Marseille Université

Jan‐Marino Ramirez

Neurological Surgery

Michelle Bévengut

Centre de Recherche en Neurobiologie - Neurophysiologie de Marseille

Laurent Vinay

Institut de Neurosciences de la Timone

H. Burnet

Centre National de la Recherche Scientifique

Patrice Coulon

Aix-Marseille Université

Alfredo J. Garcia

University of Chicago

Andrew K. Tryba

University of Chicago

Atsushi Doi

Kumamoto Health Science University

Cécile Brocard

Boehringer Ingelheim (Austria)

Cooperative Institutions

Centre National de la Recherche Scientifique

Aix-Marseille Université

Inserm

University of Chicago

Institut de Neurosciences de la Timone

The Ohio State University

Institut de Neurobiologie de la Méditerranée

Centre de Recherche en Neurobiologie - Neurophysiologie de Marseille

Centre National pour la Recherche Scientifique et Technique (CNRST)

Neurological Surgery

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Isoproterenol modulates expiratory activities in the brainstem spinal cord preparation in neonatal mice in vitro

Respiratory Physiology & Neurobiology (2024)

Jean‐Charles Viemari

Expiration

Respiratory center

Biological neural network

10.1016/j.resp.2024.104241

Cite

Citations (0)

Differential Modulation of Neural Network and Pacemaker Activity Underlying Eupnea and Sigh-Breathing Activities

Journal of Neurophysiology (2008)

Andrew K. Tryba Fernando Peña‐Ortega Steven P. Lieske Jean‐Charles Viemari Muriel Thoby‐Brisson

Many networks generate distinct rhythms with multiple frequency and amplitude characteristics. The respiratory network in the pre-Bötzinger complex (pre-Böt) generates both the low-frequency, large-amplitude sigh rhythm and a faster, smaller-amplitude eupneic rhythm. Could the same set of pacemakers generate both rhythms? Here we used an in vitro respiratory brainslice preparation. We describe a subset of synaptically isolated pacemakers that spontaneously generate two distinct bursting patterns. These two patterns resemble network activity including sigh-like bursts that occur at low frequencies and have large amplitudes and eupneic-like bursts with higher frequency and smaller amplitudes. Cholinergic neuromodulation altered the network and pacemaker bursting: fictive sigh frequency is increased dramatically, whereas fictive eupneic frequency is drastically lowered. The data suggest that timing and amplitude characteristics of fictive eupneic and sigh rhythms are set by the same set of pacemakers that are tuned by changes in the neuromodulatory state.

Bursting

Neuromodulation

10.1152/jn.01192.2007

Cite

Citations (113)

Irregular Breathing in Mice following Genetic Ablation of V2a Neurons

Journal of Neuroscience (2012)

Steven A. Crone Jean‐Charles Viemari Steven Droho Ana Mrejeru Jan‐Marino Ramirez

Neural networks called central pattern generators (CPGs) generate repetitive motor behaviors such as locomotion and breathing. Glutamatergic neurons are required for the generation and inhibitory neurons for the patterning of the motor activity associated with repetitive motor behaviors. In the mouse, glutamatergic V2a neurons coordinate the activity of left and right leg CPGs in the spinal cord enabling mice to generate an alternating gait. Here, we investigate the role of V2a neurons in the neural control of breathing, an essential repetitive motor behavior. We find that, following the ablation of V2a neurons, newborn mice breathe at a lower frequency. Recordings of respiratory activity in brainstem–spinal cord and respiratory slice preparations demonstrate that mice lacking V2a neurons are deficient in central respiratory rhythm generation. The absence of V2a neurons in the respiratory slice preparation can be compensated for by bath application of neurochemicals known to accelerate the breathing rhythm. In this slice preparation, V2a neurons exhibit a tonic firing pattern. The existence of direct connections between V2a neurons in the medial reticular formation and neurons of the pre-Bötzinger complex indicates that V2a neurons play a direct role in the function of the respiratory CPG in newborn mice. Thus, neurons of the embryonic V2a lineage appear to have been recruited to neural networks that control breathing and locomotion, two prominent CPG-driven, repetitive motor behaviors.

10.1523/jneurosci.0445-12.2012

Cite

Citations (64)

Perinatal maturation of the mouse respiratory rhythm-generator: in vivo and in vitro studies.

