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'''Pituicytes''' are the principal cell type intrinsic to the [[posterior pituitary]] gland, making up 25-30% of the volume of the gland. Most express [[glial fibrillary acidic protein]], which identifies them as a subpopulation of astrocytic glial cells. Like other [[astrocytes]], they are extensively interconnected by prominent [[gap junctions]], via which they are electrotonically coupled. The cytoplasm contains abundant [[Golgi bodies]], free [[ribosomes]] and lipid bodies. The pituicytes have long processes that extend among the neurosecretory axons that innervate the lobe and onto the basement lamina of the perivascular space. The morphology of the pituicytes changes dramatically in different physiological states.
'''Pituicytes''' are the principal cell type intrinsic to the [[posterior pituitary]] gland, making up 25-30% of the volume of the gland. Most express [[glial fibrillary acidic protein]], which identifies them as a subpopulation of astrocytic glial cells. Like other [[astrocytes]], they are extensively interconnected by prominent [[gap junctions]], via which they are electrotonically coupled. The cytoplasm contains abundant [[Golgi bodies]], free [[ribosomes]] and lipid bodies. The pituicytes have long processes that extend among the neurosecretory axons that innervate the lobe and onto the basement lamina of the perivascular space. The morphology of the pituicytes changes dramatically in different physiological states.


Because of this morphological plasticity, pituicytes have long been suspected to have a role in the regulation of neurohypophysial hormone secretion. These morphological changes are apparent in physiological states such as parturition, lactation, and dehydration. In pituicytes cultured ''in vitro'',  morphological changes ("stellation") that appear similar to those that occur physiologically  involve [[actin]] depolymerization can be induced by beta-adrenergic or A1-adenosine receptor activation, and appear to result from inhibition of the small GTPase [[RhoA]]. The neurohypophysial hormones [[vasopressin]] and [[oxytocin]] can both reverse stellation and return pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton. [[Adenosine]] and neurohormones also have opposite actions on the efflux of [[taurine]], a local messenger that is released by pituicytes in hypotonic conditions and which can inhibits vasopressin secretion from axon terminals.<ref> Rosso L, Mienville JM (2009)Pituicyte modulation of neurohormone output ''Glia'' 2009 57:235-43 PMID 18803308</ref>
Because of this morphological plasticity, pituicytes have long been suspected to have a role in the regulation of neurohypophysial hormone secretion. These morphological changes are apparent in physiological states such as parturition, lactation, and dehydration. In pituicytes cultured ''in vitro'', similar morphological changes ("stellation") involving [[actin]] depolymerization can be induced by beta-adrenergic or A1-adenosine receptor activation, and appear to result from inhibition of the small GTPase [[RhoA]]. Pituicytes express specific receptors for the neurohypophysial hormones [[vasopressin]] and [[oxytocin]], both of which can reverse stellation and return pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton. [[Adenosine]] and neurohormones also have opposite actions on the efflux of [[taurine]], a local messenger that is released by pituicytes in hypotonic conditions and which can inhibits vasopressin secretion from axon terminals.<ref> Rosso L, Mienville JM (2009)Pituicyte modulation of neurohormone output ''Glia'' 2009 57:235-43 PMID 18803308</ref>
<ref> Rosso L ''et al.'' (2004) Putative physiological significance of vasopressin V1a receptor activation in rat pituicytes ''J Neuroendocrinol'' 16:313-8 PMID 15089968 </ref>  
<ref> Rosso L ''et al.'' (2004) Putative physiological significance of vasopressin V1a receptor activation in rat pituicytes ''J Neuroendocrinol'' 16:313-8 PMID 15089968 </ref>  
<ref> Rosso L ''et al.''(2002) Vasopressin and oxytocin reverse adenosine-induced pituicyte stellation via calcium-dependent activation of Cdc42 ''Eur J Neurosci'' 16:2324-32 PMID 12492427</ref>  
<ref> Rosso L ''et al.''(2002) Vasopressin and oxytocin reverse adenosine-induced pituicyte stellation via calcium-dependent activation of Cdc42 ''Eur J Neurosci'' 16:2324-32 PMID 12492427</ref>  
<ref> Hatton GI (1988) Pituicytes, glia and control of terminal secretion. ''J Exp Biol''139:67-79 PMID 3062122</ref>
<ref> Hatton GI (1988) Pituicytes, glia and control of terminal secretion. ''J Exp Biol''139:67-79 PMID 3062122</ref>
<ref>Hatton GI ''et al.'' (1984) Dynamic neuronal-glial interactions in hypothalamus and pituitary: implications for control of hormone synthesis and release ''Peptides'' 5 Suppl 1:121-38. PMID 6384946 </ref>  
<ref>Hatton GI ''et al.'' (1984) Dynamic neuronal-glial interactions in hypothalamus and pituitary: implications for control of hormone synthesis and release ''Peptides'' 5 Suppl 1:121-38. PMID 6384946 </ref>
 
