In the present overview, our wish is to demystify some aspects of coding with spike-timing, through a simple review of well-understood technical facts regarding spike coding. Our goal is a better understanding of the extent to which computing and modeling with spiking neuron networks might be biologically plausible and computationally efficient. We intentionally restrict ourselves to a deterministic implementation of spiking neuron networks and we consider that the dynamics of a network is defined by a non-stochastic mapping. By staying in this rather simple framework, we are able to propose results, formula and concrete numerical values, on several topics: (i) general time constraints, (ii) links between continuous signals and spike trains, (iii) spiking neuron networks parameter adjustment. Beside an argued review of several facts and issues about neural coding by spikes, we propose new results, such as a numerical evaluation of the most critical temporal variables that schedule the progress of realistic spike trains. When implementing spiking neuron networks, for biological simulation or computational purpose, it is important to take into account the indisputable facts here unfolded. This precaution could prevent one from implementing mechanisms that would be meaningless relative to obvious time constraints, or from artificially introducing spikes when continuous calculations would be sufficient and more simple. It is also pointed out that implementing a large-scale spiking neuron network is finally a simple task.
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http://dx.doi.org/10.1016/j.jphysparis.2009.11.002 | DOI Listing |
Chaos
January 2025
Institut de Neurosciences des Systèmes, Aix-Marseille University, INSERM, Marseille 13005, France.
J Neurosci
January 2025
Department of Neuroscience, Brown University, Providence RI, USA.
Voltage-gated potassium conductances [Formula: see text] play a critical role not only in normal neural function, but also in many neurological disorders and related therapeutic interventions. In particular, in an important animal model of epileptic seizures, 4-aminopyridine (4-AP) administration is thought to induce seizures by reducing [Formula: see text] in cortex and other brain areas. Interestingly, 4-AP has also been useful in the treatment of neurological disorders such as multiple sclerosis (MS) and spinal cord injury, where it is thought to improve action potential propagation in axonal fibers.
View Article and Find Full Text PDFJ Neurosci
January 2025
Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, Ontario, Canada
Action potentials (spikes) are regenerated at each node of Ranvier during saltatory transmission along a myelinated axon. The high density of voltage-gated sodium channels required by nodes to reliably transmit spikes increases the risk of ectopic spike generation in the axon. Here we show that ectopic spiking is avoided because K1 channels prevent nodes from responding to slow depolarization; instead, axons respond selectively to rapid depolarization because K1 channels implement a high-pass filter.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Edmond and Lily Safra Center for Brain Sciences, The Hebrew University of Jerusalem, Jerusalem, Israel.
Theoretical neuroscientists and machine learning researchers have proposed a variety of learning rules to enable artificial neural networks to effectively perform both supervised and unsupervised learning tasks. It is not always clear, however, how these theoretically-derived rules relate to biological mechanisms of plasticity in the brain, or how these different rules might be mechanistically implemented in different contexts and brain regions. This study shows that the calcium control hypothesis, which relates synaptic plasticity in the brain to the calcium concentration ([Ca2+]) in dendritic spines, can produce a diverse array of learning rules.
View Article and Find Full Text PDFPLoS Comput Biol
January 2025
Kavli Institute for Systems Neuroscience and Centre for Algorithms in the Cortex, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Persistent homology applied to the activity of grid cells in the Medial Entorhinal Cortex suggests that this activity lies on a toroidal manifold. By analyzing real data and a simple model, we show that neural oscillations play a key role in the appearance of this toroidal topology. To quantitatively monitor how changes in spike trains influence the topology of the data, we first define a robust measure for the degree of toroidality of a dataset.
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