Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The adult hypothalamoneurohypophysial system (HNS) undergoes reversible morphological changes in response to physiological stimulation. 2. In the hypothalamus, stimulation of neurohormone secretion results in reduced astrocytic coverage of oxytocinergic somata and dendrites so that their surfaces become directly juxtaposed. Concurrently, there is a significant increase in the number of GABAergic, glutamatergic. and noradrenergic synapses impinging on the neurons. 3. In the neurohypophysis, stimulation induces retraction of pituicyte processes from the perivascular area and enlargement and multiplication of neurosecretory terminals. 4. These neuronal-glial and synaptic changes are reversible with cessation of stimulation, thus rendering the HNS an excellent model to study physiologically linked structural neuronal plasticity in the adult CNS. 5. We still do not know the cellular mechanisms and factors underlying such plasticity. Recent studies indicate, however, that the adult HNS expresses molecular characteristics normally associated with histogenesis and/or tissue reorganization in developing or regenerating neural systems. They include expression of cell adhesion molecules such as the highly sialylated isoform of the neural cell adhesion molecule, PSA-NCAM, and the glycoproteins, F3 and tenascin-C. 6. The expression of PSA-NCAM and tenascin-C does not show striking differences in terms of age, sex or physiological condition but that of F3 varies considerably with neurohypophysial stimulation. 7. We postulate that such molecular features allow magnocellular neurons and their glia to undergo neuronal-glial and synaptic plasticity throughout life, provided the proper stimulus intervenes. 8. Thus, in the hypothalamic nuclei, centrally released oxytocin acting in synergy with steroids can induce such plasticity, while adrenaline, acting through beta-adrenergic mechanisms, does so in the neurohypophysis.
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PMID:Factors governing activity-dependent structural plasticity of the hypothalamoneurohypophysial system. 953 94

A striking example of the capacity of adult astrocytes to undergo reversible morphological changes in response to stimuli which enhance neuronal activity is offered by astrocytes of the adult hypothalamo-neurohypophysial system (HNS). The HNS is composed of magnocellular neurons secreting the neurohormones oxytocin and vasopressin from axon terminals in the neurohypophysis. Upon activation of HNS secretion, glial coverage of oxytocin neurons significantly diminishes and their surfaces become extensively juxtaposed. These glial changes are invariably accompanied by structural synaptic remodelling resulting in increased numbers of GABAergic, glutamatergic, and noradrenergic afferents. In the neurohypophysis, they result in an enhanced neurohemal contact area. HNS glia in the adult continue to display "embryonic" features that may allow such activity-dependent structural plasticity. For example, supraoptic astrocytes display a radial glia-like morphology and continue to express vimentin, together with GFAP. All HNS astrocytes secrete extracellular matrix glycoproteins, like tenascin-C; they also express high levels of polysialylated NCAM or PSA-NCAM and the glycoprotein F3, molecules considered essential for neuronal-glial interactions in the developing and lesioned CNS. HNS expression of most of these proteins does not visibly vary under different conditions of neurohormone secretion. We consider them as permissive factors, therefore, allowing HNS cells to undergo remodeling whenever the proper stimuli intervene. In the hypothalamic nuclei, one such stimulus is oxytocin itself which, in synergy with steroids, can induce neuronal-glial remodelling; adrenaline does so in the neurohypophysis.
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PMID:Contribution of astrocytes to activity-dependent structural plasticity in the adult brain. 1063 28

The oxytocinergic system, which plays a major role in the control of different aspects of maternity, undergoes extensive synaptic and neuronal-glial remodelling during parturition and lactation and has thus become a remarkable example of activity-dependent morphological synaptic plasticity in the adult mammalian brain. The use of different comparative ultrastructural analyses on the rat supraoptic and paraventricular nuclei, together with identification of pre- and post-synaptic elements, has allowed us to show that there is a significant increase in the number of GABAergic, glutamatergic and noradrenergic synapses impinging on oxytocin neurons, concomitant with a reduction of glial coverage of the neurons. This synaptic plasticity involves axo-dendritic and axo-somatic contacts originating from terminals making one or several synaptic contacts in one plane of section. While noradrenergic afferents arise from medullary catecholaminergic neurons, our recent in vitro observations indicate that GABAergic and glutamatergic afferents derive, at least partly, from local intrahypothalamic neurons, in close proximity to oxytocin neurons. The cellular mechanisms underlying this morphological synaptic plasticity remain to be determined but it is highly likely that they depend on increased activity in both pre- and post-synaptic elements. Moreover, the oxytocin system continues to express 'embryonic' molecular features that may allow the morphological plasticity to occur. In particular, it expresses high levels of cell surface adhesion molecules currently thought to intervene in synaptic remodelling in the developing and lesioned central nervous system, including the weakly adhesive polysialylated isoform of the Neural Cell Adhesion Molecule, the axonal glycoprotein F3 and its ligand, the extracellular matrix glycoprotein, tenascin-C.
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PMID:Maternity leads to morphological synaptic plasticity in the oxytocin system. 1158 44

