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Anatomical remodelling of the supraoptic nucleus: changes in synaptic and extrasynaptic transmission.

Abstract : The adult hypothalamic-neurohypophysial system undergoes activity-dependent morphological plasticity that modifies the astrocytic enwrapping of its magnocellular neurones. For a long time, the functional consequences of such changes have remained hypothetical. Modifications in the glial environment of neurones are expected to have important physiological repercussions in view of the various functions played by astrocytes in the central nervous system. In particular, glial cells are essential for uptake of neurotransmitters, including glutamate, and for physically and functionally restricting diffusion of neuroactive substances within the extracellular space. Recent studies performed in the supraoptic nucleus of lactating and chronically dehydrated animals, in conditions where astrocytic coverage of neurones is reduced, have revealed a significant impairment of glutamate clearance. The resulting accumulation of the excitatory amino acid in the extracellular space around glutamatergic inputs causes an enhanced activation of presynaptic metabotropic glutamate receptors that inhibit transmitter release. In the supraoptic nucleus of lactating rats, neuroglial remodelling is accompanied by modification of the geometry, size and diffusion properties of the extracellular space. The latter observations suggest that, in the activated supraoptic nucleus, the range of action and the concentration of released neuroactive substances may be significantly enhanced. Overall, our observations indicate that the glial environment of supraoptic neurones influences synaptic glutamatergic transmission, as well as extrasynaptic forms of communication.
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https://www.hal.inserm.fr/inserm-00000069
Contributor : Stéphane Oliet <>
Submitted on : Wednesday, March 29, 2006 - 11:59:19 AM
Last modification on : Tuesday, November 5, 2019 - 10:00:07 AM

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Stéphane Oliet, Richard Piet. Anatomical remodelling of the supraoptic nucleus: changes in synaptic and extrasynaptic transmission.. J Neuroendocrinol, 2004, 16, pp.303-7. ⟨10.1111/j.0953-8194.2004.01159.x⟩. ⟨inserm-00000069⟩

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