Functional Neuronal–Glial Anatomical Remodelling in the Hypothalamus

  1. Derek J. Chadwick Organizer and
  2. Jamie Goode
  1. Stéphane H. R. Oliet1,2,
  2. Aude Panatier1,2 and
  3. Richard Piet1,2,3

Published Online: 7 OCT 2008

DOI: 10.1002/9780470032244.ch19

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276

How to Cite

Oliet, S. H. R., Panatier, A. and Piet, R. (2006) Functional Neuronal–Glial Anatomical Remodelling in the Hypothalamus, in Purinergic Signalling in Neuron-Glia Interactions: Novartis Foundation Symposium 276 (eds D. J. Chadwick and J. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/9780470032244.ch19

Author Information

  1. 1

    Inserm U378, Institut François Magendie, 33077 Bordeaux, France

  2. 2

    Université Victor Segalen, Bordeaux 2, 33077 Bordeaux, France

  3. 3

    Vollum Institute L-474, Oregon Health Sciences University, Portland, OR 97239-3098, USA

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 21 APR 2006

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470018606

Online ISBN: 9780470032244



  • supraoptic nucleus (SON) of hypothalamus;
  • hypothalamo–neurohypophysial system;
  • hypothalamus anatomical remodelling;
  • NMDA receptors and SON neuron excitability regulation;
  • astrocyte contribution in information storage


The supraoptic nucleus (SON) of the hypothalamus undergoes a striking anatomical remodelling under conditions of intense stimulations like chronic dehydration, parturition and lactation. This morphological plasticity modifies the astrocytic coverage of magnocellular neurons and their synaptic afferent inputs. These changes occur within a few hours and are completely reversible upon the cessation of the stimulation. By comparing synaptic transmission and diffusion properties before and during this neuroglial remodelling, we have been able to show that the astrocytic environment of neurons contributes to the regulation of synaptic and extrasynaptic transmission. It appears that the presence of fine astrocytic processes enveloping synapses and neuronal elements ensures two important functions. First, they control the level of activation of presynaptic metabotropic glutamate autoreceptors located on glutamatergic terminals, thereby regulating synaptic strength at excitatory synapses. Second, they constitute a physical barrier to diffusion, limiting spatially and temporally spill-over of neurotransmitters and, as a consequence, extrasynaptic transmission, a process essential for intercellular communication. Using the neuroglial anatomical remodelling of the SON as an experimental model has brought new insights into the role of glial cells in the regulation of synaptic transmission and signal processing in the brain.