98%
921
2 minutes
20
Identifying the computational roles of different neuron families is crucial for understanding neural networks. Most neural diversity is embodied in various types of γ-aminobutyric acid-mediated (GABAergic) interneurons, grouped into four major families. We collected datasets of opto-tagged neurons from all four families, along with excitatory neurons, from both the neocortex and hippocampus. The physiological features of these neurons were used to train a machine learning classifier, which subsequently inferred specific interneuron families in large-scale recordings. This combined approach enabled the reconstruction of synaptic connectivity motifs across interneuron family members. We further showed that these motifs differentially control the place field features of pyramidal neurons. Our findings attribute a prominent role to interneurons in the formation of a flexible cognitive map.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1126/science.adv5638 | DOI Listing |
Science
September 2025
Neuroscience Institute, New York University Grossman School of Medicine, New York, NY, USA.
Identifying the computational roles of different neuron families is crucial for understanding neural networks. Most neural diversity is embodied in various types of γ-aminobutyric acid-mediated (GABAergic) interneurons, grouped into four major families. We collected datasets of opto-tagged neurons from all four families, along with excitatory neurons, from both the neocortex and hippocampus.
View Article and Find Full Text PDFFront Neuroanat
August 2025
Division of Functional Neuroanatomy, Institute of Anatomy, University of Zürich, Zürich, Switzerland.
Even though bats are the second most speciose group of mammals, neuroanatomical studies of their hippocampus are rare, particularly of small echolocating bats. Here, we provide a qualitative and quantitative neuroanatomical analysis of the hippocampus of small echolocating bats (Phyllostomidae and Vespertilionidae). Calcium-binding proteins revealed species- and family-specific patterns for calbindin and calretinin.
View Article and Find Full Text PDFJ Neurosci
August 2025
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611.
In amyotrophic lateral sclerosis (ALS) motor cortex hyperexcitability is detected in both familial and sporadic cases, suggesting its centrality in the ALS phenotype; the underlying mechanisms, however, remain largely obscure. Here we utilize male and female UCHL1-eGFP (UeGFP) mice, in which the corticospinal neurons of the motor cortex are labeled with green fluorescent protein, to investigate the intrinsic excitability and synaptic inhibitory inputs on distinct neuron populations in WT-UeGFP and presymptomatic AlsinKO-UeGFP mice, which lack Alsin function and are a well-characterized mouse model for juvenile cases of ALS. We show that in the motor cortex of AlsinKO-UeGFP mice, eGFP-positive layer 5 pyramidal neurons, which represent upper motor neurons, show a decrease in intrinsic excitability compared with WT, whereas the electrophysiological properties of eGFP-negative cells, which identify callosal projection neurons, are unaffected.
View Article and Find Full Text PDFbioRxiv
July 2025
Neuroscience and Pharmacology, University of Iowa, Iowa City, Iowa 52242, USA.
Neurofibromatosis type 1 results from mutations in the gene and its encoded neurofibromin protein. This condition produces multiple symptoms, including tumors, behavioral alterations, and metabolic changes. Molecularly, neurofibromin mutations affect Ras activity, influencing multiple downstream signaling pathways, including MAPK (Raf/MEK/ERK) and PI3K/Akt/mTOR signaling.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
August 2025
Department of Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5307.
Parkinson's disease is characterized by loss of dopamine neurons that project to the dorsal striatum, and mutations in and are the most common genetic causes of familial Parkinson's disease. Previously, we showed that pathogenic mutations inhibit primary cilia formation in rare interneurons and astrocytes of the mouse and human dorsal striatum. This blocks Hedgehog signaling and reduces synthesis of neuroprotective GDNF and NRTN, which normally support dopamine neurons vulnerable in PD.
View Article and Find Full Text PDF