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Developmental origin of preBötzinger complex respiratory neuronsLaser ablation of Dbx1 neurons in the pre-Bötzinger complex stops inspiratory rhythm and impairs output in neonatal miceCumulative lesioning of respiratory interneurons disrupts and precludes motor rhythms in vitro.Dendritic calcium activity precedes inspiratory bursts in preBotzinger complex neurons.The retrotrapezoid nucleus neurons expressing Atoh1 and Phox2b are essential for the respiratory response to CO₂Robust network oscillations during mammalian respiratory rhythm generation driven by synaptic dynamics.Functional Interactions between Mammalian Respiratory Rhythmogenic and Premotor Circuitry.Transcriptome of neonatal preBötzinger complex neurones in Dbx1 reporter mice.Clonal analysis by distinct viral vectors identifies bona fide neural stem cells in the adult zebrafish telencephalon and characterizes their division properties and fate.Mechanisms Leading to Rhythm Cessation in the Respiratory PreBötzinger Complex Due to Piecewise Cumulative Neuronal Deletions(1,2,3).Sodium and calcium current-mediated pacemaker neurons and respiratory rhythm generation.Asymmetric control of inspiratory and expiratory phases by excitability in the respiratory network of neonatal mice in vitro.4-Aminopyridine-sensitive outward currents in preBötzinger complex neurons influence respiratory rhythm generation in neonatal mice.Automated cell-specific laser detection and ablation of neural circuits in neonatal brain tissue.Computer-aided neurophysiology and imaging with open-source PhysImage.A 'group pacemaker' mechanism for respiratory rhythm generation
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description
researcher ORCID ID = 0000-0003-2849-7672
@en
wetenschapper
@nl
name
John Hayes
@ast
John Hayes
@en
John Hayes
@es
John Hayes
@nl
type
label
John Hayes
@ast
John Hayes
@en
John Hayes
@es
John Hayes
@nl
altLabel
John A. Hayes
@en
prefLabel
John Hayes
@ast
John Hayes
@en
John Hayes
@es
John Hayes
@nl
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0000-0003-2849-7672