Oxytocin has profound effects on many physiological processes, and disruption of its secretion, metabolism or action results in impairment of reproductive function, social and sexual behaviours, body water balance and stress responses (1-3). The specific pattern of oxytocin secretion is directly related to the characteristics of behavioural reactions (4).Oxytocin is produced in high concentrations in specific hypothalamic nuclei, including the supraoptic nucleus (SON) and paraventricular nucleus (PVN) (5). Early in development, hypothalamic-neurohypophysial neurones, which secrete either oxytocin or vasopressin, are described morphologically as immature, but possess well-developed dendritic trees that are necessary for synapse establishment, which, in parallel with the maturation of intrinsic properties, will allow SON to express an optimal electrical pattern for axonal peptide release (3,6). Accordingly, such specific properties of hypothalamic-neurohypophysial neurones are important for the establishment of two patterns of neuropeptides secretion.In rats, oxytocin gene transcription begins on embryonic day 16, and synthesis of oxytocin is first detected by immunohistochemistry on postnatal day 2 (7). Oxytocin in neurosecretory cells is packaged into specialised organelles: large dense-cored vesicles that are transported via the microtubule cytoskeleton to the sites of secretion at axon terminals or dendrites. The involvement of SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) proteins in the release of oxytocin is still a matter of debate, and exocytosis of peptide-containing vesicles is a relatively rare event, even in this vesicle-dense system. The neurohypophysial nerve terminals possess at least two functionally distinct secretory granule pools that differ in size, rate and Ca 2+ sensitivity of exocytosis:(i) an immediately releasable pool and (ii) a readily releasable pool (Ca 2+ -dependent) (8). Two types of oxytocin secretionThere are two types of oxytocin secretion: central (within the brain) and peripheral (into the systemic blood circulation). As a result of central release, oxytocin is secreted in large amounts within the brain where it acts at specific oxytocin receptors (OTRs). Oxytocin release in the brain may be derived from two main sources: (i) the centrally projecting PVN neurones, in which axons extend to the median eminence and other extra-hypothalamic regions, such as the brainstem and spinal cord and (ii) the extensive dendrites of magnocellular oxytocin neurones located in the SON and a subregion of the PVN, which release oxytocin from vesicles into the extracellular space. Both sources of oxytocin provide the neuropeptide for different brain regions where it elicits its autocrine and paracrine functions. PVN, and presumably neurones within the medial preoptic area, are believed to be mainly responsible for mediating behavioural processes of the neuropeptide (9). Until recently, it was widely assumed that parvocellular neurones in the PVN were the origin of a...

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The expression of connexin 43 and CD38 and ADP ribosyl cyclase activity in brain cells were studied in rats with experimental hypoxic and ischemic damage to the CNS. Changes in the expression and activity of the enzyme were detected over the course of ischemic injury indicating a possible contribution of NAD(+)-converting activity and NAD(+)-transporting processes to the pathogenesis of acute cerebral ischemic injury.

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We studied the role of disturbances in cell Ca(2+) homeostasis in plasma membrane blebbing and death of thymocytes. Capacitance Ca(2+) channels of the plasma membrane and intracellular Ca(2+) stores are involved in the induction and progression of changes in the membrane and cytoskeleton and apoptosis induced by acrylonitrile.

ATP activity in mouse bone marrow cells was in vitro estimated by expression of phosphatidylserine on the outer membrane surface using FITC-labeled annexin. ATP induced apoptosis in bone marrow cells. Purinergic receptor antagonists PPADS and suramin modulated the apoptotic effect of ATP on hemopoietic cells. Acute and subacute administration of doxorubicin, an inductor of oxidative burst, decreased cell sensitivity to ATP and abolished its apoptotic effect.

We studied apoptosis and expression of peripheral benzodiazepine receptors in granulosa cells of dominant follicles from women with endocrine sterility. The expression of peripheral benzodiazepine receptors in granulosa cells depends on the degree of granulosa cell apoptosis and type of disorders in follicular steroidogenesis, which suggests the involvement of peripheral benzodiazepine receptors into the regulation of folliculogenesis in health and disease.

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