Dynamic neuronal-glial interactions in hypothalamus and pituitary: implications for control of hormone synthesis and release.
Various lines of evidence have suggested that astrocytes play a dynamic role in control of hormone synthesis and release from the CNS. The model system most studied has been the rat hypothalamo-neurohypophysial system, consisting chiefly of the supraoptic and paraventricular nuclei and their axonal terminals. Neurons of this system manufacture and secrete oxytocin and vasopressin. Electron microscopic studies have shown that certain physiological conditions (e.g., dehydration, lactation) produce increases in direct apposition among these neurosecretory cells, an effect due to withdrawal of glial processes from between the neurons. Neurohypophysial astrocytes (pituicytes) show dynamic interactions with the neurons at the level of the terminals, by engulfing them and interposing processes between the terminals and the basement membrane when hormone demand is low. Pituicyte processes retract from both areas when hormone demand is high, allowing the neuronal terminals direct access to the perivascular space. Recently, osmotic manipulations (in the physiological range) have shown that these changes can be produced in vitro in neurohypophysial explants without stimulated hormone release. Experiments on cultured adult rat pituicytes have revealed similar morphological changes in response to noradrenaline. These changes were reversed or blocked by propranolol. The increase in direct soma-somatic apposition (7-9 nm separation) of magnocellular neurons could produce a tonic rise in (K+)o which would increase protein synthesis and contribute to the raised excitability of these neurons. Also, the removal of interposed glia could allow the formation of gap junctions and specialised synapses which are known to occur between these neurons. These in turn may participate in producing the coordinated firing that maximizes hormone release. The interactions of pituicytes with the terminals in the neurohypophysis suggests that these astrocytes are also a part of the mechanism of control of hormone release.
D000200:Action Potentials; D000818:Animals; D001253:Astrocytes / Q000502:physiology; D002478:Cells, Cultured; D005260:Female; D007031:Hypothalamus / Q000502:physiology*; D007774:Lactation; D008297:Male; D008854:Microscopy, Electron; D009411:Nerve Endings / Q000502:physiology; D009457:Neuroglia / Q000502:physiology*; D009474:Neurons / Q000502:physiology* / Q000648:ultrastructure; D009994:Osmolar Concentration; D010121:Oxytocin / Q000378:metabolism; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology; D010904:Pituitary Gland, Posterior / Q000502:physiology*; D010909:Pituitary Hormones, Posterior / Q000096:biosynthesis* / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D012462:Saline Solution, Hypertonic; D013495:Supraoptic Nucleus / Q000502:physiology; D014667:Vasopressins / Q000378:metabolism; D014868:Water Deprivation
D010909:Pituitary Hormones, Posterior; D012462:Saline Solution, Hypertonic; D014667:Vasopressins; D010121:Oxytocin