Adrenergic activation modulates the signal from the Reissner fiber to cerebrospinal fluid-contacting neurons during development

The cerebrospinal fluid (CSF) contains an extracellular thread conserved in vertebrates, the Reissner fiber, which controls body axis morphogenesis in the zebrafish embryo. Yet, the signaling cascade originating from this fiber to ensure body axis straightening is not understood. Here, we explore the functional link between the Reissner fiber and undifferentiated spinal neurons contacting the CSF (CSF-cNs). First, we show that the Reissner fiber is required in vivo for the expression of urp2, a neuropeptide expressed in CSF-cNs. We show that the Reissner fiber is also required for embryonic calcium transients in these spinal neurons. Finally, we study how local adrenergic activation can substitute for the Reissner fiber-signaling pathway to CSF-cNs and rescue body axis morphogenesis. Our results show that the Reissner fiber acts on CSF-cNs and thereby contributes to establish body axis morphogenesis, and suggest it does so by controlling the availability of a chemical signal in the CSF.

Download Full-text

Adrenergic activation modulates the signal from the Reissner fiber to cerebrospinal fluid-contacting neurons during development

10.1101/2020.05.26.117341 ◽

2020 ◽

Author(s):

Cantaut-Belarif Yasmine ◽

Penru Margot ◽

Orts Del’Immagine Adeline ◽

Pézeron Guillaume ◽

Wyart Claire ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Calcium Imaging ◽

Body Axis ◽

Calcium Transients ◽

Chemical Signal ◽

Spinal Neurons ◽

Functional Link ◽

Genetic Ablation ◽

Adrenergic Activation

AbstractThe cerebrospinal fluid (CSF) contains an extracellular thread that is conserved in vertebrates and referred to as the Reissner fiber. Genetic ablation in the zebrafish revealed that the Reissner fiber controls body axis morphogenesis in the embryo. Yet, the signaling cascade originating from this fiber to ensure body axis straightening is not fully understood. Here, we explore the functional link between the Reissner fiber and undifferentiated spinal neurons contacting the CSF (CSF-cNs). First, we show that the Reissner fiber is required for the expression of urp2, a neuropeptide expressed in CSF-cNs. Using in vivo calcium imaging, we show that the Reissner fiber is also required for embryonic calcium transients in these spinal neurons. Finally, we study how local adrenergic activation directly in the CSF can substitute for the Reissner fiber-signaling pathway to CSF-cNs and rescue body axis morphogenesis. Our results suggest that the Reissner fiber acts on CSF-cNs to establish body axis morphogensis by controlling the availability of a chemical signal in the CSF.

Download Full-text

Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates

Journal of Neurophysiology ◽

10.1152/jn.00232.2013 ◽

2013 ◽

Vol 110 (7) ◽

pp. 1631-1645 ◽

Cited By ~ 13

Author(s):

R. C. Evans ◽

Y. M. Maniar ◽

K. T. Blackwell

Keyword(s):

Synaptic Plasticity ◽

Slow Wave Sleep ◽

Calcium Influx ◽

Spike Timing ◽

Medium Spiny Neuron ◽

Calcium Transients ◽

Biophysical Model ◽

Published Data ◽

High Calcium

The striatum of the basal ganglia demonstrates distinctive upstate and downstate membrane potential oscillations during slow-wave sleep and under anesthetic. The upstates generate calcium transients in the dendrites, and the amplitude of these calcium transients depends strongly on the timing of the action potential (AP) within the upstate. Calcium is essential for synaptic plasticity in the striatum, and these large calcium transients during the upstates may control which synapses undergo plastic changes. To investigate the mechanisms that underlie the relationship between calcium and AP timing, we have developed a realistic biophysical model of a medium spiny neuron (MSN). We have implemented sophisticated calcium dynamics including calcium diffusion, buffering, and pump extrusion, which accurately replicate published data. Using this model, we found that either the slow inactivation of dendritic sodium channels (NaSI) or the calcium inactivation of voltage-gated calcium channels (CDI) can cause high calcium corresponding to early APs and lower calcium corresponding to later APs. We found that only CDI can account for the experimental observation that sensitivity to AP timing is dependent on NMDA receptors. Additional simulations demonstrated a mechanism by which MSNs can dynamically modulate their sensitivity to AP timing and show that sensitivity to specifically timed pre- and postsynaptic pairings (as in spike timing-dependent plasticity protocols) is altered by the timing of the pairing within the upstate. These findings have implications for synaptic plasticity in vivo during sleep when the upstate-downstate pattern is prominent in the striatum.

