The Experts below are selected from a list of 105 Experts worldwide ranked by ideXlab platform
Gregory V Carr - One of the best experts on this subject based on the ideXlab platform.
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post weaning social isolation increases δFosB FosB protein expression in sex specific patterns in the prelimbic infralimbic cortex and hippocampus in mice
Neuroscience Letters, 2021Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with neuronal activity, chronic stress, and drug-induced neuroplasticity, is upregulated in the prelimbic/infralimbic (PL/IL) region of the cortex and hippocampus of adult C57BL/6J mice transiently isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the PL/IL in socially isolated females.In contrast, both ΔFosB and FosB are increased in male mice isolated for six weeks from weaning until tissue collection. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain and that FosB/ΔFosB expression provides a potential mechanistic link between post-weaning social isolation and associated neurological abnormalities.
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Post-weaning social isolation increases ΔFosB/FosB protein expression in sex-specific patterns in the prelimbic/infralimbic cortex and hippocampus in mice.
Neuroscience letters, 2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with neuronal activity, chronic stress, and drug-induced neuroplasticity, is upregulated in the prelimbic/infralimbic (PL/IL) region of the cortex and hippocampus of adult C57BL/6J mice transiently isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the PL/IL in socially isolated females.In contrast, both ΔFosB and FosB are increased in male mice isolated for six weeks from weaning until tissue collection. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain and that FosB/ΔFosB expression provides a potential mechanistic link between post-weaning social isolation and associated neurological abnormalities.
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post weaning social isolation increases δFosB FosB protein expression in the prefrontal cortex and hippocampus in mice
bioRxiv, 2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with chronic stress responses and drug-induced neuroplasticity, is upregulated in the medial prefrontal cortex and hippocampus of adult C57BL/6J mice isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the medial prefrontal cortex in socially isolated females. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain.
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Post-weaning social isolation increases ΔFosB/FosB protein expression in the prefrontal cortex and hippocampus in mice
2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with chronic stress responses and drug-induced neuroplasticity, is upregulated in the medial prefrontal cortex and hippocampus of adult C57BL/6J mice isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the medial prefrontal cortex in socially isolated females. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain.
Paul J Bertics - One of the best experts on this subject based on the ideXlab platform.
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activation of the Transcription Factor FosB activating protein 1 ap 1 is a prominent downstream signal of the extracellular nucleotide receptor p2rx7 in monocytic and osteoblastic cells
Journal of Biological Chemistry, 2010Co-Authors: Monica L Gavala, Lindsay M Hill, Lisa Y Lenertz, Maya R Karta, Paul J BerticsAbstract:Activation of the ionotropic P2RX7 nucleotide receptor by extracellular ATP has been implicated in modulating inflammatory disease progression. Continuous exposure of P2RX7 to ligand can result in apoptosis in many cell types, including monocytic cells, whereas transient activation of P2RX7 is linked to inflammatory mediator production and the promotion of cell growth. Given the rapid hydrolysis of ATP in the circulation and interstitial space, transient activation of P2RX7 appears critically important for its action, yet its effects on gene expression are unclear. The present study demonstrates that short-term stimulation of human and mouse monocytic cells as well as mouse osteoblasts with P2RX7 agonists substantially induces the expression of several activating protein-1 (AP-1) members, particularly FosB. The potent activation of FosB after P2RX7 stimulation is especially noteworthy considering that little is known concerning the role of FosB in immunological regulation. Interestingly, the magnitude of FosB activation induced by P2RX7 stimulation appears greater than that observed with other known inducers of FosB expression. In addition, we have identified a previously unrecognized role for FosB in osteoblasts with respect to nucleotide-induced expression of cyclooxygenase-2 (COX-2), which is the rate-limiting enzyme in prostaglandin biosynthesis from arachidonic acid and is critical for osteoblastic differentiation and immune behavior. The present studies are the first to link P2RX7 action to FosB/AP-1 regulation in multiple cell types, including a role in nucleotide-induced COX-2 expression, and support a role for FosB in the control of immune and osteogenic function by P2RX7.
