Morphological plasticity of the rat supraoptic nucleus – cellular consequences
European Journal of Neuroscience. 2010-12-01; 32(12): 1989-1994
DOI: 10.1111/j.1460-9568.2010.07514.x
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1. Eur J Neurosci. 2010 Dec;32(12):1989-94. doi: 10.1111/j.1460-9568.2010.07514.x.
Morphological plasticity of the rat supraoptic nucleus–cellular consequences.
Oliet SH(1), Bonfardin VD.
Author information:
(1)Inserm U862, Neurocentre Magendie, 146 rue Léo Saignat, 33077 Bordeaux,
France.
The supraoptic nuclei of the hypothalamus display a remarkable anatomical
plasticity during lactation, parturition and chronic dehydration, conditions
associated with massive neurohypophysial hormone secretion. This structural
remodeling is characterized by a pronounced reduction of the astrocytic coverage
of oxytocin neurons, resulting in an increase in the number and extent of
directly juxtaposed neuronal surfaces. Although the exact role played by such an
anatomical remodeling in the physiology of the hypothalamo-neurohypophysial
system is still unknown, several findings obtained over the last decade indicate
that synaptic and extrasynaptic transmissions are impacted by these structural
changes. We review these data and try to extrapolate how such changes at the
cellular level might affect the overall activity of the system. One repercussion
of the retraction of glial processes is the accumulation of glutamate in the
extracellular space. This build-up of glutamate causes an increased activation of
pre-synaptic metabotropic glutamate receptors, which are negatively coupled to
neurotransmitter release, and a switch in the mode of action of pre-synaptic
kainate receptors that control GABA release. Finally, the range of action of
substances released from astrocytes and acting on adjacent magnocellular neurons
is also affected during the anatomical remodeling. It thus appears that the
structural plasticity of the hypothalamic magnocellular nuclei strongly affects
neuron-glial interactions and, as a consequence, induces significant changes in
synaptic and extrasynaptic transmission.
© 2010 The Authors. European Journal of Neuroscience © 2010 Federation of
European Neuroscience Societies and Blackwell Publishing Ltd.
DOI: 10.1111/j.1460-9568.2010.07514.x
PMID: 21143653 [Indexed for MEDLINE]