c-fos regulates neuropeptide Y expression in mouse dentate gyrus

Wu, Yongfei; Zhang, Dongsheng; Lou, Dan; Fan, Yunxia; Aronow, Bruce J.; Xu, Ming; Zhang, Jianhua

doi:10.1016/j.neulet.2004.02.020

Cited by 18 publications

(8 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Data from both rat and mouse studies show consistently that kainate-induced seizures are also associated with increased NPY mRNA and protein levels (Arabadzisz et al, 2005;Bouilleret et al, 2000;Silva et al, 2005;Vezzani and Sperk, 2004;Wu and Li, 2005;Wu et al, 2004). As expected, this study also found prominent increases in NPY mRNA levels in the DG hilus at 6, 12, and 24 h, and in the DG granule cell layer, where NPY mRNA was expressed de novo at 6 and 12 h post-kainate.…”

Section: Discussionsupporting

confidence: 85%

“…Moreover, in mice, only the effects of kainate-induced seizures on NPY synthesis have been studied (Arabadzisz et al, 2005;Bouilleret et al, 2000;Wu and Li, 2005;Wu et al, 2004) whereas the effects on NPY receptor levels and function are still unexplored. In the present study, we therefore investigated the effects of kainate-induced seizures on levels of NPY and NPY receptor mRNA, NPY receptor binding, and NPY-stimulated [ 35 S]GTPgS functional binding.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Elbrønd-Bek

Olling

Gøtzsche

et al. 2014

Synapse

View full text Add to dashboard Cite

Kainate-induced seizures constitute a model of temporal lobe epilepsy where prominent changes are observed in the hippocampal neuropeptide Y (NPY) system. However, little is known about the functional state and signal transduction of the NPY receptor population resulting from kainate exposure. Thus, in this study, we explored functional NPY receptor activity in the mouse hippocampus and neocortex after kainate-induced seizures using NPY-stimulated [(35) S]GTPγS binding. Moreover, we also studied levels of [(125) I]-peptide YY (PYY) binding and NPY, Y1, Y2, and Y5 receptor mRNA in these kainate-treated mice. Functional NPY binding was unchanged up to 12 h post-kainate, but decreased significantly in all hippocampal regions after 24 h and 1 week. Similarly, a decrease in [(125) I]-PYY binding was found in the dentate gyrus (DG) 1 week post-kainate. However, at 2 h, 6 h, and 12 h, [(125) I]-PYY binding was increased in all regions, and in the CA1 also at 24 h post-kainate. NPY mRNA levels were prominently increased in hippocampal regions, reaching maximum at 12 and 24 h. Y1 and Y5 mRNA levels were lowered in the DG at 24 and 2 h, respectively, while Y2 mRNA levels were elevated at 24 h in the DG and CA3. This study confirms rat kainate studies by showing pronounced adaptive changes in the mouse hippocampus both with regard to NPY synthesis and NPY receptor synthesis and binding, which may contribute to regulating neuronal seizure susceptibility after kainate. However, the potential seizure-suppressant effects of increased NPY gene expression at late time points post-kainate could be attenuated by the novel finding of reduced NPY-receptor G-protein activation.

show abstract

Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Elbrønd-Bek

Olling

Gøtzsche

et al. 2014

Synapse

View full text Add to dashboard Cite

show abstract

“…injection of spexin significantly resulted in c-Fos induction in AHA and SCN (each p < 0.05), but not in ARC, DMN, LHA, PVN, SON, or VMH, suggesting that the anorectic effect of spexin may be mediated via hypothalamic AHA and SCN. Wu et al found that c-Fos could regulate NPY expression in mouse dentate gyrus [ 30 ]. We could suppose that the decrease of Npy mRNA induced by spexin might be due to the c-Fos activity in the hypothalamus.…”

