Substitution of extracellular Ca2+ by Sr2+ prolongs inspiratory burst in pre-Bötzinger complex inspiratory neurons.

Abstract:

:The pre-Bötzinger complex (preBötC) underlies inspiratory rhythm generation. As a result of network interactions, preBötC neurons burst synchronously to produce rhythmic premotor inspiratory activity. Each inspiratory burst consists of action potentials (APs) on top of a 10- to 20-mV synchronous depolarization lasting 0.3-0.8 s known as inspiratory drive potential. The mechanisms underlying the initiation and termination of the inspiratory burst are unclear, and the role of Ca(2+) is a matter of intense debate. To investigate the role of extracellular Ca(2+) in inspiratory burst initiation and termination, we substituted extracellular Ca(2+) with Sr(2+). We found for the first time an ionic manipulation that significantly interferes with burst termination. In a rhythmically active slice, we current-clamped preBötC neurons (Vm ≅ -60 mV) while recording integrated hypoglossal nerve (∫XIIn) activity as motor output. Substitution of extracellular Ca(2+) with either 1.5 or 2.5 mM Sr(2+) significantly prolonged the duration of inspiratory bursts from 653.4 ± 30.7 ms in control conditions to 981.6 ± 78.5 ms in 1.5 mM Sr(2+) and 2,048.2 ± 448.5 ms in 2.5 mM Sr(2+), with a concomitant increase in decay time and area. Substitution of extracellular Ca(2+) by Sr(2+) is a well-established method to desynchronize neurotransmitter release. Our findings suggest that the increase in inspiratory burst duration is determined by a presynaptic mechanism involving desynchronization of glutamate release within the network.

journal_name

J Neurophysiol

authors

Morgado-Valle C,Fernandez-Ruiz J,Lopez-Meraz L,Beltran-Parrazal L

doi

10.1152/jn.00705.2014

subject

Has Abstract

pub_date

2015-02-15 00:00:00

pages

1175-83

issue

4

eissn

0022-3077

issn

1522-1598

pii

jn.00705.2014

journal_volume

113

pub_type

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