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HT4PD SIGNED

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

Total Cost €

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EC-Contrib. €

0

Partnership

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 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.

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

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.

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