Corticotropin releasing factor induces proliferation of cerebellar astrocytes

Ha, Byeong Keun; Bishop, Georgia A.; King, James S.; Burry, Richard W.

doi:10.1002/1097-4547(20001215)62:6<789::aid-jnr5>3.0.co;2-5

Cited by 27 publications

(14 citation statements)

References 68 publications

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“…This unique expression pattern of CRF raised the possibility of development-specific functions, and a dendritic-modulating role has been proposed in cerebellum (49)(50)(51). The exclusive location of CRF 1 on neuronal dendrites excluded the possibility that CRF might act in concert on radial glia differentiation, suggesting instead that early postnatal CRF may influence the maturation of hippocampal neurons, specifically dendrites, directly.…”

Section: Discussionmentioning

confidence: 99%

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

Chen

Bender²,

Brunson³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

162

165

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The interplay of environmental and genetic factors in the developmental organization of the hippocampus has not been fully elucidated. The neuropeptide corticotropin-releasing factor (CRF) is released from hippocampal interneurons by environmental signals, including stress, to increase synaptic efficacy. In the early postnatal hippocampus, we have previously characterized a transient population of CRF-expressing Cajal-Retzius-like cells. Here we queried whether this stress-activated neuromodulator influences connectivity in the developing hippocampal network. Using mice deficient in the principal hippocampal CRF receptor [CRF 1(؊͞؊)] and organotypic cultures grown in the presence of synthetic CRF, or CRF receptor antagonists, we found robust effects of CRF on dendritic differentiation in hippocampal neurons. In CRF 1(؊͞؊) mice, the dendritic trees of hippocampal principal cells were exuberant, an effect that was induced in normal hippocampi in vitro by the presence of CRF 1 antagonists. In both cases, total dendritic length and dendritic branching were significantly increased. In contrast, exogenous synthetic CRF blunted the dendritic growth in hippocampal organotypic cultures. Taken together, these findings suggest that endogenous CRF, if released excessively by previous early postnatal stress, might influence neuronal connectivity and thus function of the immature hippocampus.corticotropin-releasing hormone ͉ stress ͉ corticotropin-releasing factor receptor ͉ neuropeptide ͉ Cajal-Retzius cells T he developmental organization of the hippocampal network is a complex process, requiring the interplay of genetic and environmental factors. Establishment of basic hippocampal connectivity is governed by genetically determined mechanisms, including the coordinated activation of transcription factors (1-3), and the expression of both local and more generally acting guidance molecules (4-6). Once the basic elements are in place, refinement of connectivity is achieved through environmental stimuli that influence neuronal activity (7-9). Among the elements that contribute to developmental organization of the hippocampus are the Cajal-Retzius (CR) cells (10, 11). CR cells, found in hippocampal marginal zones, release reelin, an extracellular matrix protein required for layer formation and positioning of cortical neurons (12, 13). Because lack of reelin causes perturbation of cortical lamination (14), control of neuronal positioning has been considered the major function of CR cells. However, recent results suggest additional roles for CR cells that are independent of reelin (15-18).We have previously characterized a subset of CR cells that do not express reelin but release the neuropeptide corticotropinreleasing factor (CRF).ʈ CRF functions primarily as a regulator of the neuroendocrine stress response (19,20) but is also widely expressed within the central nervous system, where it acts as a neuromodulator (21)(22)(23)(24) 5-dimethyl-N,N-dipropyl-pyrazolo[2,3-a]pyrimidin-7-amine, previously R121919} were 0.1 or 1 M (for G...

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Section: Discussionmentioning

confidence: 99%

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

Chen

Bender²,

Brunson³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

162

165

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“…The induction of TH ϩ neurons by CRF in the presence of BDNF may possibly result from 1) the rescue of a subpopulation of TH ϩ cells for which CRF was a survival factor, as described previously (Radulovic et al, 2003); 2) a mitogenic effect of CRF on BDNF-induced TH ϩ cells via cAMP-dependent signaling (Ha et al, 2000); 3) the restoration of a phenotype lost transiently as the result of cell suffering or lack of appropriate trophic stimulation during the processing of the embryonic tissue; 4) the recruitment of postmitotic neurons, which…”

Section: Discussionmentioning

confidence: 99%

The Phenotypic Differentiation of Locus Ceruleus Noradrenergic Neurons Mediated by Brain-Derived Neurotrophic Factor Is Enhanced by Corticotropin Releasing Factor through the Activation of a cAMP-Dependent Signaling Pathway

