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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. They 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.
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'''Pituicytes''' are the main cell type within the [[posterior pituitary]] gland, a [[neuroendocrine]] gland at the base of the brain from which the hormones [[oxytocin]] and [[vasopressin]] are secreted. The pituicytes do not themselves make these hormones; oxytocin and vasopressin are synthesised by large [[neuroendocrine neurons]] of the [[hypothalamus]] whose axons project into the posterior pituitary gland. The pituicytes are closely associated with these axons, they express receptors by which they respond directly to oxytocin and vasopressin, and their morphology can change dramatically in different physiological states. Exactly what their role is remains incompletely understood. They are thought to have an influence upon secretion of vasopressin and oxytocin, in particular by releasing the inhibitory amino acid [[taurine]] in response to hypo-osmotic challenge <ref>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</ref>. They are thought to be important for the growth of the neurosecretory axons, including regrowth of axons after damage <ref>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</ref>
<ref>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</ref>. They are also thought to be involved in the autophagic destruction of damaged axons.
 
 
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. Pituicytes also respond to [[dynorphin]], an [[opioid peptide]] that is co-secreted with both vasopressin and oxytocin <ref>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</ref> [[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.''(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 ''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>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</ref>
 
==References==
{{reflist}}
 
<ref>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</ref>
<ref>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</ref>
<ref>Burnard DM, Pittman QJ, Macvicar BA (1991) Neurotransmitter-mediated changes in the electrophysiological properties of pituicytes. ''J Neuroendocrinol'' 3:433-9 PMID 19215489</ref>[[Category:Suggestion Bot Tag]]

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Pituicytes are the main cell type within the posterior pituitary gland, a neuroendocrine gland at the base of the brain from which the hormones oxytocin and vasopressin are secreted. The pituicytes do not themselves make these hormones; oxytocin and vasopressin are synthesised by large neuroendocrine neurons of the hypothalamus whose axons project into the posterior pituitary gland. The pituicytes are closely associated with these axons, they express receptors by which they respond directly to oxytocin and vasopressin, and their morphology can change dramatically in different physiological states. Exactly what their role is remains incompletely understood. They are thought to have an influence upon secretion of vasopressin and oxytocin, in particular by releasing the inhibitory amino acid taurine in response to hypo-osmotic challenge [1]. They are thought to be important for the growth of the neurosecretory axons, including regrowth of axons after damage [2] [3]. They are also thought to be involved in the autophagic destruction of damaged axons.


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. Pituicytes also respond to dynorphin, an opioid peptide that is co-secreted with both vasopressin and oxytocin [4] 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. [5] [6] [7] [8] [9] [10]

References

  1. ↑ 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
  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. ↑ 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
  5. ↑ Rosso L, Mienville JM (2009)Pituicyte modulation of neurohormone output Glia 2009 57:235-43 PMID 18803308
  6. ↑ Rosso L et al. (2004) Putative physiological significance of vasopressin V1a receptor activation in rat pituicytes J Neuroendocrinol 16:313-8 PMID 15089968
  7. ↑ 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
  8. ↑ Hatton GI (1988) Pituicytes, glia and control of terminal secretion. J Exp Biol139:67-79 PMID 3062122
  9. ↑ 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
  10. ↑ 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

[1] [2] [3]

  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. ↑ 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
  3. ↑ 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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