Intermittent hypoxia promotes recovery of respiratory motor function in spinal cord injured mice depleted of serotonin in the central nervous system

We examined the effect of repeated daily exposure to intermittent hypoxia (IH) on the recovery of respiratory and limb motor function in mice genetically depleted of central nervous system serotonin. Electroencephalography, diaphragm activity, ventilation, core body temperature and limb mobility were measured in spontaneously breathing wild type (Tph2^+/+) and tryptophan hydroxylase 2 knockout (Tph2^-/-) mice. Following a C₂ hemisection the mice were exposed daily to IH (i.e. twelve 4-min episodes of 10% oxygen interspersed with 4-min normoxic periods followed by a 90-min end recovery period) or normoxia (i.e. sham protocol - 21% oxygen) for 10 consecutive days. Diaphragm activity recovered to pre-hemisection levels in the Tph2^+/+ and Tph2^-/- mice following exposure to IH but not normoxia (Tph2^+/+ 1.3 ± 0.2 vs. 0.3 ± 0.2; Tph2^-/- 1.06 ± 0.1 vs. 0.3 ± 0.1, standardized to pre-hemisection values, p < 0.01). Likewise, recovery of tidal volume and breathing frequency was evident, although breathing frequency values did not return to pre-hemisection levels within the time frame of the protocol. Partial recovery of limb motor function was also evident two weeks after spinal cord hemisection. However, recovery was not dependent on IH or the presence of serotonin in the central nervous system. We conclude that IH promotes recovery of respiratory function but not basic motor tasks. Moreover, we conclude that spontaneous or treatment induced recovery of respiratory and motor limb function is not dependent on serotonin in the central nervous system in a mouse model of spinal cord injury.

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