Second messager

Résumé

Les messagers secondaires, ou seconds messagers sont des molécules permettant la transduction d'un signal provenant de l'extérieur d'une cellule, vers l'intérieur ou la surface de celle-ci. Généralement un ligand (une hormone) se lie à un récepteur membranaire. Cette liaison est à l'origine de la libération d'un messager secondaire dans le cytoplasme, ou dans la membrane plasmique selon l'affinité chimique (hydrophile/hydrophobe) de celui-ci. Ce messager secondaire peut entraîner une cascade de réactions (ce qui amplifie le signal) débouchant sur une réponse cellulaire (transcription de gène-cible, libération du contenu de vésicules d'exocytose, etc.) Définition de second messager Le second messager doit présenter un certain nombre de propriétés pour être considéré comme tel:

Il doit présenter une élévation temporaire de sa concentration due à la présence du premier messager (le ligand)

Il doit précéder l'effet biologique

On doit pouvoir reproduire l'action du

Source officielle

https://fr.wikipedia.org/wiki/Second_messager

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Presentation of selected signalling pathways with emphasis on both the mechanism of action of the molecules involved, molecular interactions and the role of their spatio-temporal organization within the cell, considering cellular dimensions and conditions.

The goal of the course is to guide students through the essential aspects of molecular neuroscience and neurodegenerative diseases. The student will gain the ability to dissect the molecular basis of disease in the nervous system in order to begin to understand and identify therapeutic strategies.

Basic course in biochemistry as well as cellular and molecular biology for non-life science students enrolling at the Master or PhD thesis level from various engineering disciplines. It reviews essential notions necessary for a training in biology-related engineering fields.

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Molecular Hydrogen Messengers Can Lead to Structural Infidelity: A Cautionary Tale of Protonated Glycine

Antoine Louis Claude Masson, Thomas Rizzo, Evan Rowland Williams

The effects of tagging protonated glycine with either He or with between 1 and 14 H2 molecules on the infrared photodissociation (IRPD) spectra and the ion structure was investigated. Differences in the IR spectra with either a single He atom or H2 molecule attached indicate that even a single H2 molecule can affect the frequencies of some vibrational bands of this simple ion. The protonation site is the preferred location of the tag with He and with up to two H2 molecules, but evidence for H2 attachment to the hydrogen atom of the uncharged carboxylic acid is observed for ions tagged with three or more H2 molecules. This results in a 55 cm-1 red shift in the carboxylic acid OH stretch, and evidence for some structural isomers where the hydrogen bond between the protonated nitrogen and the carbonyl oxygen is partially broken as a result H2 molecules attached to this site is observed. These results are supported by theory, which indicates that H2 molecules can effectively break this weak hydrogen bond with three or more H2 molecules. These results indicate that large spectral shifts as a result of H2 molecules attaching to sites remote from the charge can occur and affect stretching frequencies as a result of charge transfer, and that tagging with multiple H2 molecules can change the structure of the ion itself.

American Institute of Physics2015

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Phorbol esters modulate spontaneous and Ca2+-evoked transmitter release via acting on both munc13 and protein kinase C

Natalya Korogod, Ralf Schneggenburger

Diacylglycerol (DAG) and phorbol esters strongly potentiate transmitter release at synapses by activating protein kinase C (PKC) and members of the Munc13 family of presynaptic vesicle priming proteins. This PKC/Munc13 pathway has emerged as a crucial regulator of release probability during various forms of activity-dependent enhancement of release. Here, we investigated the relative roles of PKC and Munc13-1 in the phorbol ester potentiation of evoked and spontaneous transmitter release at the calyx of Held synapse. The phorbol ester phorbol 12,13-dibutyrate (1 mu M) potentiated the frequency of miniature EPSCs, and the amplitudes of evoked EPSCs with a similar time course. Preincubating slices with the PKC blocker Ro31-82200 reduced the potentiation, mainly by affecting a late phase of the phorbol ester potentiation. The Ro31-8220-insensitive potentiation was most likely mediated by Munc13-1, because in organotypic slices of Munc13-1H567K knock-in mice, in which DAG binding to Munc13-1 is abolished, the potentiation of spontaneous release by phorbol ester was strongly suppressed. Using direct presynaptic depolarizations in paired recordings, we show that the phorbol ester potentiation does not go along with an increase in the number of readily releasable vesicles, despite an increase in the cumulative EPSC amplitude during 100 Hz stimulation trains. Our data indicate that activation of Munc13 and PKC both contribute to an enhancement of the fusion probability of readily releasable vesicles. Thus, docked and readily releasable vesicles are a substrate for modulation via intracellular second-messenger pathways that act via Munc13 and PKC.

Society for Neuroscience2008

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Vasoactive intestinal peptide, pituitary adenylate cyclase-activating peptide, and noradrenaline induce the transcription factors CCAAT/enhancer binding protein (C/EBP)-beta and C/EBP delta in mouse cortical astrocytes: involvement in cAMP-regulated glycogen metabolism

Jean-René Cardinaux, Pierre Magistretti

We have described previously a transcription-dependent induction of glycogen resynthesis by the vasoactive intestinal peptide (VIP) or noradrenaline (NA) in astrocytes, which is mediated by cAMP. Because it has been postulated that the cAMP-mediated regulation of energy balance in hepatocytes and adipocytes is channeled at least in part through the CCAAT/enhancer binding protein (C/EBP) family of transcription factors, we tested the hypothesis that C/EBP isoforms could be expressed in mouse cortical astrocytes and that their level of expression could be regulated by VIP, by the VIP-related neuropeptide pituitary adenylate cyclase-activating peptide (PACAP), or by NA. We report in this study that in these cells, C/EBP beta and C/EBP delta are induced by VIP, PACAP, or NA via the cAMP second-messenger pathway. Induction of C/EBP beta and -delta mRNA by VIP occurs in the presence of a protein synthesis inhibitor. Thus, c/ebp beta and c/ebp delta behave as cAMP-inducible immediate-early genes in astrocytes. Moreover, transfection of astrocytes with expression vectors selectively producing the transcriptionally active form of C/EBP beta, termed liver-enriched transcriptional activator protein, or C/EBP delta enhance the glycogen resynthesis elicited by NA, whereas an expression vector producing the transcriptionally inactive form of C/EBP beta, termed liver-enriched transcriptional inhibitory protein, reduces this resynthesis. These results support the idea that C/EBP beta and -delta regulate gene expression of energy metabolism-related enzymes in astrocytes.

1996

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