Plasticity of Central and Peripheral Sources of Noradrenaline in Rats during Ontogenesis.
The morphogenesis of individual organs and the whole organism occurs under the control of intercellular chemical signals mainly during the perinatal period of ontogenesis in rodents. In this study, we tested our hypothesis that the biologically active concentration of noradrenaline (NA) in blood in perinatal ontogenesis of rats is maintained due to humoral interaction between its central and peripheral sources based on their plasticity. As one of the mechanisms of plasticity, we examined changes in the secretory activity (spontaneous and stimulated release of NA) of NA-producing organs under deficiency of its synthesis in the brain. The destruction of NA-ergic neurons was provoked by administration of a hybrid molecular complex - antibodies against dopamine-β-hydroxylase associated with the cytotoxin saporin - into the lateral cerebral ventricles of neonatal rats. We found that 72 h after the inhibition of NA synthesis in the brain, its spontaneous release from hypothalamus increased, which was most likely due to a compensatory increase of NA secretion from surviving neurons and can be considered as one of the mechanisms of neuroplasticity aimed at the maintenance of its physiological concentration in peripheral blood. Noradrenaline secretion from peripheral sources (adrenal glands and the organ of Zuckerkandl) also showed a compensatory increase in this model. Thus, during the critical period of morphogenesis, the brain is integrated into the system of NA-producing organs and participates in their reciprocal humoral regulation as manifested in compensatory enhancement of NA secretion in each of the studied sources of NA under specific inhibition of NA production in the brain.
Koltzov Institute of Developmental Biology, Russian Academy of Sciences, Moscow, 119334, Russia. aliya_mr89@mail.ru.
N S
NS
Bondarenko
L K
LK
Dilmukhametova
A Yu
AY
Kurina
A R
AR
Murtazina
A Ya
AY
Sapronova
A P
AP
Sysoeva
M V
MV
Ugrumov
D000311:Adrenal Glands / Q000254:growth & development / Q000378:metabolism; D059331:Adrenergic Neurons / Q000378:metabolism*; D000818:Animals; D002552:Cerebral Ventricles / Q000254:growth & development / Q000378:metabolism; D004299:Dopamine beta-Hydroxylase / Q000378:metabolism; D007031:Hypothalamus / Q000254:growth & development / Q000378:metabolism; D008297:Male; D009638:Norepinephrine / Q000378:metabolism*; D010220:Para-Aortic Bodies / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D054789:Ribosome Inactivating Proteins, Type 1 / Q000633:toxicity; D000076985:Saporins
D054789:Ribosome Inactivating Proteins, Type 1; D004299:Dopamine beta-Hydroxylase; D000076985:Saporins; D009638:Norepinephrine