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J Neurophysiol 79: 2383-2393, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 79 No. 5 May 1998, pp. 2383-2393
Copyright ©1998 The American Physiological Society

Thalamic Locus Mediates Hypoxic Inhibition of Breathing in Fetal Sheep

Brian J. Koos, Andrew Chau, Masahiko Matsuura, Oscar Punla, and Lawrence Kruger

Departments of Obstetrics and Gynecology and Neurobiology, Nicholas S. Assali Perinatal Research Laboratory, Brain Research Institute, UCLA School of Medicine, Los Angeles, California 90095-1740

Koos, Brian J., Andrew Chau, Masahiko Matsuura, Oscar Punla, and Lawrence Kruger. Thalamic locus mediates hypoxic inhibition of breathing in fetal sheep. J. Neurophysiol. 79: 2383-2393, 1998. The effects of lesions rostral to the brain stem on breathing responses to hypoxia were determined in chronically catheterized fetal sheep (>0.8 term). These studies were designed to test the hypothesis that the diencephalon is involved in hypoxic inhibition of fetal breathing. As in normal fetuses, hypoxia inhibited breathing with transection rostral to the thalamus or transection resulting in virtual destruction of the thalamus but sparing most of the parafascicular nuclear complex. Neuronal lesions were produced in the fetal diencephalon by injecting ibotenic acid through cannulas implanted in the brain. Hypoxic inhibition of breathing was abolished when the lesions encompassed the parafascicular nuclear complex but was retained when the lesions spared the parafascicular nuclear region or when the vehicle alone was injected. A new locus has been identified immediately rostral to the midbrain, which is crucial to hypoxic inhibition of fetal breathing. This thalamic sector involves the parafascicular nuclear complex and may link central O2-sensing cells to motoneurons that inhibit breathing.




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