OT binds to specific G- protein coupled cell surface receptors (OT- Rs) on target cells to mediate a variety of effects largely concerned with reproductive function. Historically, attention has focused on the role of OT in the regulation of lactation; parturition; and reproductive behaviour. Data from animal models lacking oxytocin because of targeted disruption of the oxytocin gene have challenged this dogma, forcing a review of the physiological roles of the hormone.

Oxytocin and Lactation

In the rat, the stimulation of sensory afferents in the nipple by the act of suckling trigger a reflex cascade leading to synchronized firing bursts of oxytocic magnocellular neurones, with pulsatile OT release corresponding to this burst activity. The released OT acts on OT- Rs on smooth muscle cells lining the milk ducts of the breast, initiating milk ejection. OT is essential for completion of this milk ejection re f lex in rodent. Mice lacking OT fail to transfer milk to their suckling young, and this deficit is corrected by injection of OT. In contrast, Women lacking posterior pituitary function can breast feed normally, illustrating that OT is not necessary for lactation in Humans.

Oxytocin and Parturition

OT is a powerful uterotonic agent. In many mammals there is both an increase in OT secretion during parturition, and an increase in uterine responsiveness to OT at term. These data suggest a key role for the hormone in the initiation and progression of labour.

It is believed that falling progesterone concentrations toward the end of pregnancy lead to up- regulation of uterine myometrial OT- Rs, enhanced contractility, and increased sensitivity to circulating OT. Stretching of the ‘birth canal’ during parturition leads to the stimulation of specific autonomic afferents, triggering increased burst firing of oxytocic magnocellular neurones and OT release. A positive feedback loop is formed, with OT both stimulating uterine contraction further and enhancing the production of local uterotonic mediators. It has been difficult to demonstrate increased circulating OT levels in women during labour, due in part to the difficulties of analysing pulsatile release coupled with the short circulating half- life of the hormone due to the action of placental cysteine aminopeptidase. In mice lacking OT, parturition is normal. Moreover, Women with absent posterior pituitary function can have a normal labour. However, the importance of OT in the birth process is highlighted by the effectiveness of OT antagonists in the management of preterm labour.

OT may have key additional offspring- facing roles in parturition. Maternal OT produces a switch in fetal central nervous system (CNS) neurotransmission with enhanced inhibitory GABAergic signalling. This increases fetal neuronal resistance to hypoxaemic damage that may occur during delivery, part of adaptive mother- fetal signalling during parturition in which OT is a major player.

Oxytocin and Behaviour

OT- R expression is widespread in the CNS of many species. There is clear evidence that OT has important influences on reproductive behaviour in rat; facilitating both lordosis and the development of maternal behaviour patterns. However, mice lacking OT exhibit normal sexual and maternal behaviour, indicating these effects may be species dependent. Central oxytocic transmission appears to re duce anxiety and hypothalamo- pituitary- adrenal stress responses in female rats. However, the same central oxytotic function may be required for normal adrenocorticotropin responses to stress. OT release from both dendrites and nerve terminals of hypothalamic magnocellular neurons can be regulated by other neuropeptides, highlighting the potential for magnocellular OT to integrate with central neurotransmission.

Central OT pathways have been implicated complex behaviour: social recognition, affiliation, and social bonding. This clustering has raised interest in the role of OT and OT pathways in the development of autism. A number of association studies have demonstrated linkage between autism and OT- R polymorphisms. Together, these data suggest a complex role for OT in the stress and other behavioural responses, with species and context- dependent differential effects.

Integrated Physiology of Oxytocin

 How are the proposed roles of OT in reproductive function reconciled with both human and mouse data that highlight normal function in the absence of the hormone? Clearly there are interspecies differences in OT- modulated processes that contribute important qualifications to the data. The mouse gravid uterus does not ex press OT- Rs, in contrast to human and rat. It is perhaps not surprising therefore, that parturition is normal in the OT null- mouse. Similarly, in contrast to rat, maternal behaviour evolves gradually in mouse, and is not acquired rapidly in the postpartum period. Mouse may therefore not be a good model for the uterine and behavioural effects of OT. Secondly, there is clearly variable redundancy in some of the physiological pathways in which OT is involved. This redundancy may vary between species. The extrapolation of OT’s role in normal physiology from those responses found in its absence should thus be made with caution.

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مواضيع ذات صلة

Syndrome of Inappropriate Antidiuresis

Hypothalamic Diabetes Insipidus

Regulation and Biological Actions of Growth Hormone and Prolactin

Hypothalamic Control of Growth Hormone Secretion

Corticotropin-Releasing Hormone

The Physiology of Vasopressin

Gonadotropin-Releasing Hormone

Thyrotropin-Releasing Hormone

Biosynthesis of Adrenal Cortex Mineralocorticoids, Glucocorticoids, and Some Androgens

Mechanisms of hormone action: Cell Signaling by Membrane Receptors

Biosynthesis of Peptide and Protein Hormones

Hormones and Their Communication Systems