Synaptic and neuronal-glial plasticity in the adult oxytocinergic system in response to physiological stimuli.
Magnocellular oxytocinergic neurons in the hypothalamus offer a striking example of a mammalian neuronal system whose basic architecture and synaptic circuitry can be reversibly modified in adulthood. During parturition, lactation and prolonged osmotic stimulation, glial coverage of oxytocinergic neurons markedly diminishes and their surfaces are left in extensive juxtaposition; concurrently, there is formation of new synapses, which are predominantly GABAergic and which couple two or more oxytocinergic neurons simultaneously. These structural changes do not permanently modify the anatomy of the system since upon cessation of stimulation, neuronal juxtapositions and shared synapses disappear, to reappear upon new stimulation. At present, we can only speculate about the cellular mechanisms and factors responsible for these reversible neuroanatomical changes. However, oxytocin itself appears to be of primary importance since it can induce similar anatomical changes when chronically infused into the third ventricle.
D000818:Animals; D003681:Dehydration / Q000503:physiopathology; D005260:Female; D007774:Lactation / Q000502:physiology; D009457:Neuroglia / Q000502:physiology* / Q000648:ultrastructure; D009473:Neuronal Plasticity / Q000187:drug effects*; D010121:Oxytocin / Q000494:pharmacology / Q000502:physiology*; D011247:Pregnancy; D051381:Rats; D013495:Supraoptic Nucleus / Q000254:growth & development* / Q000502:physiology / Q000648:ultrastructure; D013569:Synapses / Q000502:physiology* / Q000648:ultrastructure
D010121:Oxytocin