Relationship of glia to GnRH axonal outgrowth from third ventricular grafts in hpg hosts

Silverman, Rachel C.; Gibson, M.E.; Silverman, Ann‐Judith

doi:10.1016/0014-4886(91)90152-3

Cited by 46 publications

(34 citation statements)

References 60 publications

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“…In rodents, LHRH fibers travel caudally until they reach the level of the median eminence region. There, instead of continuing toward the neurohypophysis, they travel in close association with tanycytic processes toward the external layer of the median eminence (Kozlowski and Coates, 1985;Silverman et al, 1991), where they gain access to the portal vasculature that drains the median eminence of their neurosecretory products. Electron and confocal microscopy studies aimed at defining the dynamics of this neuro-hemal-tanycytic relationship either during the estrous cycle or after manipulation of the steroid milieu have led to the concept that tanycytic plasticity is a required component of reproductive cyclicity (Kozlowski and Coates, 1985;King and Letourneau, 1994;King and Rubin, 1996;Prevot et al, 1998Prevot et al, , 1999, and cycling changes in the association of tanycytes to LHRH neurosecretory processes defines the capability of the terminals to access the endothelial wall of the portal vessels and, thus, to release LHRH into the portal circulation (King and Letourneau, 1994;Prevot et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity

et al. 2003

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The activation of transforming growth factor ␣ (TGF␣)-erbB-1 and neuregulin-erbB-4 signaling pathways in hypothalamic astrocytes has been shown to play a key role in the process by which the neuroendocrine brain controls luteinizing hormone-releasing hormone (LHRH) secretion. Earlier studies suggested that tanycytes, an ependymoglial cell type of the median eminence, regulate LHRH release during the estrous cycle by undergoing plastic changes that alternatively allow or prevent direct access of the LHRH nerve terminals to the portal vasculature. Neither the molecules responsible for these plastic changes nor the underlying controlling mechanisms have been identified. Here we show that cultured tanycytes express erbB-1 and erbB-2, two of the four members of the erbB receptor family, and respond to TGF␣ with receptor phosphorylation, release of prostaglandin E 2 (PGE 2 ), and a PGE 2 -dependent increase in the release of TGF␤ 1 , a growth factor previously implicated in the glial control of LHRH secretion. Blockade of either erbB-1 receptor signal transduction or prostaglandin synthesis prevented the stimulatory effect of TGF␣ on both PGE 2 and TGF␤ 1 release. Time-lapse studies revealed that TGF␣ and TGF␤ 1 have dramatically opposite effects on tanycyte plasticity. Whereas TGF␣ promotes tanycytic outgrowth, TGF␤ 1 elicits retraction of tanycytic processes. Blockade of metalloproteinase activity abolished the effect of TGF␤ 1 , suggesting that TGF␤ 1 induces tanycytic retraction by facilitating dissolution of the extracellular matrix. Prolonged (Ͼ12 hr) exposure of tanycytes to TGF␣ resulted in focal tanycytic retraction, an effect that was abolished by immunoneutralization of TGF␤ 1 action, indicating that the retraction was attributable to TGF␣-induced TGF␤ 1 formation. These in vitro results identify tanycytes as targets of TGF␣ action and demonstrate that activation of erbB-1-mediated signaling in these cells results in plastic changes that, involving PGE 2 and TGF␤ 1 as downstream effectors, mimic the morphological plasticity displayed by tanycytes during the hours encompassing the preovulatory surge of LHRH.

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Section: Discussionmentioning

confidence: 99%

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity

et al. 2003

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“…Tanycytes are specialized bipolar glial cells, located in the arcuate nucleus and the median eminence, that play a key role in neuroendocrine regulation. Tanycytes contribute to the regulation of GnRH release by extension and retraction of end-foot processes that are interposed between GnRH synaptic terminals and the portal vasculature of the median eminence (Kobayashi et al 1972, Kozlowski & Coates 1985, Ugrumov et al 1985, 1989, Silverman et al 1991, King & Letourneau 1994, Prevot et al 1999.…”

Section: The Role Of Glial Cells In the Maturation Of Neuronal Circuimentioning

confidence: 99%

The role of glia in the hypothalamus: implications for gonadal steroid feedback and reproductive neuroendocrine output

Garcia-Segura

Lorenz²,

DonCarlos³

2008

Reproduction

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Neuron-to-glia, glia-to-neuron, and glia-to-glia communication are implicated in the modulation of neuronal activity and synaptic transmission relevant to reproduction. Glial cells play an important role in neuroendocrine regulation and participate in the sexual differentiation of neuronal connectivity of brain regions involved in the control of reproductive neuroendocrine output. During puberty, modifications in the morphology and chemistry of astrocytes and tanycytes in the hypothalamus and median eminence influence the maturation of the neuronal circuits controlling the secretion of GnRH. During adult reproductive life, the glial cells participate in the transient remodeling of neuronal connectivity in the preoptic area, the arcuate nucleus, the median eminence, and other brain regions involved in the control of reproduction. Gonadal hormones regulate glial plasticity by direct and indirect effects and regulate various other endocrine signals, local soluble factors and adhesion molecules that also affect glial function and glia-to-neuron communication. The glial cells, therefore, are central to the coordination of endocrine and local inputs that bring about neural plasticity and adapt reproductive capacity to homeostatic signals.

