The role of catecholamines in memory impairment in chicks following reduced gas exchange in ovo.
We have shown previously that reducing gas exchange to chick embryos by half wrapping eggs with an impermeable membrane from either days 14-18 (W14-18) or days 10-18 (W10-18) of the 21 day incubation results in post-hatch memory deficits. In the W10-18 chicks, short-term memory following training is impaired, whereas in the W14-18 chicks, memory is intact for 30 min but does not consolidate into long-term storage. The reduction in gas exchange caused by half wrapping eggs resulted in alterations in hematocrit, O2 and CO2 tensions suggesting that the embryos are hypoxic and hypercapnic. Our aim was to test the hypothesis that increases in circulating levels of catecholamines in ovo, as a result of hypoxia, lead to a disturbance of the central noradrenergic pathways resulting in cognitive impairment. Noradrenaline is critical for memory consolidation and a disturbance during development could compromise cognitive ability. In the present study, plasma noradrenaline levels were significantly elevated compared with control levels 2 days after hatch in W14-18 chicks. There was also a decrease in tissue noradrenaline concentration in the anterior forebrain in both W14-18 and W10-18 chicks. The differential ability of centrally administered beta2- and beta3-adrenoceptor agonists to overcome the memory deficit post-training, suggests altered responsiveness of central beta2-adrenoceptors to noradrenaline in W14-18 chicks. By comparing the W10-18 and W14-18 chicks with those from eggs wrapped from W10-14 we show that it is the timing of the prenatal hypoxia, rather than its duration, that determines the nature of cognitive dysfunction. We conclude that prenatal hypoxia induced by restriction of gas exchange can disrupt or alter central noradrenergic transmission causing cognitive impairment.
Camm
E J
EJ
Fetal and Neonatal Research Group, Department of Physiology, Monash University, Clayton, Victoria 3800, Australia.
Harding
R
R
Lambert
G W
GW
Gibbs
M E
ME
D058666:Adrenergic beta-2 Receptor Agonists; D058667:Adrenergic beta-3 Receptor Agonists; D000818:Animals; D001362:Avoidance Learning / Q000502:physiology; D002642:Chick Embryo; D002645:Chickens; D004193:Discrimination Learning / Q000502:physiology; D004195:Disease Models, Animal; D004298:Dopamine / Q000097:blood / Q000378:metabolism*; D004837:Epinephrine / Q000097:blood / Q000378:metabolism*; D005311:Fetal Hypoxia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D002534:Hypoxia, Brain / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D008568:Memory / Q000502:physiology; D008569:Memory Disorders / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D009434:Neural Pathways / Q000378:metabolism / Q000503:physiopathology; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism*; D016548:Prosencephalon / Q000378:metabolism* / Q000503:physiopathology; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology; D013997:Time Factors; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
D058666:Adrenergic beta-2 Receptor Agonists; D058667:Adrenergic beta-3 Receptor Agonists; D018343:Receptors, Adrenergic, beta-2; D022702:Receptors, Adrenergic, beta-3; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine