Synaptic Pathways to Phrenic Motoneurons Are Enhanced by Chronic Intermittent Hypoxia after Cervical Spinal Cord Injury
Phrenic nerve
Intermittent hypoxia
Hypoxia
DOI:
10.1523/jneurosci.23-07-02993.2003
Publication Date:
2018-04-13T22:30:51Z
AUTHORS (4)
ABSTRACT
Spinal hemisection at C2 reveals caudal synaptic pathways that cross the spinal midline (crossed phrenic pathways) and can restore inspiratory activity in ipsilateral motoneurons. Intermittent hypoxia induces plasticity cervical cord, resulting enhanced motor output. We hypothesized chronic intermittent (CIH) (alternating 11% O(2) air; 5 min periods; 12 hr per night; 7 nights) would strengthen crossed pathways. Experiments were performed on anesthetized, vagotomized, paralyzed, ventilated, spinally injured (C2 hemisection) rats exposed to either normoxia or CIH before acute injury (preconditioning) after (postconditioning). Spontaneous bursts compound action potentials evoked via stimulation of ventrolateral funiculus (contralateral injury) recorded both nerves. minimal absent all acutely regardless preconditioning. In postconditioned with normoxia, observed occasionally during baseline conditions always chemoreceptor (hypoxia hypercapnia). However, had substantially larger baseline, hypoxia, hypercapnia (all p < 0.05 vs normoxic group). Short-latency (0.7 msec) also by conditioning chronically (p 0.05). conclude induced cord plasticity-enhanced This required preconditions established injury.
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