==References==
==References==
<references/>
<references/>

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Pituicytes are the principal cell type intrinsic to the posterior pituitary gland, making up 25-30% of the volume of the gland. Most express glial fibrillary acidic protein, which identifies them as a subpopulation of astrocytic glial cells. Like other astrocytes, they are extensively interconnected by prominent gap junctions, via which they are electrotonically coupled. The cytoplasm contains abundant Golgi bodies, free ribosomes and lipid bodies. The pituicytes have long processes that extend among the neurosecretory axons that innervate the lobe and onto the basement lamina of the perivascular space. The morphology of the pituicytes changes dramatically in different physiological states.

Because of this morphological plasticity, pituicytes have long been suspected to have a role in the regulation of neurohypophysial hormone secretion. These morphological changes are apparent in physiological states such as parturition, lactation, and dehydration. In pituicytes cultured in vitro, similar morphological changes ("stellation") involving actin depolymerization can be induced by beta-adrenergic or A1-adenosine receptor activation, and appear to result from inhibition of the small GTPase RhoA. Pituicytes express specific receptors for the neurohypophysial hormones vasopressin and oxytocin, both of which can reverse stellation and return pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton. Adenosine and neurohormones also have opposite actions on the efflux of taurine, a local messenger that is released by pituicytes in hypotonic conditions and which can inhibits vasopressin secretion from axon terminals.[1] [2] [3] [4] [5]

References

  1. ↑ Rosso L, Mienville JM (2009)Pituicyte modulation of neurohormone output Glia 2009 57:235-43 PMID 18803308
  2. ↑ Rosso L et al. (2004) Putative physiological significance of vasopressin V1a receptor activation in rat pituicytes J Neuroendocrinol 16:313-8 PMID 15089968
  3. ↑ Rosso L et al.(2002) Vasopressin and oxytocin reverse adenosine-induced pituicyte stellation via calcium-dependent activation of Cdc42 Eur J Neurosci 16:2324-32 PMID 12492427
  4. ↑ Hatton GI (1988) Pituicytes, glia and control of terminal secretion. J Exp Biol139:67-79 PMID 3062122
  5. ↑ Hatton GI et al. (1984) Dynamic neuronal-glial interactions in hypothalamus and pituitary: implications for control of hormone synthesis and release Peptides 5 Suppl 1:121-38. PMID 6384946

[1] [2] [3] [4] [5] [6] [7] [8]

  1. ↑ Dellmann HD et al. (1991) Fine structural changes in explants of the neural lobe of the rat hypophysis J Neuroendocrinol 1991 Jun 1;3(3):339-47 PMID 19215473
  2. ↑ Dellmann HD, Carithers J (1993) Intrahypothalamically transected neurosecretory axons do not regenerate in the absence of glial cells J Neural Transplant Plast 4:127-37 PMID 8110864
  3. ↑ Ouassat M, Dellmann HD (1998)Regeneration of neurosecretory axons into various types of intrahypothalamic grafts is promoted by the absence of blood brain barrier: fine structural analysis. J Chem Neuroanat 14:181-94
  4. ↑ Wang D et al. (2009) The expression of voltage-gated ca2+ channels in pituicytes and the up-regulation of L-type ca2+ channels during water deprivation J Neuroendocrinol 21:858-66 PMID 19686441
  5. ↑ Miyata S et al. (1999) Morphological plasticity and rearrangement of cytoskeletons in pituicytes cultured from adult rat neurohypophysis. Neurosci Res 33:299-306 PMID 10401983
  6. ↑ Miyata S et al. (1997) Taurine in rat posterior pituitary: localization in astrocytes and selective release by hypoosmotic stimulation. J Comp Neurol 381:513-23 PMID 9136807
  7. ↑ Boersma CJ et al. (1983) Dynorphin 1-17 delays the vasopressin induced mobilization of intracellular calcium in cultured astrocytes from the rat neural lobe. J Neuroendocrinol 5:583-90 PMID 8680428
  8. ↑ Burnard DM, Pittman QJ, Macvicar BA (1991) Neurotransmitter-mediated changes in the electrophysiological properties of pituicytes. J Neuroendocrinol 3:433-9 PMID 19215489
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