The central nervous system is organized into different neural circuits, each with particular functions and properties. Studying neural circuits is essential to understanding brain function and neuronal diseases. Microfluidic systems are widely used for reconstructing and studying neural circuits but still need improvement to allow modulation and monitoring of the physiological properties of circuits. In this study, we constructed an improved microfluidic device that supports the electrical modulation of neural circuits and proper reassembly. We demonstrated that our microfluidic device provides a platform for electrically modulating and monitoring the physiological function of neural circuits with genetic indicators for synaptic functionality in corticostriatal (CStr) circuits. In particular, our microfluidic device measures activity-driven Ca dynamics using Ca indicators (synaptophysin-GCaMP6f and Fluo5F-AM), as well as activity-driven synaptic transmission and retrieval using vGlut-pHluorin. Overall, our findings indicate that the improved microfluidic platform described here is an invaluable tool for studying the physiological properties of specific neural circuits.
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http://dx.doi.org/10.1186/s13041-023-01007-z | DOI Listing |
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Brain Electrophysiology and Epilepsy Lab (BEE-L), Epilepsy and EEG Unit, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
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View Article and Find Full Text PDFNeurosci Biobehav Rev
January 2025
Department of Cognitive Neuroscience, Radboud University Medical Centre, Donders Institute for Brain, Cognition and Behaviour Netherlands.
Neurosci Bull
January 2025
School of Brain Science and Brain Medicine, Zhejiang University School of Medicine, Hangzhou, 310058, China.
Alzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Inhibitory interneurons normally regulate neural networks underlying memory and cognition, but are disrupted in Alzheimer's disease. Proper interneuron activity reduces amyloid-beta, whereas hyperexcitability elevates amyloid levels. Still, the underlying pathologic processes mediating interneuron dysfunction remain unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Cornell University, Ithaca, NY, USA.
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