Interneurons play a key role in cortical function and dysfunction, yet organization of cortical interneuronal circuitry remains poorly understood. Cortical Layer 1 (L1) contains 2 general GABAergic interneuron groups, namely single bouquet cells (SBCs) and elongated neurogliaform cells (ENGCs). SBCs predominantly make unidirectional inhibitory connections (SBC→) with L2/3 interneurons, whereas ENGCs frequently form reciprocal inhibitory and electric connections (ENGC↔) with L2/3 interneurons. Here, we describe a systematic investigation of the pyramidal neuron targets of L1 neuron-led interneuronal circuits in the rat barrel cortex with simultaneous octuple whole-cell recordings and report a simple organizational scheme of the interneuronal circuits. Both SBCs→ and ENGC ↔ L2/3 interneuronal circuits connect to L2/3 and L5, but not L6, pyramidal neurons. SBC → L2/3 interneuronal circuits primarily inhibit the entire dendritic-somato-axonal axis of a few L2/3 and L5 pyramidal neurons located within the same column. In contrast, ENGC ↔ L2/3 interneuronal circuits generally inhibit the distal apical dendrite of many L2/3 and L5 pyramidal neurons across multiple columns. Finally, L1 interneuron-led circuits target distinct subcellular compartments of L2/3 and L5 pyramidal neurons in a L2/3 interneuron type-dependent manner. These results suggest that L1 neurons form canonical interneuronal circuits to control information processes in both supra- and infragranular cortical layers.
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http://dx.doi.org/10.1093/cercor/bhu020 | DOI Listing |
Brain
January 2025
Department of Neurology, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
Epilepsy is a network disorder, involving neural circuits at both the micro- and macroscale. While local excitatory-inhibitory imbalances are recognized as a hallmark at the microscale, the dynamic role of distinct neuron types during seizures remain poorly understood. At the macroscale, interactions between key nodes within the epileptic network, such as the central median thalamic nucleus (CMT), are critical to the, hippocampal epileptic process.
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January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
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January 2025
Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Hodological patterning refers to developmental mechanisms that link the location of neurons in the brain or spinal cord to specific axonal trajectories that direct connectivity to synaptic targets either within the central nervous system or in the periphery. In vertebrate motor circuits, hodological patterning has been demonstrated at different levels, from the final motor output of somatic and preganglionic autonomic neurons targeting peripheral motoneurons and ganglion cells, to premotor inputs from spinal and brainstem neuron populations targeting the somatic motoneurons and preganglionic autonomic neurons, to cortical neurons that delegate movement commands to the brainstem and spinal neurons. In many cases molecular profiling reveals potential underlying mechanisms whereby selective gene expression creates the link between location and axon trajectory.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
In the ventricular-subventricular-zone (V-SVZ) of the postnatal mammalian brain, immature neurons (neuroblasts) are generated from neural stem cells throughout their lifetime. These V-SVZ-derived neuroblasts normally migrate to the olfactory bulb through the rostral migratory stream, differentiate into interneurons, and are integrated into the preexisting olfactory circuit. When the brain is injured, some neuroblasts initiate migration toward the lesion and attempt to repair the damaged neuronal circuitry, but their low regeneration efficiency prevents functional recovery.
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January 2025
Oregon Hearing Research Center, Oregon Health & Science University, Portland, OR, United States.
Introduction: The brainstem vestibular nuclei neurons receive synaptic inputs from inner ear acceleration-sensing hair cells, cerebellar output neurons, and ascending signals from spinal proprioceptive-related neurons. The lateral (LVST) and medial (MVST) vestibulospinal (VS) tracts convey their coded signals to the spinal circuits to rapidly counter externally imposed perturbations to facilitate stability and provide a framework for self-generated head movements.
Methods: The present study describes the morphological characteristics of intraaxonally recorded and labeled VS neurons monosynaptically connected to the 8th nerve.
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