Gain control of sensory input across polysynaptic circuitries in mouse visual cortex by a single G protein-coupled receptor type (5-HT2A)

Ruxandra Barzan, Beyza Bozkurt, Mohammadreza M. Nejad, Sandra T. Süß, Tatjana Surdin, Hanna Böke, Katharina Spoida, Zohre Azimi, Michelle Grömmke, Dennis Eickelbeck, Melanie D. Mark, Lennard Rohr, Ida Siveke, Sen Cheng, Stefan Herlitze and Dirk Jancke ()
Additional contact information
Ruxandra Barzan: Ruhr University Bochum
Beyza Bozkurt: Ruhr University Bochum
Mohammadreza M. Nejad: Ruhr University Bochum
Sandra T. Süß: Ruhr University Bochum
Tatjana Surdin: Ruhr University Bochum
Hanna Böke: Ruhr University Bochum
Katharina Spoida: Ruhr University Bochum
Zohre Azimi: Ruhr University Bochum
Michelle Grömmke: Ruhr University Bochum
Dennis Eickelbeck: Ruhr University Bochum
Melanie D. Mark: Ruhr University Bochum
Lennard Rohr: Ruhr University Bochum
Ida Siveke: Ruhr University Bochum
Sen Cheng: Ruhr University Bochum
Stefan Herlitze: Ruhr University Bochum
Dirk Jancke: Ruhr University Bochum

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: Abstract Response gain is a crucial means by which modulatory systems control the impact of sensory input. In the visual cortex, the serotonergic 5-HT2A receptor is key in such modulation. However, due to its expression across different cell types and lack of methods that allow for specific activation, the underlying network mechanisms remain unsolved. Here we optogenetically activate endogenous G protein-coupled receptor (GPCR) signaling of a single receptor subtype in distinct mouse neocortical subpopulations in vivo. We show that photoactivation of the 5-HT2A receptor pathway in pyramidal neurons enhances firing of both excitatory neurons and interneurons, whereas 5-HT2A photoactivation in parvalbumin interneurons produces bidirectional effects. Combined photoactivation in both cell types and cortical network modelling demonstrates a conductance-driven polysynaptic mechanism that controls the gain of visual input without affecting ongoing baseline levels. Our study opens avenues to explore GPCRs neuromodulation and its impact on sensory-driven activity and ongoing neuronal dynamics.

Date: 2024
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DOI: 10.1038/s41467-024-51861-1

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