Humans are able to continually learn new information and acquire skills that meet the demands of an ever-changing environment. Yet, this new learning does not necessarily occur at the expense of old memories. The specialised biological mechanisms that permit continual learning in humans and other mammals are not fully understood. Here I explore the possibility that neural inhibition plays an important role. I present recent findings from studies in humans that suggest inhibition regulates the stability of neural networks to gate cortical plasticity and memory retrieval. These studies use non-invasive methods to obtain an indirect measure of neural inhibition and corroborate comparable findings in animals. Together these studies reveal a model whereby neural inhibition protects memories from interference to permit continual learning. Neural inhibition may, therefore, play a critical role in the computations that underlie higher-order cognition and adaptive behaviour.
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http://dx.doi.org/10.1016/j.conb.2020.09.007 | DOI Listing |
J Neuroimmunol
January 2025
Centre for Critical Care Medicine, The First Affiliated Hospital of Xinjiang Medical University, Urumchi 830054, China. Electronic address:
This study aimed to investigate the effects of MCC950 in a rat model of sepsis-associated encephalopathy (SAE). Adult male rats were randomly assigned to 12 groups according to the surgery or treatment received and evaluation times. The SAE model was established using the cecal ligation and puncture (CLP) method.
View Article and Find Full Text PDFStem Cell Res Ther
January 2025
Department of Neurosurgery, The First Medical Centre, Chinese PLA General Hospital, Beijing, 100853, China.
Background: Closed head injury (CHI) provokes a prominent neuroinflammation that may lead to long-term health consequences. Microglia plays pivotal and complex roles in neuroinflammation-mediated neuronal insult and repair following CHI. We previously reported that induced neural stem cells (iNSCs) can block the effects of CXCL12/CXCR4 signaling on NF-κB activation in activated microglia by CXCR4 overexpression.
View Article and Find Full Text PDFSci Rep
January 2025
Key Laboratory for Stem Cells and Tissue Engineering Ministry of Education, Guangdong Provincial Key Laboratory of Brain Function and Disease, Institute of Spinal Cord Injury, Department of Histology and Embryology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Neuromuscular diseases usually manifest as abnormalities involving motor neurons, neuromuscular junctions, and skeletal muscle (SkM) in postnatal stage. Present in vitro models of neuromuscular interactions require a long time and lack neuroglia involvement. Our study aimed to construct rodent bioengineered spinal cord neural network-skeletal muscle (NN-SkM) assembloids to elucidate the interactions between spinal cord neural stem cells (SC-NSCs) and SkM cells and their biological effects on the development and maturation of postnatal spinal cord motor neural circuits.
View Article and Find Full Text PDFToxicol In Vitro
January 2025
School of Public Health, Nantong University, Nantong 226019, Jiangsu, China. Electronic address:
2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD) belongs to the category of persistent environmental pollutants, and gestational exposure to TCDD can lead to cognitive, memory, and motor deficits, as well as altered neuron development in rodents. However, the molecular mechanisms underlying TCDD's neurotoxicity remine unclear. Neural stem cells (NSCs) possess the capacity for self-renewal and can generate various cell types within the brain, playing fundamental roles in brain development and regeneration.
View Article and Find Full Text PDFNeuron
January 2025
Department of Biochemistry, Weill Cornell Medicine, New York, NY 10065, USA; Department of Psychiatry, Weill Cornell Medicine, New York, NY 10065, USA. Electronic address:
Dissecting how membrane receptors regulate neural circuits is critical for deciphering principles of neuromodulation and mechanisms of drug action. Here, we use a battery of optical approaches to determine how presynaptic metabotropic glutamate receptor 2 (mGluR2) in the basolateral amygdala (BLA) controls anxiety-related behavior in mice. Using projection-specific photopharmacological activation, we find that mGluR2-mediated presynaptic inhibition of ventromedial prefrontal cortex (vmPFC)-BLA, but not posterior insular cortex (pIC)-BLA, connections produces a long-lasting decrease in spatial avoidance.
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