HAL (Le Centre pour la Communication Scientifique Directe) (2003)

Jean‐Charles Viemari H. Burnet Michelle Bévengut Gérard Hilaire

Source

Cite

Citations (3)

Neuronal Bursting Properties in Focal and Parafocal Regions in Pediatric Neocortical Epilepsy Stratified by Histology

Journal of Clinical Neurophysiology (2010)

Charles J. Marcuccilli Andrew K. Tryba Wim van Drongelen Henner Koch Jean‐Charles Viemari

To test the hypothesis that focal and parafocal neocortical tissue from pediatric patients with intractable epilepsy exhibits cellular and synaptic differences, the authors characterized the propensity of these neurons to generate (a) voltage-dependent bursting and (b) synaptically driven paroxysmal depolarization shifts. Neocortical slices were prepared from tissue resected from patients with intractable epilepsy. Multiunit network activity and simultaneous whole-cell patch recordings were made from neurons from three patient groups: (1) those with normal histology; (2) those with mild and severe cortical dysplasia; and (3) those with abnormal pathology but without cortical dysplasia. Seizure-like activity was characterized by population bursting with concomitant bursting in intracellularly recorded cortical neurons (n = 59). The authors found significantly more N-methyl-d-aspartic acid-driven voltage-dependent bursting neurons in focal versus parafocal tissue in patients with severe cortical dysplasia (P < 0.01). Occurrence of paroxysmal depolarization shifts and burst amplitude and burst duration were significantly related to tissue type: focal or parafocal (P < 0.05). The authors show that functional differences between focal and parafocal tissue in patients with severe cortical dysplasia exist. There are functional differences between patient groups with different histology, and bursting properties can be significantly associated with the distinction between focal and parafocal tissue.

Bursting

Histology

10.1097/wnp.0b013e3181fe06d8

Cite

Citations (22)

Contribution of the potassium-chloride co-transporter KCC2 to the modulation of lumbar spinal networks in mice

European Journal of Neuroscience (2011)

Aurélie Stil Céline Jean-Xavier Sylvie Liabeuf Cécile Brocard Eric Delpire

Spontaneous activity is observed in most developing neuronal circuits, such as the retina, hippocampus, brainstem and spinal cord. In the spinal cord, spontaneous activity is important for generating embryonic movements critical for the proper development of motor axons, muscles and synaptic connections. A spontaneous bursting activity can be recorded in vitro from ventral roots during perinatal development. The depolarizing action of the inhibitory amino acids γ-aminobutyric acid and glycine is widely proposed to contribute to spontaneous activity in several immature systems. During development, the intracellular chloride concentration decreases, leading to a shift of equilibrium potential for Cl(-) ions towards more negative values, and thereby to a change in glycine- and γ-aminobutyric acid-evoked potentials from depolarization/excitation to hyperpolarization/inhibition. The up-regulation of the outward-directed Cl(-) pump, the neuron-specific potassium-chloride co-transporter type 2 KCC2, has been shown to underlie this shift. Here, we investigated whether spontaneous and locomotor-like activities are altered in genetically modified mice that express only 8-20% of KCC2, compared with wild-type animals. We show that a reduced amount of KCC2 leads to a depolarized equilibrium potential for Cl(-) ions in lumbar motoneurons, an increased spontaneous activity and a faster locomotor-like activity. However, the left-right and flexor-extensor alternating pattern observed during fictive locomotion was not affected. We conclude that neuronal networks within the spinal cord are more excitable in KCC2 mutant mice, which suggests that KCC2 strongly modulates the excitability of spinal cord networks.

Hyperpolarization

Bursting

Aminobutyric acid

10.1111/j.1460-9568.2010.07592.x

Cite

Citations (45)

Ret deficiency in mice impairs the development of A5 and A6 neurons and the functional maturation of the respiratory rhythm

European Journal of Neuroscience (2005)

Jean‐Charles Viemari Gilles Maussion Michelle Bévengut H. Burnet J. M. Pequignot

Abstract Although a normal respiratory rhythm is vital at birth, little is known about the genetic factors controlling the prenatal maturation of the respiratory network in mammals. In Phox2a mutant mice, which do not express A6 neurons, we previously hypothesized that the release of endogenous norepinephrine by A6 neurons is required for a normal respiratory rhythm to occur at birth. Here we investigated the role of the Ret gene, which encodes a transmembrane tyrosine kinase receptor, in the maturation of norepinephrine and respiratory systems. As Ret ‐null mutants ( Ret–/– ) did not survive after birth, our experiments were performed in wild‐type (wt) and Ret–/– fetuses exteriorized from pregnant heterozygous mice at gestational day 18. First, in wt fetuses, quantitative in situ hybridization revealed high levels of Ret transcripts in the pontine A5 and A6 areas. Second, in Ret–/– fetuses, high‐pressure liquid chromatography showed significantly reduced norepinephrine contents in the pons but not the medulla. Third, tyrosine hydroxylase immunocytochemistry revealed a significantly reduced number of pontine A5 and A6 neurons but not medullary norepinephrine neurons in Ret–/– fetuses. Finally, electrophysiological and pharmacological experiments performed on brainstem ‘en bloc’ preparations demonstrated impaired resting respiratory activity and abnormal responses to central hypoxia and norepinephrine application in Ret–/– fetuses. To conclude, our results show that Ret gene contributes to the prenatal maturation of A6 and A5 neurons and respiratory system. They support the hypothesis that the normal maturation of the respiratory network requires afferent activity corresponding to the A6 excitatory and A5 inhibitory input balance.

