Epileptic seizure is typically characterized by highly synchronized episodes of neural activity. Existing stimulation therapies focus purely on suppressing the pathologically synchronized neuronal firing patterns during the ictal (seizure) period. While these strategies are effective in suppressing seizures when they occur, they fail to prevent the re-emergence of seizures once the stimulation is turned off. Previously, we developed a novel neurostimulation motif, which we refer to as "Forced Temporal Spike-Time Stimulation" (FTSTS) that has shown remarkable promise in long-lasting desynchronization of excessively synchronized neuronal firing patterns by harnessing synaptic plasticity. In this paper, we build upon this prior work by optimizing the parameters of the FTSTS protocol in order to efficiently desynchronize the pathologically synchronous neuronal firing patterns that occur during epileptic seizures using a recently published computational model of neocortical-onset seizures. We show that the FTSTS protocol applied during the ictal period can modify the excitatory-to-inhibitory synaptic weight in order to effectively desynchronize the pathological neuronal firing patterns even after the ictal period. Our investigation opens the door to a possible new neurostimulation therapy for epilepsy.
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http://dx.doi.org/10.3389/fncom.2023.1084080 | DOI Listing |
Hippocampus
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UCL Institute of Cognitive Neuroscience, University College London, London, UK.
Grid and place cells typically fire at progressively earlier phases within each cycle of the theta rhythm as rodents run across their firing fields, a phenomenon known as theta phase precession. Here, we report theta phase precession relative to turning angle in theta-modulated head direction cells within the anteroventral thalamic nucleus (AVN). As rodents turn their heads, these cells fire at progressively earlier phases as head direction sweeps over their preferred tuning direction.
View Article and Find Full Text PDFElife
March 2025
Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, Netherlands.
Human autonomic neuronal cell models are emerging as tools for modelling diseases such as cardiac arrhythmias. In this systematic review, we compared thirty-three articles applying fourteen different protocols to generate sympathetic neurons and three different procedures to produce parasympathetic neurons. All methods involved the differentiation of human pluripotent stem cells, and none employed permanent or reversible cell immortalization.
View Article and Find Full Text PDFActa Physiol (Oxf)
April 2025
Department of Physiology, Faculty of Medicine, Yeditepe University, Istanbul, Turkey.
Aim: Mitochondria play key roles in neuronal activity, particularly in modulating agouti-related protein (AgRP) and proopiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC), which regulates food intake. FAM163A, a newly identified protein, is suggested to be part of the mitochondrial proteome, though its functions remain largely unknown. This study aimed to investigate the effects of Fam163a knockdown and mitochondrial dysfunction on food intake, AgRP neuron activity, and mitochondrial function in the hypothalamus.
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March 2025
Michael Smith Laboratories, University of British Columbia. 2185 East Mall. Vancouver, B.C., V6T 1Z4, Canada.
T-type calcium channels shape neuronal excitability driving burst firing, plasticity and neuronal oscillations that influence circuit activity. The three biophysically distinct T-type channel subtypes (Cav3.1, Cav3.
View Article and Find Full Text PDFJ Neurol Sci
February 2025
International Collaboration on Repair Discoveries (ICORD), Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Experimental Medicine, Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Division of Physical Medicine & Rehabilitation, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
Nerve transfer surgery (NTS) shows promise in restoring movement to muscles paralyzed by spinal cord (SCI) and peripheral nerve injury (PNI). Yet, motor outcomes vary, and the neurophysiological factors influencing responders and non-responders remain unclear. As the fundamental goal of NTS is to reinnervate paralyzed muscles by creating new motor units (MUs), we examined MU properties after NTS for individuals with SCI and PNI.
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