STRESSEDASTROCYTES
The interplay between astrocytes and neurons in the progression of stress-induced cognitive disorders
| Coordinatore | UNIVERSIDADE DO MINHO
Organization address
address: Largo do Paco contact info |
| Nazionalità Coordinatore | Portugal [PT] |
| Totale costo | 153˙047 € |
| EC contributo | 153˙047 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-2010-IEF |
| Funding Scheme | MC-IEF |
| Anno di inizio | 2012 |
| Periodo (anno-mese-giorno) | 2012-12-03 - 2014-12-29 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
UNIVERSIDADE DO MINHO
Organization address
address: Largo do Paco contact info |
PT (BRAGA) | coordinator | 153˙047.20 |
Mappa
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Obiettivo del progetto (Objective)
'Stress exposure sets primarily a response to restore physiological homeostasis and promote behavioural adaptation. However, prolonged stressful experience may trigger maladaptive responses that lead to severe manifestations such as depressive-like behaviour, learning and memory deficits. Indeed, advances in neurobiology reported clear morphological deficits in neurons of both hippocampus and prefrontal cortex (PFC) after chronic-stress exposure. However, the classical paradigm that brain information processing is exclusively a neuronal process has been challenged by an emerging body of evidence. In fact, there is a lack of information regarding stress effects on glial cells, whose importance is rising due to exciting data supporting dynamic neuron-glia interactions. Blockade of neurotransmitter release from astrocytes in vivo contributed to unexpected behaviour modulation, namely affecting sleep control. Moreover, ex vivo immunohistochemistry pointed out astrocytic loss in regions affected by stress exposure. In light of these thrilling observations, it is predictable that astrocyte function may be implicated in stress-induced cognitive impairments. Therefore, we propose here the multidisciplinary and innovative dissection of the astrocytic contribution to the progression of stress-related cognitive disorders across the PFC and hippocampus by: (1) assessing the extent of the stress-induced effects, through a battery of behaviour tests for cognitive and depressive-like behaviour, after conditioned genetic or pharmacological blockade of astrocytic function; (2) combining three complementary electrophysiological in vivo techniques and producing a thorough characterization of the astrocytic contribution to stress-induced changes throughout time; and (3) associating ex vivo patch-clamp recordings and a comprehensive immunohistochemical analysis to reveal specific morphological implications in the disorder progression, both in neurons and astrocytes.'