Neuronal-glial remodeling: a structural basis for neuronal-glial interactions in the adult hypothalamus.
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.
Langle
Sarah L
SL
INSERM U378 Neuroendocrinologie Morphofonctionelle, Institut François Magendie, 1 Rue Camille Saint-Saëns, F33077 Bordeaux Cedex, France.
Poulain
Dominique A
DA
Theodosis
Dionysia T
DT
D000367:Age Factors; D000818:Animals; D002450:Cell Communication / Q000502:physiology*; D007031:Hypothalamus / Q000166:cytology* / Q000502:physiology; D009457:Neuroglia / Q000166:cytology*; D009473:Neuronal Plasticity / Q000502:physiology; D009474:Neurons / Q000166:cytology*