Download Full-text

The functions of Reelin in membrane trafficking and cytoskeletal dynamics: implications for neuronal migration, polarization and differentiation

Biochemical Journal ◽

10.1042/bcj20160628 ◽

2017 ◽

Vol 474 (18) ◽

pp. 3137-3165 ◽

Cited By ~ 24

Author(s):

Jessica Santana ◽

María-Paz Marzolo

Keyword(s):

Membrane Trafficking ◽

Neuronal Migration ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Signaling Cascade ◽

Low Density ◽

Lipoprotein Receptor ◽

Density Lipoprotein Receptor ◽

Reelin Signaling

Reelin is a large extracellular matrix protein with relevant roles in mammalian central nervous system including neurogenesis, neuronal polarization and migration during development; and synaptic plasticity with its implications in learning and memory, in the adult. Dysfunctions in reelin signaling are associated with brain lamination defects such as lissencephaly, but also with neuropsychiatric diseases like autism, schizophrenia and depression as well with neurodegeneration. Reelin signaling involves a core pathway that activates upon reelin binding to its receptors, particularly ApoER2 (apolipoprotein E receptor 2)/LRP8 (low-density lipoprotein receptor-related protein 8) and very low-density lipoprotein receptor, followed by Src/Fyn-mediated phosphorylation of the adaptor protein Dab1 (Disabled-1). Phosphorylated Dab1 (pDab1) is a hub in the signaling cascade, from which several other downstream pathways diverge reflecting the different roles of reelin. Many of these pathways affect the dynamics of the actin and microtubular cytoskeleton, as well as membrane trafficking through the regulation of the activity of small GTPases, including the Rho and Rap families and molecules involved in cell polarity. The complexity of reelin functions is reflected by the fact that, even now, the precise mode of action of this signaling cascade in vivo at the cellular and molecular levels remains unclear. This review addresses and discusses in detail the participation of reelin in the processes underlying neurogenesis, neuronal migration in the cerebral cortex and the hippocampus; and the polarization, differentiation and maturation processes that neurons experiment in order to be functional in the adult brain. In vivo and in vitro evidence is presented in order to facilitate a better understanding of this fascinating system.

Download Full-text

In vivo LPS administration alters S100B protein content in cerebrospinal fluid, but not in serum

Neurology Psychiatry and Brain Research ◽

10.1016/j.npbr.2012.02.015 ◽

2012 ◽

Vol 18 (2) ◽

pp. 54-55

Author(s):

Lucas Silva Tortorelli ◽

Maria Cristina Guerra ◽

Fabiana Galland ◽

Carollina Da Ré ◽

Elisa Negri ◽

...

Keyword(s):

Cerebrospinal Fluid ◽

Protein Content ◽

S100b Protein

Download Full-text

Microdialysis Sampling of Carbamazepine, Phenytoin and Phenobarbital in Subcutaneous Extracellular Fluid and Subdural Cerebrospinal Fluid in Humans: An in vitro and in vivo Study of Adsorption to the Sampling Device

Pharmacology & Toxicology ◽

10.1034/j.1600-0773.2002.910402.x ◽

2002 ◽

Vol 91 (4) ◽

pp. 158-165 ◽

Cited By ~ 26

Author(s):

Martin Lindberger ◽

Torbjörn Tomson ◽

Lars Ståhle

Keyword(s):

Cerebrospinal Fluid ◽

Extracellular Fluid ◽

In Vivo Study ◽

Microdialysis Sampling ◽

Sampling Device

Download Full-text

Mapping and Functional Characterization of the TAF11 Interaction with TFIIA

Molecular and Cellular Biology ◽

10.1128/mcb.25.3.945-957.2005 ◽

2005 ◽

Vol 25 (3) ◽

pp. 945-957 ◽

Cited By ~ 19

Author(s):

M. M. Robinson ◽

G. Yatherajam ◽

R. T. Ranallo ◽

A. Bric ◽

M. R. Paule ◽

...

Keyword(s):

Functional Characterization ◽

Regulation Of Gene Expression ◽

Small Subunit ◽

Molecular Organization ◽

Functional Link ◽

Essential Information ◽

Histone Fold ◽

Histone Fold Domain ◽

Promoter Dna

ABSTRACT TFIIA interacts with TFIID via association with TATA binding protein (TBP) and TBP-associated factor 11 (TAF11). We previously identified a mutation in the small subunit of TFIIA (toa2-I27K) that is defective for interaction with TAF11. To further explore the functional link between TFIIA and TAF11, the toa2-I27K allele was utilized in a genetic screen to isolate compensatory mutants in TAF11. Analysis of these compensatory mutants revealed that the interaction between TAF11 and TFIIA involves two distinct regions of TAF11: the highly conserved histone fold domain and the N-terminal region. Cells expressing a TAF11 allele defective for interaction with TFIIA exhibit conditional growth phenotypes and defects in transcription. Moreover, TAF11 imparts changes to both TFIIA-DNA and TBP-DNA contacts in the context of promoter DNA. These alterations appear to enhance the formation and stabilization of the TFIIA-TBP-DNA complex. Taken together, these studies provide essential information regarding the molecular organization of the TAF11-TFIIA interaction and define a mechanistic role for this association in the regulation of gene expression in vivo.

Download Full-text