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rdf:type
lifeskim:mentions
pubmed:dateCreated
2010-12-14
pubmed:abstractText
We studied preBötzinger Complex (preBötC) inspiratory interneurons to determine the cellular mechanisms that influence burst termination in a mammalian central pattern generator. Neonatal mouse slice preparations that retain preBötC neurons generate respiratory motor rhythms in vitro. Inspiratory-related bursts rely on inward currents that flux Na(+), thus outward currents coupled to Na(+) accumulation are logical candidates for assisting in, or causing, burst termination. We examined Na(+)/K(+) ATPase electrogenic pump current (I(pump)), Na(+)-dependent K(+) current (I(K-Na)), and ATP-dependent K(+) current (I(K-ATP)). The pharmacological blockade of I(pump), I(K-Na), or I(K-ATP) caused pathological depolarization akin to a burst that cannot terminate, which impeded respiratory rhythm generation and reversibly stopped motor output. By simulating inspiratory bursts with current-step commands in synaptically isolated preBötC neurons, we determined that each current generates approximately 3-8?mV of transient post-burst hyperpolarization that decays in 50-1600?ms. I(pump), I(K-Na), and - to a lesser extent - I(K-ATP) contribute to terminating inspiratory bursts in the context of respiratory rhythm generation by responding to activity dependent cues such as Na(+) accumulation.
pubmed:language
eng
pubmed:journal
pubmed:status
PubMed-not-MEDLINE
pubmed:issn
1662-5110
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
124
pubmed:year
2010
pubmed:articleTitle
Outward Currents Contributing to Inspiratory Burst Termination in preBötzinger Complex Neurons of Neonatal Mice Studied in Vitro.
pubmed:affiliation
Department of Applied Science, The College of William and Mary Williamsburg, VA, USA.
pubmed:publicationType
Journal Article