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Activation of the Transcription Factor FosB/Activating Protein-1 (AP-1) Is a Prominent Downstream Signal of the Extracellular Nucleotide Receptor P2RX7 in Monocytic and Osteoblastic Cells
The Journal of biological chemistry, 2010Co-Authors: Monica L Gavala, Lindsay M Hill, Lisa Y Lenertz, Maya R Karta, Paul J BerticsAbstract:Activation of the ionotropic P2RX7 nucleotide receptor by extracellular ATP has been implicated in modulating inflammatory disease progression. Continuous exposure of P2RX7 to ligand can result in apoptosis in many cell types, including monocytic cells, whereas transient activation of P2RX7 is linked to inflammatory mediator production and the promotion of cell growth. Given the rapid hydrolysis of ATP in the circulation and interstitial space, transient activation of P2RX7 appears critically important for its action, yet its effects on gene expression are unclear. The present study demonstrates that short-term stimulation of human and mouse monocytic cells as well as mouse osteoblasts with P2RX7 agonists substantially induces the expression of several activating protein-1 (AP-1) members, particularly FosB. The potent activation of FosB after P2RX7 stimulation is especially noteworthy considering that little is known concerning the role of FosB in immunological regulation. Interestingly, the magnitude of FosB activation induced by P2RX7 stimulation appears greater than that observed with other known inducers of FosB expression. In addition, we have identified a previously unrecognized role for FosB in osteoblasts with respect to nucleotide-induced expression of cyclooxygenase-2 (COX-2), which is the rate-limiting enzyme in prostaglandin biosynthesis from arachidonic acid and is critical for osteoblastic differentiation and immune behavior. The present studies are the first to link P2RX7 action to FosB/AP-1 regulation in multiple cell types, including a role in nucleotide-induced COX-2 expression, and support a role for FosB in the control of immune and osteogenic function by P2RX7.
Michael Noback - One of the best experts on this subject based on the ideXlab platform.
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post weaning social isolation increases δFosB FosB protein expression in sex specific patterns in the prelimbic infralimbic cortex and hippocampus in mice
Neuroscience Letters, 2021Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with neuronal activity, chronic stress, and drug-induced neuroplasticity, is upregulated in the prelimbic/infralimbic (PL/IL) region of the cortex and hippocampus of adult C57BL/6J mice transiently isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the PL/IL in socially isolated females.In contrast, both ΔFosB and FosB are increased in male mice isolated for six weeks from weaning until tissue collection. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain and that FosB/ΔFosB expression provides a potential mechanistic link between post-weaning social isolation and associated neurological abnormalities.
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Post-weaning social isolation increases ΔFosB/FosB protein expression in sex-specific patterns in the prelimbic/infralimbic cortex and hippocampus in mice.
Neuroscience letters, 2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with neuronal activity, chronic stress, and drug-induced neuroplasticity, is upregulated in the prelimbic/infralimbic (PL/IL) region of the cortex and hippocampus of adult C57BL/6J mice transiently isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the PL/IL in socially isolated females.In contrast, both ΔFosB and FosB are increased in male mice isolated for six weeks from weaning until tissue collection. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain and that FosB/ΔFosB expression provides a potential mechanistic link between post-weaning social isolation and associated neurological abnormalities.
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post weaning social isolation increases δFosB FosB protein expression in the prefrontal cortex and hippocampus in mice
bioRxiv, 2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with chronic stress responses and drug-induced neuroplasticity, is upregulated in the medial prefrontal cortex and hippocampus of adult C57BL/6J mice isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the medial prefrontal cortex in socially isolated females. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain.
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Post-weaning social isolation increases ΔFosB/FosB protein expression in the prefrontal cortex and hippocampus in mice
2020Co-Authors: Michael Noback, Gongliang Zhang, Noelle White, James C Barrow, Gregory V CarrAbstract:Social isolation is a growing public health concern across the lifespan. Specifically, isolation early in life, during critical periods of brain development, increases the risk of psychiatric disorders later in life. Previous studies of isolation models in mice have shown distinct neurological abnormalities in various regions of the brain, but the mechanism linking the experience of isolation to these phenotypes is unclear. In this study, we show that ΔFosB, a long-lived Transcription Factor associated with chronic stress responses and drug-induced neuroplasticity, is upregulated in the medial prefrontal cortex and hippocampus of adult C57BL/6J mice isolated for two weeks post-weaning. Additionally, a related Transcription Factor, FosB, is also increased in the medial prefrontal cortex in socially isolated females. These results show that short-term isolation during the critical post-weaning period has long-lasting and sex-dependent effects on gene expression in brain.
