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MODULATION OF SLOW-WAVE ACTIVITY USING A MUSCARINIC PHOTOSWITCHABLE DRUG IN LAYER II/III OF THE MOUSE SOMATOSENSORY CORTEX
Nayeli Fernanda Pérez Pérezand 13 co-authors
Institut de Bioenginyeria de Catalunya (IBEC)
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-648
Presentation
Date TBA
Board: PS03-08AM-648
Event Information
Poster Board
PS03-08AM-648
Poster
View posterAbstract
Current pharmacological therapies for modulating brain states such as consciousness and sleep act systemically, lacking the spatiotemporal precision necessary to intervene in specific neural circuits. This lack of selectivity frequently generates side effects and limits their clinical applicability.
To overcome these barriers, we have characterized a novel photosensitive agonist of the muscarinic acetylcholine receptor M1. This compound remains inactive in the dark and isomerizes to its bioactive form only under amber light (590 nm), allowing for the local and temporally controlled activation of mAChR M1 signaling.
Through in vivo experiments and recordings of neuronal activity in layers 2/3 of the somatosensory cortex, we demonstrated the efficacy of this drug.
Focal photopharmacological neuromodulation with this drug allows us to decrease delta band activity associated with deep sleep and, furthermore, increase the frequency of slow-wave activity, characteristics that correlate with less deep sleep states. All animals recovered without behavioural deficits, indicating the absence of acute toxicity. This approach represents an innovative strategy for targeted neurological therapies and allows for the high-precision dissection of the dynamics of the neural circuits underlying brain states.
To overcome these barriers, we have characterized a novel photosensitive agonist of the muscarinic acetylcholine receptor M1. This compound remains inactive in the dark and isomerizes to its bioactive form only under amber light (590 nm), allowing for the local and temporally controlled activation of mAChR M1 signaling.
Through in vivo experiments and recordings of neuronal activity in layers 2/3 of the somatosensory cortex, we demonstrated the efficacy of this drug.
Focal photopharmacological neuromodulation with this drug allows us to decrease delta band activity associated with deep sleep and, furthermore, increase the frequency of slow-wave activity, characteristics that correlate with less deep sleep states. All animals recovered without behavioural deficits, indicating the absence of acute toxicity. This approach represents an innovative strategy for targeted neurological therapies and allows for the high-precision dissection of the dynamics of the neural circuits underlying brain states.
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