In insects, four types of motoneurons have long been known, including fast motoneurons, slow motoneurons, common inhibitory motoneurons, and DUM neurons. They innervate the same muscle and control its contraction together. Recent studies in Drosophila have suggested the existence of another type of motoneuron, the common excitatory motoneuron. Here, we found that shakB-GAL4 produced by labels this type of motoneuron in Drosophila larvae. We found that Drosophila larvae have two common excitatory motoneurons in each abdominal segment, RP2 for dorsal muscles and MNSNb/d-Is for ventral muscles. They innervate most of the internal longitudinal or oblique muscles on the dorsal or ventral body wall with type-Is terminals and use glutamate as a transmitter. Electrophysiological recording indicated that stimulation of the RP2 axon evoked excitatory junctional potential in a dorsal muscle.
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http://dx.doi.org/10.2108/zsj.24.504 | DOI Listing |
Brain Commun
January 2025
Department of Biological Sciences, Southern Methodist University, Dallas, TX 75275, USA.
Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related death, likely stemming from seizure activity disrupting vital brain centres controlling heart and breathing function. However, understanding of SUDEP's anatomical basis and mechanisms remains limited, hampering risk evaluation and prevention strategies. Prior studies using a neuron-specific conditional knockout mouse model of SUDEP identified the primary importance of brain-driven mechanisms contributing to sudden death and cardiorespiratory dysregulation; yet, the underlying neurocircuits have not been identified.
View Article and Find Full Text PDFFront Neurol
December 2024
Department of Pediatrics, Peking University First Hospital, Beijing, China.
Introduction: Neonatal seizures are the most common clinical manifestation of neurological dysfunction in newborns, with an incidence ranging from 1 to 5‰. However, the therapeutic efficacy of current pharmacological treatments remains suboptimal. This study aims to utilize genetically modified hamsters with hypertriglyceridaemia (HTG) to investigate the effects of elevated triglycerides on neuronal excitability and to elucidate the underlying mechanisms.
View Article and Find Full Text PDFHeliyon
January 2025
Department of Pediatric Neurology, University of Health Sciences, Gülhane Training and Research Hospital, Ankara, the Republic of Türkiye.
Objective: Epilepsy is one of the most common neurological diseases in the pediatric population. Orexins are excitatory peptides and associated with energy homeostasis, eating and drinking behaviors, sleep regulation, sleep-wake periods, analgesia, and cognitive activities such as attention, learning, and memory. The aim of this study was to reveal the relationship between plasma orexin levels and seizures in pediatric epilepsy patients with seizures, epilepsy patients in remission, and healthy control group with similar demographic characteristics.
View Article and Find Full Text PDFRegen Ther
March 2025
Department of Physiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
Introduction: Tau protein plays a pivotal role in the pathogenesis of Alzheimer's disease (AD) and in regulating neuronal excitability. Among tau-coding microtubule associated protein tau () gene mutations, the A152T mutation is reported to increase the risk of AD and neuronal excitability in mouse models.
Methods: To investigate the effects of gene expression and its mutations on neuronal activity in human neurons, we employed genome editing technology to introduce the A152T or P301S mutations into induced pluripotent stem cells (iPSCs).
PLoS Comput Biol
January 2025
Department of Mathematics and Statistics, Middlebury College, Middlebury, Vermont, United States of America.
Chronic pain is a wide-spread condition that is debilitating and expensive to manage, costing the United States alone around $600 billion in 2010. In a common symptom of chronic pain called allodynia, non-painful stimuli produce painful responses with highly variable presentations across individuals. While the specific mechanisms remain unclear, allodynia is hypothesized to be caused by the dysregulation of excitatory-inhibitory (E-I) balance in pain-processing neural circuitry in the dorsal horn of the spinal cord.
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