Elaine Aparecida Del Bel - One of the best experts on this subject based on the ideXlab platform.
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anti dyskinetic effect of the neuronal nitric oxide synthase inhibitor is linked to decrease of FosB deltaFosB expression
Neuroscience Letters, 2013Co-Authors: Fernando E Padovanneto, Nadia Rubia Ferreira, Danielle De Oliveiratavares, Daniele De Aguiar, C A Silva, Rita Raismanvozari, Elaine Aparecida Del BelAbstract:Abstract Rodents with lesion of dopaminergic pathway when receiving repeated l -3,4-dihydroxiphenylalanine ( l -DOPA) treatment develop abnormal involuntary movements called dyskinesia. We demonstrated that nitric oxide synthase (NOS) inhibitors mitigate l -DOPA-induced dyskinesia in rodents. The aim of the present study was to verify if the in vivo preferential neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI) affect the expression of the Transcription Factor FosB/ΔFosB in the lesioned striatum, an indicator of neuronal activity associated with dyskinesia. Male Wistar rats with unilateral microinjection (medial forebrain bundle) of either the neurotoxin 6-hydroxidopamine (6-OHDA; n = 4–6/group) or saline (sham; n = 6/group) were provided with l -DOPA (30 mg/kg plus benserazide 7.5 mg/kg/day, oral gavage), once a day during 22 days. 6-OHDA-lesioned animals developed abnormal involuntary movements (AIMs) classified as axial, limb, orofacial and locomotive dyskinesia and presented FosB/ΔFosB increase in the dopamine-depleted striatum. Administration of 7-NI (30 mg/kg, i.p.), 30 min prior to l -DOPA reduced the severity of AIMs (≈65% for axial, limb and orofacial and 74% for locomotive AIMs scores), without interfering with the rotarod performance. Simultaneously, 7-NI attenuated the expression of FosB/ΔFosB in dopamine-depleted striatum (≈65% in medial and ≈54% in lateral striatum, bregma 0.48 mm). FosB/ΔFosB expression in lateral striatum was correlated with l -DOPA-induced dyskinesia. The findings described here corroborate a new approach to the management of l -DOPA-therapy in Parkinson's disease (PD) treatment.
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Anti-dyskinetic effect of the neuronal nitric oxide synthase inhibitor is linked to decrease of FosB/deltaFosB expression.
Neuroscience letters, 2013Co-Authors: Fernando E. Padovan-neto, Nadia Rubia Ferreira, Daniele De Aguiar, C A Silva, Danielle De Oliveira-tavares, Rita Raisman-vozari, Elaine Aparecida Del BelAbstract:Abstract Rodents with lesion of dopaminergic pathway when receiving repeated l -3,4-dihydroxiphenylalanine ( l -DOPA) treatment develop abnormal involuntary movements called dyskinesia. We demonstrated that nitric oxide synthase (NOS) inhibitors mitigate l -DOPA-induced dyskinesia in rodents. The aim of the present study was to verify if the in vivo preferential neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI) affect the expression of the Transcription Factor FosB/ΔFosB in the lesioned striatum, an indicator of neuronal activity associated with dyskinesia. Male Wistar rats with unilateral microinjection (medial forebrain bundle) of either the neurotoxin 6-hydroxidopamine (6-OHDA; n = 4–6/group) or saline (sham; n = 6/group) were provided with l -DOPA (30 mg/kg plus benserazide 7.5 mg/kg/day, oral gavage), once a day during 22 days. 6-OHDA-lesioned animals developed abnormal involuntary movements (AIMs) classified as axial, limb, orofacial and locomotive dyskinesia and presented FosB/ΔFosB increase in the dopamine-depleted striatum. Administration of 7-NI (30 mg/kg, i.p.), 30 min prior to l -DOPA reduced the severity of AIMs (≈65% for axial, limb and orofacial and 74% for locomotive AIMs scores), without interfering with the rotarod performance. Simultaneously, 7-NI attenuated the expression of FosB/ΔFosB in dopamine-depleted striatum (≈65% in medial and ≈54% in lateral striatum, bregma 0.48 mm). FosB/ΔFosB expression in lateral striatum was correlated with l -DOPA-induced dyskinesia. The findings described here corroborate a new approach to the management of l -DOPA-therapy in Parkinson's disease (PD) treatment.