Pons

Medulla

10.1111/j.1460-9568.2005.04441.x

Cite

Citations (39)

Growth restriction induced by chronic prenatal hypoxia affects breathing rhythm and its pontine catecholaminergic modulation

Journal of Neurophysiology (2016)

K. Tree Jean‐Charles Viemari Florence Cayetanot Julie Peyronnet

Impaired transplacental supply of oxygen leads to intrauterine growth restriction, one of the most important causes of perinatal mortality and respiratory morbidity. Breathing rhythm depends on the central respiratory network modulated by catecholamines. We investigated the impact of growth restriction, using prenatal hypoxia, on respiratory frequency, on central respiratory-like rhythm, and on its catecholaminergic modulation after birth. At birth, respiratory frequency was increased and confirmed in en bloc medullary preparations, where the frequency of the fourth cervical (C4) ventral root discharge was increased, and in slice preparations containing the pre-Bötzinger complex with an increased inspiratory rhythm. The inhibition of C4 burst discharge observed in pontomedullary preparations was stronger in the growth-restricted group. These results cannot be directly linked by the tyrosine hydroxylase activity increase of A 1 /C 1 and A 2 /C 2 cell groups in the medulla since blockade of α 1 - and α 2 -adrenergic receptors did not abolish the difference between both groups. However, in pontomedullary preparations, the stronger inhibition of C4 burst discharge is probably supported by an increased inhibition of A 5 , a respiratory rhythm inhibitor pontine group of neurons displaying increased tyrosine hydroxylase activity, because blockade of α 2 -adrenergic receptors abolished the difference between the two groups. Taken together, these results indicate that growth restriction leads to a perturbation of the breathing frequency, which finds, at least in part, its origin in the modification of catecholaminergic modulation of the central breathing network.

Medulla

Pons

Catecholaminergic cell groups

10.1152/jn.00869.2015

Cite

Citations (6)

Neonatal apneic phenotype in a murine congenital central hypoventilation syndrome model is induced through non‐cell autonomous developmental mechanisms

Brain Pathology (2020)

Diego Alzate‐Correa Jillian Mei‐ling Liu Mikayla Jones Talita M. Silva Michele Joana Alves

Congenital central hypoventilation syndrome (CCHS) represents a rare genetic disorder usually caused by mutations in the homeodomain transcription factor PHOX2B. Some CCHS patients suffer mainly from deficiencies in CO2 and/or O2 respiratory chemoreflex, whereas other patients present with full apnea shortly after birth. Our goal was to identify the neuropathological mechanisms of apneic presentations in CCHS. In the developing murine neuroepithelium, Phox2b is expressed in three discrete progenitor domains across the dorsal-ventral axis, with different domains responsible for producing unique autonomic or visceral motor neurons. Restricting the expression of mutant Phox2b to the ventral visceral motor neuron domain induces marked newborn apnea together with a significant loss of visceral motor neurons, RTN ablation, and preBötzinger complex dysfunction. This finding suggests that the observed apnea develops through non-cell autonomous developmental mechanisms. Mutant Phox2b expression in dorsal rhombencephalic neurons did not generate significant respiratory dysfunction, but did result in subtle metabolic thermoregulatory deficiencies. We confirm the expression of a novel murine Phox2b splice variant which shares exons 1 and 2 with the more widely studied Phox2b splice variant, but which differs in exon 3 where most CCHS mutations occur. We also show that mutant Phox2b expression in the visceral motor neuron progenitor domain increases cell proliferation at the expense of visceral motor neuron development. We propose that visceral motor neurons may function as organizers of brainstem respiratory neuron development, and that disruptions in their development result in secondary/non-cell autonomous maldevelopment of key brainstem respiratory neurons.

Forebrain

Neuroepithelial cell

10.1111/bpa.12877

Cite

Citations (13)

Noradrénaline, maturation et fonctionnement du réseau respiratoire central : Etude in vivo et in vitro chez le foetus et le nouveau-né de souris normales ou mutantes

Jean‐Charles Viemari

Source

Cite

Citations (0)