Selective losses of brainstem catecholamine neurons after hypoxia-ischemia in the immature rat pup.
Hypoxic-ischemic (HI) injury in the preterm neonate incurs numerous functional deficits, however little is known about the neurochemically-defined brain nuclei that may underpin them. Key candidates are the brainstem catecholamine neurons. Using an immature animal model, the postnatal day (P)-3 (P3) rat pup, we investigated the effects of HI on brainstem catecholamine neurons in the locus coeruleus, nucleus tractus solitarius (NTS), and ventrolateral medulla (VLM). On P21, we found that prior P3 HI significantly reduced numbers of catecholaminergic neurons in the locus coeruleus, NTS, and VLM. Only locus coeruleus A6, NTS A2, and VLM A1 noradrenergic neurons, but not NTS C2 and VLM C1 adrenergic neurons, were lost. There was also an associated reduction in dopamine-beta-hydroxylase-positive immunolabeling in the forebrain. These findings suggest neonatal HI can affect specific neurochemically-defined neuronal populations in the brainstem and that noradrenergic neurons are particularly vulnerable to HI injury.
Buller
Kathryn M
KM
Perinatal Research Centre, University of Queensland, Queensland 4029, Australia. K.Buller@uq.edu.au
Wixey
Julie A
JA
Pathipati
Praneeti
P
Carty
Michelle
M
Colditz
Paul B
PB
Williams
Christopher E
CE
Scheepens
Arjan
A
D000818:Animals; D000831:Animals, Newborn; D001933:Brain Stem / Q000378:metabolism / Q000473:pathology*; D002395:Catecholamines / Q000378:metabolism*; D002452:Cell Count; D004195:Disease Models, Animal; D005260:Female; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism / Q000473:pathology*; D008125:Locus Coeruleus / Q000378:metabolism / Q000473:pathology; D009186:Myelin Sheath / Q000378:metabolism; D009474:Neurons / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D017552:Solitary Nucleus / Q000378:metabolism / Q000473:pathology; D014697:Ventromedial Hypothalamic Nucleus / Q000378:metabolism / Q000473:pathology
D002395:Catecholamines