Opendata, web and dolomites

HT4PD SIGNED

The role of the serotonin 5-HT4 receptor in motor and non-motor symptoms of Parkinson’s disease

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 HT4PD project word cloud

Explore the words cloud of the HT4PD project. It provides you a very rough idea of what is the project "HT4PD" about.

striatum    htr4    ventral    depression    depressive    ing    lid    substrate    termed    dyskinesia    dorsolateral    serotonin    shows    transgenic    altered    knockdown    patients    investigation    dspns    alpha    lids    markers    coupled    involuntary    excitability    hippocampus    balance    onset    enriched    pointing    implicated    dopa    ht    attenuate    antidepressant    receptor    disease    modulate    anti    manipulate    disrupted    symptoms    motor    probe    contrast    cellular    unilaterally    candidate    effect    cortex    virally    90    depressant    inhibitors    projection    behaviors    expression    re    unknown    protein    caused    altering    reduce    lesioned    bilaterally    ohda    overexpress    ltd    pharmacologically    striatal    linked    neuron    le    uncontrollably    severity    symptom    models    htr1a    counteract    spiny    ltp    mechanism    dopamine    release    neurons    serotonergic    action    agonists    striatally    dopaminergic    anxiety    diminished    parkinson    mice    treatment    movements    d2    yield    overexpression    occurring    ispns    pd    behavior    paradigms    depotentiation    metabolism    examined    ssris   

Project "HT4PD" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country France [FR]
 Total cost 295˙061 €
 EC max contribution 295˙061 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2019
 Funding Scheme MSCA-IF-EF-CAR
 Starting year 2021
 Duration (year-month-day) from 2021-01-01   to  2023-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 295˙061.00

Map

 Project objective

Parkinson’s Disease (PD) is caused by dopaminergic neuron loss resulting in motor symptoms that are treated with L-DOPA. However, ≤90% of patients develop involuntary movements, termed L-DOPA induced dyskinesia (LID). Another less well studied, but highly occurring PD symptom is depression. There is evidence that the serotonin system is implicated in both, LID and PD-linked depression. Serotonergic (5-HT) neurons uncontrollably release L-DOPA-derived dopamine, and HTR1a/b agonists counteract such release and LIDs. Serotonin re-uptake inhibitors (SSRIs) also attenuate LID, through a still unknown mechanism. The striatally enriched Gαs-coupled receptor, HTR4, has the potential to enhance excitability of spiny projection neurons, to affect the balance of striatal pathways that is disrupted in PD and is a candidate to modulate LID and PD-depression. D2 agonists reduce depressive behavior in PD models, pointing towards a role for the striatum. Specifically, the dorsolateral striatum shows diminished metabolism, in contrast to non-PD-depression where the ventral striatum is a substrate. HTR4 in cortex and hippocampus was linked to antidepressant action. Agonists and overexpression yield anti-depressant-like responses, however, striatal HTR4 in PD-depression has not been examined. 1. We will determine HTR4 protein expression on a cellular level (dSPNs, iSPNs) in transgenic mice. We will virally overexpress, knockdown and pharmacologically manipulate HTR4 and assess striatally-driven behaviors. 2. We will probe HTR4 in motor symptoms by altering expression/activity in unilaterally 6-OHDA lesioned mice. We will evaluate LID onset/severity, dyskinesia markers and LTP, depotentiation and LTD. 3. We will test bilaterally-lesioned mice with altered HTR4 expression/activity in depression/anxiety paradigms. We will determine the effect on the action of D2, HTR1a agonists and SSRIs. Our comprehensive investigation of HTR4 will lead to a new understanding and treatment of PD.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "HT4PD" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

The information about "HT4PD" are provided by the European Opendata Portal: CORDIS opendata.

More projects from the same programme (H2020-EU.1.3.2.)

GENESE 17 (2018)

Geometries of Exotic NuclEar StructurE 17

Read More  

EGeoCC (2019)

Ethnic geography and civil conflict

Read More  

GAiNS (2020)

Gibberellic acid signaling and dynamics during arbuscular mycorrhizal symbiosis and rhizobial-legume symbiosis

Read More