The messenger RNA encoding VGF, a neuronal peptide precursor, is rapidly regulated in the rat central nervous system by neuronal activity, seizure and lesion

Snyder, Susan E.; Cheng, Helen; Murray, Karl D.; Isackson, Paul J.; McNeill, Thomas H.; Salton, Stephen R.J.

doi:10.1016/s0306-4522(97)00280-7

Cited by 56 publications

(49 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The VGF gene has a CREB binding site, which is necessary for its induction by other neurotrophic factors (Salton et al, 2000), and suggests a point of convergence for transcriptional regulation by 5-HT and BDNF. Furthermore, expression of VGF is induced by BDNF (Eagleson et al, 2001;Alder et al, 2003) as well as in models of neuronal activity such as learning, LTP, seizure, and synaptogenesis (Lombardo et al, 1995;Benson and Salton, 1996;Hevroni et al, 1998;Snyder et al, 1998;Alder et al, 2003;Newton et al, 2003;Altar et al, 2004). In support of our findings of an increase in VGF expression after imipramine treatment, an increase in VGF mRNA was observed in the hippocampus of animals after electroconvulsive therapy (Newton et al, 2003;Altar et al, 2004;Conti et al, 2007).…”

Section: Vgf In Depression Modelssupporting

confidence: 83%

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

Krol²,

et al. 2007

View full text Add to dashboard Cite

Brain-derived neurotrophic factor (BDNF) is upregulated in the hippocampus by antidepressant treatments, and BDNF produces antidepressant-like effects in behavioral models of depression. In our previous work, we identified genes induced by BDNF and defined their specific roles in hippocampal neuronal development and plasticity. To identify genes downstream of BDNF that may play roles in psychiatric disorders, we examined a subset of BDNF-induced genes also regulated by 5-HT (serotonin), which includes the neuropeptide VGF (nonacronymic). To explore the function of VGF in depression, we first investigated the expression of the neuropeptide in animal models of depression. VGF was downregulated in the hippocampus after both the learned helplessness and forced swim test (FST) paradigms. Conversely, VGF infusion in the hippocampus of mice subjected to FST reduced the time spent immobile for up to 6 d, thus demonstrating a novel role for VGF as an antidepressant-like agent. Recent evidence indicates that chronic treatment of rodents with antidepressants increases neurogenesis in the adult dentate gyrus and that neurogenesis is required for the behavioral effects of antidepressants. Our studies using

show abstract

Section: Vgf In Depression Modelssupporting

confidence: 83%

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

Krol²,

et al. 2007

View full text Add to dashboard Cite

show abstract

“…The mechanism by which VGF and TLQP-62 mediate fear memory formation involves the activation of BDNF-TrkB signaling pathways and subsequent neuronal cytoskeletal reorganization, potentially affecting synaptic structure and function (Hale et al, 2011;Deinhardt and Chao, 2014;Lynch et al, 2014). Our data suggest that adult VGF expression is required to potentiate BDNF-TrkB receptor signaling, which contributes critically to a positive autoregulatory feedback loop that mediates hippocampal-dependent memory consolidation (Canossa et al, 1997;Cheng et al, 2011;Bambah-Mukku et al, 2014).…”

Section: Introductionmentioning

confidence: 82%

“…Neuronal VGF expression is induced by increased neuronal activity in vivo (Snyder et al, 1998b), cellular depolarization in vitro (Salton et al, 1991;Bonni et al, 1999), and the BDNF signaling pathway in vitro and in vivo (Snyder et al, 1998b;Bonni et al, 1999;Eagleson et al, 2001;Alder et al, 2003;Cazzin et al, 2011). Here, we found increased expression of VGF mRNA and protein in dorsal hippocampus during the early phase of memory consolidation.…”

Section: Discussionmentioning

confidence: 99%

“…The expression of VGF in neurons is robustly regulated by neurotrophic growth factors (Salton et al, 1991;Alder et al, 2003) and by neuronal activity (Snyder et al, 1998b). VGF is widely expressed in the developing and adult brain, including in cerebral cortex, hypothalamus, and hippocampus (van den Pol et al, 1994;Lombardo et al, 1995;Snyder and Salton, 1998;Snyder et al, 1998a).…”

