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

Project description

Gaining a deeper understanding of PD and more effective treatments

Parkinson’s disease (PD) is caused by dopaminergic neuron loss that leads to motor symptoms currently treated with L-DOPA. Unfortunately, up to 90 % of patients develop involuntary movements, termed L-DOPA induced dyskinesia (LID), often accompanied by PD-associated depression. The serotonin system is implicated in LID and depression in PD patients. The striatally enriched serotonin receptor HTR4 has the potential to enhance the excitability of spiny projection neurons, affecting the balance of striatal pathways that are disrupted in PD. Thus, HTR4 is an obvious candidate for the modulation of LID and depression related to PD. The EU-funded HT4PD project aims to comprehensively investigate the role of HTR4 in the development of PD-associated symptoms using transgenic mice models, leading to a deeper understanding of PD and more effective treatments.

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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MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2019

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Coordinator

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 295 061,76
Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 295 061,76
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