Traver¹,

Marien²,

Martin³

et al. 2006

Molecular Pharmacology

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We have developed a model system of locus ceruleus (LC) neurons in culture, in which brain-derived neurotrophic factor (BDNF) induces the emergence of noradrenergic neurons attested by the presence of tyrosine hydroxylase (TH) and dopamine-␤-hydroxylase and the absence of phenylethanolamine N-methyl-transferase. Although inactive in itself, the neuropeptide corticotropin releasing factor (CRF) strongly amplified the effect of BDNF, increasing the number of cells expressing TH and the active accumulation of noradrenaline by a factor of 2 to 3 via a mechanism that was nonmitogenic. CRF also acted cooperatively with neurotrophin-4, which like BDNF is a selective ligand of the TrkB tyrosine kinase receptor. The effect of CRF but not that of BDNF was prevented by astressin, a nonselective CRF-1/CRF-2 receptor antagonist. However, only CRF-1 receptor transcripts were detectable in LC cultures, suggesting that this receptor subtype mediated the effect of CRF. Consistent with the positive coupling of CRF-1 receptors to adenylate cyclase, the trophic action of CRF was mimicked by cAMP elevating agents. Epac, a guanine nucleotide exchange factor directly activated by cAMP, contributed to the effect of CRF through the stimulation of extracellular signalregulated kinases (ERKs) 1/2. However, downstream of ERK1/2 activation by CRF, the phenotypic induction of noradrenergic neurons relied upon the stimulation of the phosphatidylinositol-3-kinase/Akt transduction pathway by BDNF. Together, our results suggest that CRF participates to the phenotypic differentiation of LC noradrenergic neurons during development. Whether similar mechanisms account for the high degree of plasticity of these neurons in the adult brain remains to be established.The majority of noradrenergic (NA) neurons in the brain are localized within a single brainstem nucleus, the locus ceruleus (LC). However, because of a widespread projection system, these neurons innervate almost the entire central nervous system (Berridge and Waterhouse, 2003). Because of the ubiquitous distribution of NA, the LC-NA system plays a prominent role in a variety of brain functions and behaviors that include vigilance, attention, arousal, memory acquisition, locomotor control, and response to stress (Berridge and Waterhouse, 2003). LC NA neurons are also interesting for other reasons: 1) via their neurotransmitter, they influence the development and survival of other populations of neuronal cells either during development of the brain or later in life (Meier et al., 1991;Marien et al., 2004); 2) some of them can recover in the adult brain a phenotype that they transiently expressed during development (Bezin et al., 2000); and 3) they are vulnerable to neurodegenerative conditions such as Alzheimer's and Parkinson's diseases (Zarow et al., 2003) and represent a potential target for pharmacological This work was supported by Centre de Recherche Pierre Fabre and Institut National de la Santé et de la Recherche Médicale.Article, publication date, and citation information can...

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“…CRH has been shown to promote or inhibit cell proliferation via interacting with CRH‐R1 in several cell types (McGillis et al . 1989; Singh 1989; Ha et al . 2000; Carlson et al .…”

Section: Discussionmentioning

confidence: 99%

Corticotropin‐releasing hormone induces proliferation and TNF‐α release in cultured rat microglia via MAP kinase signalling pathways

Wang¹,

Ji²,

Dow³

2002

Journal of Neurochemistry

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We have previously demonstrated that corticotropin-releasing hormone (CRH) receptor 1 (CRH-R1) is functionally expressed in rat microglia. In the present study, we show that CRH, acting on CRH-R1, promoted cell proliferation and tumour necrosis factor-a (TNF-a) release in cultured rat microglia. Exogenous CRH resulted in an increase in BrdU incorporation compared with control cells, which was observed in a range of concentrations of CRH between 10 and 500 nM, with a maximal response at 50 nM. The effect of CRH on BrdU incorporation was inhibited by a CRH antagonist astressin but not by a cAMP-dependent protein kinase inhibitor H89. Exposure of microglial cells to CRH resulted in a transient and rapid increase in TNF-a release in a dosedependent manner. In the presence of astressin, the effects of CRH on TNF-a release were attenuated. CRH effects on TNF-a release were also inhibited by specific inhibitors of MEK, the upstream kinase of the extracellular signal-regulated protein kinase (ERK) (PD98059) or p38 mitogen-activated protein kinase (SB203580), but not by H89. Furthermore, CRH induced rapid phosphorylation of ERK and p38 kinases. Astressin, PD98059, and SB230580 were able to inhibit CRH-induced kinase phosphorylation. These results suggest that CRH induces cell proliferation and TNF-a release in cultured microglia via MAP kinase signalling pathways, thereby providing insight into the interactions between CRH and inflammatory mediators.

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Corticotropin releasing factor induces proliferation of cerebellar astrocytes

Cited by 27 publications

References 68 publications

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

Modulation of dendritic differentiation by corticotropin-releasing factor in the developing hippocampus

The Phenotypic Differentiation of Locus Ceruleus Noradrenergic Neurons Mediated by Brain-Derived Neurotrophic Factor Is Enhanced by Corticotropin Releasing Factor through the Activation of a cAMP-Dependent Signaling Pathway

Corticotropin‐releasing hormone induces proliferation and TNF‐α release in cultured rat microglia via MAP kinase signalling pathways

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