Structural Plasticity in the Hypothalamo Neurohypophysial System

The role of PSA has also been intensively investigated in the hypothalamo-neurohypophysial system. Oxytocin-secreting neurons of this system undergo reversible morphological changes during physiological stimulation. In the hypothalamus, such structural plasticity is represented by modifications in the size and shape of their somata and dendrites, as well as the extent to which their surfaces are covered by glia. Due to retraction of astrocytic processes, adjacent somata and dendrites of oxytocinergic neurons become extensively juxtaposed and receive an increased number of synapses. In the neurohypophysis, there is a parallel reduction in glial coverage of their axons together with retraction of glial processes from the perivascular basal lamina and an increase in the number and size of axon terminals. These changes occur rapidly, within a few hours, and are reversible upon termination of physiological stimulation65.

Evidently this plasticity requires dynamic cell interactions that must bring into play cell surface and extracellular matrix molecules such as those intervening in developing neuronal systems. Indeed, neurons and glial cells of the adult hypothalamo-neurohypophysial system continue to express such molecules, including PSA-NCAM and the extracellular matrix glycoprotein tenascin-C. Furthermore, removal of PSA with endo-N prevents withdrawal of astrocytic processes and increases the number of synaptic contacts normally induced by lactation and dehydration66. Endo-N also prevents a significant reduction in the number of GABAergic axo-somatic synapses normally induced by estradiol in the adult female arcuate nucleus67. In vitro experiments involving stimulation of the neurohypophysis by exposure to hyperosmotic conditions or a beta-adrenergic agonist also revealed a suppression of axonal and glial changes by endo-N68. Thus, PSA promotes structural plasticity in the hypothalamo-neurohypophysial system. Not only PSA is important for this process but the rest of NCAM glycoprotein seems to be involved as well, since the supraoptic nucleus displays diminished astrocytic coverage and increased synaptic input in NCAM-deficient mice. This correlated with enhanced plasma and intranuclear concentrations of oxytocin and reduced anxiety-related behavior, showing hyperactivity of the oxytocin system in NCAM-deficient mice69.

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