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PIANISM SIGNED

Prefrontal Cortex Circuit Dynamics underlying Working Memory and its Serotonin Modulation

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EC-Contrib. €

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Partnership

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 PIANISM project word cloud

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

pyramidal    intrinsic    gain    pv    electrophysiology    ionic    5ht    density    ve    enabled    action    causing    plan    examine    protein    memory    networks    modulated    regulation    neuronal    intracellular    gabaergic    axons    cellular    mediated    raphe    subtypes    slices    sst    neurons    initial    currents    transmission    imaging    serotonin    dysfunctional    deficits    firing    fulfill    disorders    link    sustained    supports    therapeutic    deficiency    experiments    calcium    optogenetically    coupled    projected    dependent    underlying    genetically    perform    cognitive    nuclei    voltage    sensitive    mechanistic    clamp    sodium    ketamine    deficiencies    serotonergic    mechanism    drive    types    synaptic    poorly    patch    model    cortex    na    cell    trpc    decision    alterations    encoded    indicators    mice    chronic    iuml    cells    outlasts    inward    understand    vip    pharmacologically    data    experimental    wm    acute    mental    modulation    learning    receptor    mechanisms    pfc    deficient    prefrontal    circuits    express    impaired    excitatory    persistent    maintenance    dysfunctions    optical    signalling    schizophrenia   

Project "PIANISM" data sheet

The following table provides information about the project.

Coordinator
IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE 

Organization address
address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD
city: LONDON
postcode: SW7 2AZ
website: http://www.imperial.ac.uk/

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 United Kingdom [UK]
 Total cost 212˙933 €
 EC max contribution 212˙933 € (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-ST
 Starting year 2020
 Duration (year-month-day) from 2020-05-01   to  2022-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE UK (LONDON) coordinator 212˙933.00

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 Project objective

The prefrontal cortex (PFC) is essential for higher cognitive tasks such as learning, decision making and, in particular, working memory (WM). To fulfill these tasks, PFC neurons express several serotonin (5HT) receptor subtypes that are modulated by a high density of serotonergic axons projected from the raphe nuclei. Alterations of the neuronal mechanisms within PFC lead to an impaired top-down regulation, causing cognitive dysfunctions in mental disorders such as schizophrenia. A key cellular mechanism related to WM formation and maintenance in the PFC is sustained action potential firing of neurons that outlasts the initial excitatory drive. Persistent firing is likely enabled by synaptic networks and intracellular ionic mechanisms, including voltage sensitive sodium and calcium inward currents or G-Protein-coupled receptor mediated TRPC/ CAN currents. Moreover, experimental data supports a link between dysfunctional serotonergic modulation in the PFC and WM deficits, but yet, the underlying mechanisms are poorly understood. Here, I plan to gain a mechanistic understanding of the serotonergic modulation of WM at the cellular level including the link between 5HT receptor activity and prefrontal cellular circuits dependent WM formation and the role of 5HT in WM-related persistent firing. I will perform patch-clamp electrophysiology and optical voltage imaging (genetically encoded voltage indicators) of prefrontal pyramidal and GABAergic cells (PV-, SST-, VIP-subtypes) in acute slices from naïve and WM deficient mice (chronic ketamine model of schizophrenia), and examine how the activity of these cell types are modulated by optogenetically and pharmacologically controlled 5HT signalling. These experiments aim to understand the serotonergic transmission and intrinsic properties within the PFC involved in WM formation, maintenance and deficiency. Better understanding of these mechanisms will help to develop new and specific therapeutic targets for WM deficiencies.

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