Key result
Electrical stimulation of the rostral fastigial nucleus alters ventilation ~35%, abolished by nucleus gigantocellularis lesions.
Why the study?
The dependence of fastigial nucleus-mediated respiratory responses on the integrity of the medullary gigantocellular nucleus was unclear.
Answers are grounded in this paper and cite their sources.
The nucleus gigantocellularis of the medulla receives monosynaptic inputs from the rostral fastigial nucleus and is required for FNr-mediated respiratory responses.
Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 +/- 11.0% (P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 +/- 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO(2)-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.
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Xu et al. (2001) studied this question. Electrical stimulation of the rostral fastigial nucleus (FNr) before and after NGC lesions vs. Sham controls was evaluated on Alteration in ventilation (p=< 0.01). Electrical stimulation of the rostral fastigial nucleus altered ventilation by 35.2% (P<0.01), a response that was abolished by lesions of the nucleus gigantocellularis.
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