Section: Discussionmentioning

confidence: 99%

Peripheral Spexin Inhibited Food Intake in Mice

Zhou

Feng

et al. 2020

International Journal of Endocrinology

View full text Add to dashboard Cite

Spexin (SPX, NPQ), a novel endogenous neuropeptide, was firstly identified by bioinformatics. Spexin gene and protein widely distributed in the central nervous system and peripheral tissues, such as the hypothalamus and digestive tract. The role of spexin in appetite regulation in mammalian is still unclear. The present study was designed to investigate the mechanism and effect of peripheral spexin on food intake in mice. During the light period, an intraperitoneal (i.p.) injection of spexin (10 nmol/mouse) significantly inhibited cumulative food intake at 2, 4, and 6 h after treatment in fasted mice. During the dark period, spexin (1 and 10 nmol/mouse, i.p.) significantly suppressed cumulative food intake at 4 and 6 h after treatment in freely feeding mice. The GALR3 antagonist SNAP37889, not GALR2 antagonist, significantly antagonized the inhibitory effect on cumulative food intake (0–6 h) induced by spexin. Spexin significantly reduced the mRNA level of Npy mRNA, not Agrp, Pomc, Cart, Crh, Orexin, or Mch, in the hypothalamus. Spexin (10 nmol/mouse, i.p.) increased the number of c-Fos positive neurons in hypothalamic AHA and SCN, but not in ARC, DMN, LHA, PVN, SON, or VMH. The hypothalamic p-CaMK2 protein expression was upregulated by spexin. This study indicated that acute peripheral injection of spexin inhibited mouse food intake. The anorectic effect may be mediated by GALR3, and inhibiting neuropeptide Y (NPY) via p-CaMK2 and c-Fos in the hypothalamus.

show abstract

“…In comparison, the analysis of the neuronal regulon of other PRTFs has received less attention. The few available studies exploring SRF-dependent (Etkin et al, 2006;Stritt et al, 2009;Parkitna et al, 2010) and FOS-dependent (Wu et al, 2004;Paletzki et al, 2008) neuronal gene expression show disparate results and limited overlap, likely because of the technical reasons stated above. A remarkable difference between our screen and those previous studies is the possibility to quantitatively compare the changes triggered by the expression of each one of these PRTFs.…”

Section: Discussionmentioning

confidence: 99%

cAMP Response Element-Binding Protein Is a Primary Hub of Activity-Driven Neuronal Gene Expression

Benito¹,

Valor²,

Jiménez-Minchan³

et al. 2011

J. Neurosci.

111

View full text Add to dashboard Cite

Long-lasting forms of neuronal plasticity require de novo gene expression, but relatively little is known about the events that occur genome-wide in response to activity in a neuronal network. Here, we unveil the gene expression programs initiated in mouse hippocampal neurons in response to different stimuli and explore the contribution of four prominent plasticity-related transcription factors (CREB, SRF, EGR1, and FOS) to these programs. Our study provides a comprehensive view of the intricate genetic networks and interactions elicited by neuronal stimulation identifying hundreds of novel downstream targets, including novel stimulus-associated miRNAs and candidate genes that may be differentially regulated at the exon/promoter level. Our analyses indicate that these four transcription factors impinge on similar biological processes through primarily non-overlapping gene-expression programs. Meta-analysis of the datasets generated in our study and comparison with publicly available transcriptomics data revealed the individual and collective contribution of these transcription factors to different activity-driven genetic programs. In addition, both gain-and loss-of-function experiments support a pivotal role for CREB in membrane-to-nucleus signal transduction in neurons. Our data provide a novel resource for researchers wanting to explore the genetic pathways associated with activity-regulated neuronal functions.

show abstract

c-fos regulates neuropeptide Y expression in mouse dentate gyrus

Cited by 18 publications

References 17 publications

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Peripheral Spexin Inhibited Food Intake in Mice

cAMP Response Element-Binding Protein Is a Primary Hub of Activity-Driven Neuronal Gene Expression

Contact Info

Product

Resources

About

c-fos regulates neuropeptide Y expression in mouse dentate gyrus

Cited by 18 publications

References 17 publications

Neuropeptide Y-stimulated [35S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Neuropeptide Y-stimulated [35S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Peripheral Spexin Inhibited Food Intake in Mice

cAMP Response Element-Binding Protein Is a Primary Hub of Activity-Driven Neuronal Gene Expression

Contact Info

Product

Resources

About

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice

Neuropeptide Y-stimulated [³⁵S]GTPγs functional binding is reduced in the hippocampus after kainate-induced seizures in mice