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Benjamin Portal, Post-doc researcher

Benjamin Portal

External scholarship

About me

From behavioral observations to neuronal and glial activity, I made my PhD in France. It was focused on the role of astroglial Cx43 in depression and drug response. We demonstrated that astroglial glutamate, release through Cx43 hemichannel, plays a key role in antidepressant response. Still interested in astrocytic glutamate, I moved to Mia Lindskog's lab in February 2020 to get more insights on the role of this gliotransmitter in the early phases of Alzheimer’s diseases.

This project is supported by the Swedish Axel Wenner-Gren foundation for international exchange of scientists.

Research description

Amyloid plaques and neurofibrillary tangles are one of the hallmarks of Alzheimer’s disease (AD) (Querfurth and LaFerla., 2010). Moreover, recent evidences emphasize the strong comorbidity between AD and psychiatric disorders such as Parkinson’s disease, Schizophrenia or Major Depression (Dossi et al., 2018). Despite shared dysfunctions between neurodegenerative and psychiatric illnesses (i.e. neuroinflammation, high microglial activation), astroglial dysfunctions remain yet to be solved. It is now clear that at the tripartite synapse (Araque et al., 1999), astrocytes can release gliotransmitters such as glutamate (Orellana et al., 2011), ATP (Kang et al., 2008) and D-serine (Papouin et al., 2017). It has been shown that those molecules can modulate either neuronal activity (Pannasch et al., 2011) or drug response (Portal et al., 2020). So far, astrocytes are an interesting pharmacological target in psychiatric and neurodegenerative disorders (Rivera and But, 2019).

The hypothesis of my work is that astroglial glutamate can regulate neuronal activity therefore contributing to the appearance of observed neuro-behavioral dysfunctions in AD.  We aim at exploring the early glial changes, with respect to synaptic changes. In particular, the use of the state-of-the art mouse model of AD would help to understand astrocytic alterations which may lead to amyloid plaques formation. My main goal is to decipher early astrocytic changes which may explain, at least in part, neuronal deficits in AD.

Teaching portfolio

2018/2019 - Teaching assistant, Neuroscience, University of Toulouse - Paul Sabatier (Toulouse, France)

2017/2018 - Teaching assistant, Molecular Biology, University of Toulouse - Paul Sabatier (Toulouse, France)


2019 - PhD in Neuroscience, University of Toulouse - Paul Sabatier (Toulouse, France)

2016 - MSc in Pharmaceutical Science, University of Paris-Saclay (Paris, France)

2014 - BSc in Cell Biology and Physiology, University of Toulouse - Paul Sabatier (Toulouse, France)

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