Increasing evidence is establishing that adult neurons and their associated glia can undergo state-dependent changes in their morphology and in consequence, in their relationships and functional interactions. A neuronal system that illustrates this kind of neuronal-glial plasticity in an exemplary fashion is that responsible for the secretion of the neurohormone oxytocin (OT). As shown by comparative ultrastructural analysis, during physiological conditions like lactation and dehydration, which result in enhanced peripheral and central release of the peptide, astrocytic coverage of OT neurons is markedly reduced and their surfaces are left directly juxtaposed. Such reduced glial coverage is of consequence to neuronal activity since it modifies extracellular ionic homeostasis and glutamate neurotransmission. In addition, it is probably prerequisite to the synaptic remodeling that occurs concurrently, and results in an enhanced number of inhibitory (GABAergic) and excitatory (glutamatergic, noradrenergic) synapses, thus further affecting neuronal function. The neuronal-glial and synaptic changes occur rapidly, within a matter of hours, and are reversible with termination of stimulation. The adult OT system retains many juvenile molecular features that may allow such plasticity, including expression of cell adhesion molecules implicated in neuronal-glial interactions during development, like polysialylated NCAM, F3/contactin and its ligand, the matrix glycoprotein, tenascin-C. On the other hand, OT itself can induce the changes since in vivo (ventricular microinfusion) or in vitro (on acute hypothalamic slices) application leads to glial and neuronal transformations similar to those induced by physiological stimuli.
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PMID:Neuronal-glial remodeling: a structural basis for neuronal-glial interactions in the adult hypothalamus. 1244 93

The adult hypothalamo-neurohypophysial system (HNS) undergoes activity-dependent morphological plasticity which modifies astrocytic coverage of its oxytocinergic neurons and their synaptic inputs. Thus, during physiological conditions that enhance central and peripheral release of oxytocin (OT), adjacent somata and dendrites of OT neurons become extensively juxtaposed, without intervening astrocytic processes and receive an increased number of synapses. The morphological changes occur within a few hours and are reversible with termination of stimulation. The reduced astrocytic coverage has direct functional consequences since it modifies extracellular ionic homeostasis, synaptic transmission, and the size and geometry of the extracellular space. It also contributes indirectly to neuronal function by permitting formation of synapses on neuronal surfaces freed of astrocytic processes. Overall, such remodeling is expected to potentiate activated neuronal firing, especially in clusters of tightly packed neurons, an anatomical arrangement characterizing OT neurons. This plasticity connotes dynamic cell interactions that must bring into play cell surface and extracellular matrix adhesive proteins like those intervening in developing neuronal systems undergoing neuronal-glial and synaptogenic transformations. It is worth noting, therefore, that adult HNS neurons and glia continue to express such molecules, including polysialic acid (PSA)-enriched neural cell adhesion molecule (PSA-NCAM) and the glycoprotein, tenascin-C. PSA is a large, complex sugar on the extracellular domain of NCAM considered a negative regulator of adhesion; it occurs in large amounts on the surfaces of HNS neurons and astrocytes. Tenascin-C, on the other hand, possesses adhesive and repulsive properties; it is secreted by HNS astrocytes and occurs in extracellular spaces and on cell surfaces after interaction with appropriate ligands. These molecules have been considered permissive factors for morphological plasticity. However, because of their localization and inherent properties, they may also serve to modulate the extracellular environment and in consequence, synaptic and volume transmission in a system in which the extracellular compartment is constantly being modified.
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PMID:Neuronal, glial and synaptic remodeling in the adult hypothalamus: functional consequences and role of cell surface and extracellular matrix adhesion molecules. 1518 15