Monica L Gavala - One of the best experts on this subject based on the ideXlab platform.
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activation of the Transcription Factor FosB activating protein 1 ap 1 is a prominent downstream signal of the extracellular nucleotide receptor p2rx7 in monocytic and osteoblastic cells
Journal of Biological Chemistry, 2010Co-Authors: Monica L Gavala, Lindsay M Hill, Lisa Y Lenertz, Maya R Karta, Paul J BerticsAbstract:Activation of the ionotropic P2RX7 nucleotide receptor by extracellular ATP has been implicated in modulating inflammatory disease progression. Continuous exposure of P2RX7 to ligand can result in apoptosis in many cell types, including monocytic cells, whereas transient activation of P2RX7 is linked to inflammatory mediator production and the promotion of cell growth. Given the rapid hydrolysis of ATP in the circulation and interstitial space, transient activation of P2RX7 appears critically important for its action, yet its effects on gene expression are unclear. The present study demonstrates that short-term stimulation of human and mouse monocytic cells as well as mouse osteoblasts with P2RX7 agonists substantially induces the expression of several activating protein-1 (AP-1) members, particularly FosB. The potent activation of FosB after P2RX7 stimulation is especially noteworthy considering that little is known concerning the role of FosB in immunological regulation. Interestingly, the magnitude of FosB activation induced by P2RX7 stimulation appears greater than that observed with other known inducers of FosB expression. In addition, we have identified a previously unrecognized role for FosB in osteoblasts with respect to nucleotide-induced expression of cyclooxygenase-2 (COX-2), which is the rate-limiting enzyme in prostaglandin biosynthesis from arachidonic acid and is critical for osteoblastic differentiation and immune behavior. The present studies are the first to link P2RX7 action to FosB/AP-1 regulation in multiple cell types, including a role in nucleotide-induced COX-2 expression, and support a role for FosB in the control of immune and osteogenic function by P2RX7.
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Activation of the Transcription Factor FosB/Activating Protein-1 (AP-1) Is a Prominent Downstream Signal of the Extracellular Nucleotide Receptor P2RX7 in Monocytic and Osteoblastic Cells
The Journal of biological chemistry, 2010Co-Authors: Monica L Gavala, Lindsay M Hill, Lisa Y Lenertz, Maya R Karta, Paul J BerticsAbstract:Activation of the ionotropic P2RX7 nucleotide receptor by extracellular ATP has been implicated in modulating inflammatory disease progression. Continuous exposure of P2RX7 to ligand can result in apoptosis in many cell types, including monocytic cells, whereas transient activation of P2RX7 is linked to inflammatory mediator production and the promotion of cell growth. Given the rapid hydrolysis of ATP in the circulation and interstitial space, transient activation of P2RX7 appears critically important for its action, yet its effects on gene expression are unclear. The present study demonstrates that short-term stimulation of human and mouse monocytic cells as well as mouse osteoblasts with P2RX7 agonists substantially induces the expression of several activating protein-1 (AP-1) members, particularly FosB. The potent activation of FosB after P2RX7 stimulation is especially noteworthy considering that little is known concerning the role of FosB in immunological regulation. Interestingly, the magnitude of FosB activation induced by P2RX7 stimulation appears greater than that observed with other known inducers of FosB expression. In addition, we have identified a previously unrecognized role for FosB in osteoblasts with respect to nucleotide-induced expression of cyclooxygenase-2 (COX-2), which is the rate-limiting enzyme in prostaglandin biosynthesis from arachidonic acid and is critical for osteoblastic differentiation and immune behavior. The present studies are the first to link P2RX7 action to FosB/AP-1 regulation in multiple cell types, including a role in nucleotide-induced COX-2 expression, and support a role for FosB in the control of immune and osteogenic function by P2RX7.