Section: Introductionmentioning

confidence: 99%

“…VGF is widely expressed in the developing and adult brain, including in cerebral cortex, hypothalamus, and hippocampus (van den Pol et al, 1994;Lombardo et al, 1995;Snyder and Salton, 1998;Snyder et al, 1998a). Decreased VGF levels in CSF, hippocampus, or prefrontal cortex have been reported in patients with Alzheimer's disease, frontotemporal dementia, and psychiatric disorders including bipolar disorder, schizophrenia, and social anhedonia (Rüetschi et al, 2005;Simonsen et al, 2008;Thakker-Varia et al, 2010;Ramos et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

VGF and Its C-Terminal Peptide TLQP-62 Regulate Memory Formation in Hippocampus via a BDNF-TrkB-Dependent Mechanism

Lin¹,

Jiang²,

Sadahiro³

et al. 2015

Journal of Neuroscience

128

View full text Add to dashboard Cite

Regulated expression and secretion of BDNF, which activates TrkB receptor signaling, is known to play a critical role in cognition. Identification of additional modulators of cognitive behavior that regulate activity-dependent BDNF secretion and/or potentiate TrkB receptor signaling would therefore be of considerable interest. In this study, we show in the adult mouse hippocampus that expression of the granin family gene Vgf and secretion of its C-terminal VGF-derived peptide TLQP-62 are required for fear memory formation. We found that hippocampal VGF expression and TLQP-62 levels were transiently induced after fear memory training and that sequestering secreted TLQP-62 peptide in the hippocampus immediately after training impaired memory formation. Reduced VGF expression was found to impair learning-evoked Rac1 induction and phosphorylation of the synaptic plasticity markers cofilin and synapsin in the adult mouse hippocampus. Moreover, TLQP-62 induced acute, transient activation of the TrkB receptor and subsequent CREB phosphorylation in hippocampal slice preparations and its administration immediately after training enhanced long-term memory formation. A critical role of BDNF-TrkB signaling as a downstream effector in VGF/TLQP-62-mediated memory consolidation was further revealed by posttraining activation of BDNF-TrkB signaling, which rescued impaired fear memory resulting from hippocampal administration of anti-VGF antibodies or germline VGF ablation in mice. We propose that VGF is a critical component of a positive BDNF-TrkB regulatory loop and, upon its induced expression by memory training, the TLQP-62 peptide rapidly reinforces BDNF-TrkB signaling, regulating hippocampal memory consolidation.

show abstract

Developmental expression of VGF mRNA in the prenatal and postnatal rat

1998

View full text Add to dashboard Cite

VGF is a developmentally regulated, secretory peptide precursor that is expressed by neurons and neuroendocrine cells and that has its transcription and secretion induced rapidly by neurotrophins and by depolarization. To gain insight into the possible functions and regulation of VGF in vivo, we have characterized the distribution of VGF mRNA in the developing rat nervous system. VGF expression was first detectable at embryonic day 11.5 in the primordia of cranial, sympathetic, and dorsal root ganglia, and its distribution expanded throughout development to include significant expression throughout the brain, spinal cord, and retina of the adult rat. The earliest expression of VGF, therefore, appeared in the peripheral nervous system as developing neurons settled in their designated ganglia. In many regions of the brain, VGF mRNA levels were found to be highest during periods when axonal outgrowth and synaptogenesis predominate. Areas of the central nervous system that contain predominantly dividing cells never displayed any VGF mRNA expression, nor did the vast majority of nonneural tissues.

show abstract

The messenger RNA encoding VGF, a neuronal peptide precursor, is rapidly regulated in the rat central nervous system by neuronal activity, seizure and lesion

Cited by 56 publications

References 54 publications

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

The Neuropeptide VGF Produces Antidepressant-Like Behavioral Effects and Enhances Proliferation in the Hippocampus

VGF and Its C-Terminal Peptide TLQP-62 Regulate Memory Formation in Hippocampus via a BDNF-TrkB-Dependent Mechanism

Developmental expression of VGF mRNA in the prenatal and postnatal rat

Contact Info

Product

Resources

About