Elsevier

Neuroscience Letters

Volume 221, Issues 2–3, 17 January 1997, Pages 77-80
Neuroscience Letters

Perinatal asphyxia-induced changes in rat brain tyrosine hydroxylase-immunoreactive cell body number: effects of nicotine treatment

https://doi.org/10.1016/S0304-3940(96)13293-6Get rights and content

Abstract

Perinatal asphyxia (15–22 min) was induced to male Sprague–Dawley rat pups during the last day of gestation and the surviving pups were sacrificed at 4 weeks of age. Brain sections were stained for tyrosine hydroxylase immunoreactivity and Cresyl violet. With increasing duration of perinatal asphyxia a reduction in the number of tyrosine hydroxylase immunoreactive (TH-IR) nerve cell bodies was found in the locus ceruleus, probably reflecting an increased death of noradrenaline nerve cell bodies. In contrast, perinatal asphyxia (15–20 min) resulted in an increased number of TH-IR nerve cell bodies in the A9 (zona compacta of the substantia nigra) and the A10 (ventral tegmental area) regions of the mesencephalon, probably reflecting an increased survival of dopamine nerve cell bodies. Perinatal asphyxia for longer than 20 min periods reduced the number of TH-IR cell bodies in the 4 week old rat, even below those found in control animals, indicating that when asphyxia is induced for a period leading to almost 100% mortality, a long-term reduction of the number of mesencephalic dopamine neurons is produced. It has previously been shown that a 4 week postnatal nicotine (0.2 μmol/kg per h) treatment counteracts the asphyxia-induced increase in TH-IR cell body number in the substantia nigra and ventral tegmental area. Such nicotine treatment did not influence the reduction in TH-IR cell bodies in the locus ceruleus following 15–20 min of perinatal asphyxia.

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Acknowledgements

This work has been supported by grants from the Swedish Medical Research Council (10362, 10649, 8669, 10797), Karolinska Institute Research Founds, the foundations of Magnus Bergvall, Harald and Greta Jeansson, Loo and Hans Osterman, General Maternity Hospital, Wenner-Gren Center, Åke Wiberg, Samariten and the Swedish Tobacco Research Council, the Deutsche Forschungsgemeinschaft (Gr 1256/1–1) and NIH grant MH 45212. We are grateful to Miss Julia Heldt and Miss Gaby Åström for skilful technical

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