Analysis of neuronal subpopulations in mice over-expressing suppressor of cytokine signaling-2

Ransome, Mark I.; Turnley, Ann M.

doi:10.1016/j.neuroscience.2004.12.041

Cited by 28 publications

(23 citation statements)

References 51 publications

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“…We have previously demonstrated that GH-R2/2 and SOCS-2 Tg mice have altered brain anatomy with increased densities in total and subpopulations of cortical neurons (Ransome et al, 2004;Ransome and Turnley, 2005). Young GH-R2/2 mice are reported to have normal behavioral traits including hippocampal-dependent cognition (Kinney et al, 2001;Kinney-Forshee et al, 2004;Bartke, 2005).…”

Section: Introductionmentioning

confidence: 99%

Growth hormone signaling and hippocampal neurogenesis: Insights from genetic models

Ransome

Turnley

2008

Hippocampus

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Adult hippocampal neurogenesis (AHN) is modulated by a variety of factors through effects on the proliferation-differentiation-survival regulatory axis. We have employed growth hormone receptor knockout (GH-R-/-) and suppressor of cytokine signaling-2 transgenic (SOCS-2 Tg) mice as models of altered GH-signaling to assess their affects on basal and exercised-induced hippocampal neurogenesis. Assessment of proliferation 24-h after 7-days of bromodeoxyuridine (BrdU) labeling with or without voluntary running showed that the density of BrdU(+) cells in the subgranular zone remained unchanged between genotypes in control housing, while running induced significant increases in BrdU-labeled cells in WT, GH-R-/-, and SOCS-2 Tg mice. The proportion of BrdU/doublecortin and BrdU/S100beta cells did not vary between genotype or running conditions at this time-point. Assessment of cell survival 28-days after BrdU labeling showed that SOCS-2 Tg animals had significantly higher BrdU(+) cell densities in the granule cell layer compared to WT and GH-R-/- animals in control housing and after voluntary running. There were no differences in cell survival between WT and GH-R-/- mice with or without running. Mature phenotype analysis showed similar proportions of BrdU/NeuN and BrdU/S100beta in all groups. While SOCS-2 Tg mice had similar social interaction behaviors and sensorimotor gating, they appeared to be less anxious with heightened basal locomotor activity and showed enhanced performance in the Morris watermaze test. Overall, our data indicated that mice over-expressing SOCS-2 showed increased survival of neurons generated during AHN, which correlated with improved performance in a hippocampal-dependent cognitive task. Furthermore, voluntary running increased AHN in WT, SOCS-2 Tg, and serum-IGF-1-deficient GH-R-/- mice.

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Section: Introductionmentioning

confidence: 99%

Growth hormone signaling and hippocampal neurogenesis: Insights from genetic models

Ransome

Turnley

2008

Hippocampus

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“…In-vitro, neural stem cells from SOCS2 -/-mice show a marked reduction in the number of neurons generated [171], as opposed to SOCS2Tg mice which show an increase in neuron number [172][173][174]. Additionally, PC12 cells and neural cells from SOCS2Tg mice demonstrate increased neurite outgrowth in tissue culture [171,[174][175][176].…”

Section: Socs2 In the Brainmentioning

confidence: 98%

Regulation of Basal and Injury-Induced Fate Decisions of Adult Neural Precursor Cells: Focus on SOCS2 and Related Signalling Pathways

Basrai¹,

Christie²,

Turnley³

2013

Trends in Cell Signaling Pathways in Neuronal Fate Decision

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“…Mice with altered growth hormone responsiveness, including SOCS2KO (hyper-responsive), SOCS2TG (hypo-responsive) and GH receptor null (GHRKO) (non-responsive) mice, exhibit a variety of alterations in neural architecture (Ransome et al, 2004; Ransome and Turnley, 2005). The changes in neural architecture observed in SOCS2TG and SOCS2KO mice implicate this gene in neuronal differentiation and neurite outgrowth.…”

Section: The Suppressors Of Cytokine Signaling (Socs) In the Nervous mentioning

confidence: 99%

“…The changes in neural architecture observed in SOCS2TG and SOCS2KO mice implicate this gene in neuronal differentiation and neurite outgrowth. Interestingly, despite the fact that loss of SOCS2 has an effect on mouse body and organ size (Metcalf et al, 2000), it has no effect on brain size, although there was an effect on neuronal density and composition (Ransome et al, 2004; Ransome and Turnley, 2005). The SOCS2KO mice have decreased cortical neuron density whereas the SOCS2TG and GHRKO mice exhibit an increased cortical neuron density.…”

Section: The Suppressors Of Cytokine Signaling (Socs) In the Nervous mentioning

confidence: 99%

“…Furthermore, the overall number of gamma-aminobutyric acid positive interneurons did not appear to change between genotypes. The altered expression of cortical interneuron markers observed in SOCS2TG and SOCS2KO mice suggests that SOCS2 may regulate expression of specific transcription factors required for interneuron subtype specification or that expression of the interneuron markers might be modulated by the amount of synaptic activity within a cell and thus the altered levels of expression in the SOCS2TG and SOCS2KO mice might simply arise from changes in neuronal circuitry and synaptic activity (Ransome and Turnley, 2005). Juxtaposition of the neuroanatomical phenotypes of mice with altered responsiveness to GH signaling (SOCS2KO hyper-responsive > SOCS2TG hypo-responsive > GHRKO non-responsive) reveals that whilst cortical neuron density correlates with increasing responsiveness to GH, the measures of dendritic branching or some interneuron populations do not.…”

Section: The Suppressors Of Cytokine Signaling (Socs) In the Nervous mentioning

confidence: 99%

See 1 more Smart Citation

Regulation of neurotrophin receptor (Trk) signaling: suppressor of cytokine signaling 2 (SOCS2) is a new player

Uren

Turnley

2014

Front. Mol. Neurosci.

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The classic neurotrophins Nerve Growth Factor (NGF), Brain Derived Neurotrophic Factor (BDNF) and Neurotrophins NT-3 and NT-4 are well known to regulate various aspects of neuronal differentiation, survival and growth. They do this by binding to their cognate receptors, members of the Tropomyosin-related kinase (Trk) receptor tyrosine kinase family, namely TrkA, TrkB, and TrkC. These receptors are then internalized and localized to different cellular compartments, where signal transduction occurs. Conversely, members of the suppressor of cytokine signaling (SOCS) family are best known as negative regulators of signaling via the JAK/STAT pathway. Some members of the family, and in particular SOCS2, have roles in the nervous system that at least partially overlap with that of neurotrophins, namely neuronal differentiation and neurite outgrowth. Recent evidence suggests that SOCS2 is a novel regulator of NGF signaling, altering TrkA cellular localization and downstream signaling to affect neurite growth but not neuronal survival. This review first discusses regulation of Trk receptor signaling, followed by the role of SOCS2 in the nervous system and finishes with a discussion of possible mechanisms by which SOCS2 may regulate TrkA function.

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Analysis of neuronal subpopulations in mice over-expressing suppressor of cytokine signaling-2

Cited by 28 publications

References 51 publications

Growth hormone signaling and hippocampal neurogenesis: Insights from genetic models

Growth hormone signaling and hippocampal neurogenesis: Insights from genetic models

Regulation of Basal and Injury-Induced Fate Decisions of Adult Neural Precursor Cells: Focus on SOCS2 and Related Signalling Pathways

Regulation of neurotrophin receptor (Trk) signaling: suppressor of cytokine signaling 2 (SOCS2) is a new player

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