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“…Glial processes seem to provide a permissive substrate for GnRH axonal extension, and the presence of a chemotropic factor, i.e. basic fibroblast growth factor (bFGF), provides specificity in the ME, which underlies the accurate navigation of the growing axon (Silverman et al 1991). The fact that the GnRH axon displays a remarkable degree of outgrowth during a time of extensive glial hypertrophy and hyperplasia suggests that glial cells may play a facilitatory or permissive role in GnRH axonal extension (Silverman et al 1991).…”

Section: Introductionmentioning

confidence: 99%

“…basic fibroblast growth factor (bFGF), provides specificity in the ME, which underlies the accurate navigation of the growing axon (Silverman et al 1991). The fact that the GnRH axon displays a remarkable degree of outgrowth during a time of extensive glial hypertrophy and hyperplasia suggests that glial cells may play a facilitatory or permissive role in GnRH axonal extension (Silverman et al 1991). Glial cell have been shown to regulate GnRH secretion via two related mechanisms, plastic rearrangements and direct cell-cell communication and, both mechanisms require the participation of growth factors (Ojeda et al 2003).…”

Section: Introductionmentioning

confidence: 99%

Neuronal-glial plasticity in gonadotropin-releasing hormone release in adult female rats: role of the polysialylated form of the neural cell adhesion molecule

Parkash¹,

Kaur²

2005

Journal of Endocrinology

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The gonadotropin-releasing hormone (GnRH) neurosecretory system undergoes marked structural and functional changes during the ovarian cycle. The aim of this study was to examine the neuroanatomical relationship between GnRH neurons and a polysialylated form of neural cell adhesion molecule (PSA-NCAM), a known marker of neuronal plasticity. Using immunohistofluorescent dual labeling, we determined that axon terminals of GnRH in the median arcuate nucleus (ME-ARC) region of the hypothalamus in the proestrous phase of the estrous cycle were intimately associated with PSA-NCAM. To further examine whether PSA-NCAM expression associated with GnRH neuron terminals varies in conjugation with cyclic changes in ovarian steroid hormone levels, we examined GnRH and PSA-NCAM dual expression in ovariectomized (OVX) and estrogen-progesterone-primed OVX (EBP-OVX) rats. The expression of PSA-NCAM immunoreactivity associated with the GnRH neurons in the proestrous phase and EBP-OVX rats was significantly higher than during the diestrous phase and in OVX rats where GnRH secretion declines. We further examined whether the structural changes in GnRH axon terminals in the ME-ARC region are also associated with glial plasticity. By extension and retraction of the glial processes, the GnRH neuron terminals in the ME-ARC region could undergo dynamic plastic changes that control GnRH release during the proestrous phase. PSA-NCAM expression was also seen on glial cells in the ME-ARC region. The close association between PSA-NCAM on GnRH and glial cells in the ME-ARC region of the hypothalamus in the rat showed dynamic structural changes in GnRH neuron terminals during the estrous cycle. These observations suggested that PSA-NCAM may act as a molecular substrate to promote neuroplastic changes in the GnRH neurosecretory system.

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Relationship of glia to GnRH axonal outgrowth from third ventricular grafts in hpg hosts

Cited by 46 publications

References 60 publications

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity

The role of glia in the hypothalamus: implications for gonadal steroid feedback and reproductive neuroendocrine output

Neuronal-glial plasticity in gonadotropin-releasing hormone release in adult female rats: role of the polysialylated form of the neural cell adhesion molecule

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Relationship of glia to GnRH axonal outgrowth from third ventricular grafts in hpg hosts

Cited by 46 publications

References 60 publications

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β1Release via Prostaglandin E2Production and Induces Cell Plasticity

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β1Release via Prostaglandin E2Production and Induces Cell Plasticity

The role of glia in the hypothalamus: implications for gonadal steroid feedback and reproductive neuroendocrine output

Neuronal-glial plasticity in gonadotropin-releasing hormone release in adult female rats: role of the polysialylated form of the neural cell adhesion molecule

Contact Info

Product

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Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity

Activation of erbB-1 Signaling in Tanycytes of the Median Eminence Stimulates Transforming Growth Factor β₁Release via Prostaglandin E₂Production and Induces Cell Plasticity