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Oxytocin neuron activation in NCAM-deficient mice: anatomical and functional consequences.

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Title: Oxytocin neuron activation in NCAM-deficient mice: anatomical and functional consequences.
Authors: Theodosis, D. T. (AUTHOR), Schachner, M. (AUTHOR), Neumann, I. D. (AUTHOR)
Source: European Journal of Neuroscience. Dec2004, Vol. 20 Issue 12, p3270-3280. 11p.
Subjects: Neurons, Oxytocin, Laboratory mice, Neuroglia, Neural stimulation, Cell adhesion
Abstract: During stimulated neurosecretion in the rat, oxytocin neurons display a reduced glial coverage and receive an increased number of synapses, changes that are reversed on arrest of stimulation. We identified polysialic acid on the neural cell adhesion molecule (NCAM) as an important mediator of such plasticity. To investigate further the role of this cell surface glycoprotein, we examined the oxytocin system in mice genetically deficient in NCAM. First, ultrastructural analyses revealed that in wild-type mice, the supraoptic nucleus (SON) underwent the same remodelling as in the rat because oxytocin neurons had a diminished astrocytic coverage and increased synaptic input during lactation or chronic salt loading. Surprisingly, the SON displayed this morphology in NCAM-deficient mice as well, whether they were nongestating and hydrated, lactating or dehydrated. The oxytocin system in NCAM-deficient mice was abnormally hyperactive, as illustrated by enhanced plasma and intranuclear concentrations of oxytocin and reduced anxiety-related behaviour. Plasma oxytocin concentrations were also high in lactating NCAM-deficient dams but certain parameters of lactation and maternal behaviour were impaired. NCAM-deficient mice survived ingestion of 2% saline for 7 days and had increased plasma oxytocin but they did not cope with more severe osmotic challenges. Our observations highlight further the remarkable capacity of the adult oxytocin system to undergo neuronal and glial remodelling whenever it is activated. That lack of NCAM did not prevent remodelling indicates that NCAM can be substituted by other molecular mechanisms. Finally, while NCAM deficiency greatly enhanced oxytocin release, it led to impaired oxytocin-dependent physiological and behavioural responses. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Oxytocin neuron activation in NCAM-deficient mice: anatomical and functional consequences.
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  Data: <searchLink fieldCode="AR" term="%22Theodosis%2C+D%2E+T%2E%22">Theodosis, D. T.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Schachner%2C+M%2E%22">Schachner, M.</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Neumann%2C+I%2E+D%2E%22">Neumann, I. D.</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Dec2004, Vol. 20 Issue 12, p3270-3280. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Neurons%22">Neurons</searchLink><br /><searchLink fieldCode="DE" term="%22Oxytocin%22">Oxytocin</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+mice%22">Laboratory mice</searchLink><br /><searchLink fieldCode="DE" term="%22Neuroglia%22">Neuroglia</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+stimulation%22">Neural stimulation</searchLink><br /><searchLink fieldCode="DE" term="%22Cell+adhesion%22">Cell adhesion</searchLink>
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  Label: Abstract
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  Data: During stimulated neurosecretion in the rat, oxytocin neurons display a reduced glial coverage and receive an increased number of synapses, changes that are reversed on arrest of stimulation. We identified polysialic acid on the neural cell adhesion molecule (NCAM) as an important mediator of such plasticity. To investigate further the role of this cell surface glycoprotein, we examined the oxytocin system in mice genetically deficient in NCAM. First, ultrastructural analyses revealed that in wild-type mice, the supraoptic nucleus (SON) underwent the same remodelling as in the rat because oxytocin neurons had a diminished astrocytic coverage and increased synaptic input during lactation or chronic salt loading. Surprisingly, the SON displayed this morphology in NCAM-deficient mice as well, whether they were nongestating and hydrated, lactating or dehydrated. The oxytocin system in NCAM-deficient mice was abnormally hyperactive, as illustrated by enhanced plasma and intranuclear concentrations of oxytocin and reduced anxiety-related behaviour. Plasma oxytocin concentrations were also high in lactating NCAM-deficient dams but certain parameters of lactation and maternal behaviour were impaired. NCAM-deficient mice survived ingestion of 2% saline for 7 days and had increased plasma oxytocin but they did not cope with more severe osmotic challenges. Our observations highlight further the remarkable capacity of the adult oxytocin system to undergo neuronal and glial remodelling whenever it is activated. That lack of NCAM did not prevent remodelling indicates that NCAM can be substituted by other molecular mechanisms. Finally, while NCAM deficiency greatly enhanced oxytocin release, it led to impaired oxytocin-dependent physiological and behavioural responses. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/j.1460-9568.2004.03779.x
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        Text: English
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      – SubjectFull: Laboratory mice
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      – SubjectFull: Neuroglia
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      – SubjectFull: Cell adhesion
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              Text: Dec2004
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