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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Delayed increase of tyrosine hydroxylation in the rat A2 medullary neurons upon long-term hypoxia.

In vivo and in vitro activity of tyrosine hydroxylase ( TH) was estimated in the catecholaminergic A2 cell group of the nucleus tractus solitarius (NTS) in rats exposed to normobaric hypoxia (10% O2 in nitrogen) for 2 h, 3, 7, 14 or 21 days. The A2 cell group was subdivided into two subgroups. In the caudal A2 subgroup located caudal to the calamus scriptorius, long-term but not acute hypoxia elicited an increase of in vivo tyrosine hydroxylation rate after 7 days of exposure (+60% above normoxic controls). The increase of in vivo TH activity was maintained at the same level at the end of hypoxic exposure. In vitro TH activity was increased transiently after 7 days of hypoxia (+92% above normoxic (controls). In thr rostral A2 subgroup, hypoxia elicited a significant increase of in vivo tyrosine hydroxylation at 7 days (+38%) but did not alter in vitro TH activity throughout the whole exposure. Hypoxia produced no detectable change in TH activity in other noradrenergic cell groups of the brain stem (locus coeruleus, A5) except for a transient inhibition of in vivo TH activity in A5 after 2 h. Immunocytochemical analyses confirmed that the catecholaminergic neurons in the caudal A2 area are not only of a noradrenergic nature. The neurons were located in the commissural subnucleus of the NTS. On the other hand, the rostral A2 area contains noradrenergic neurons intermingled with a small number of adrenergic cell bodies.(ABSTRACT TRUNCATED AT 250 WORDS)[1]


  1. Delayed increase of tyrosine hydroxylation in the rat A2 medullary neurons upon long-term hypoxia. Soulier, V., Dalmaz, Y., Cottet-Emard, J.M., Kitahama, K., Pequignot, J.M. Brain Res. (1995) [Pubmed]
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