ArticlePLoS computational biology2020
Chloride dynamics alter the input-output properties of neurons.
Article in PLoS computational biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Learning Dynamics in Biophysical Spiking Network Models Are Shaped by KCC2/NKCC1 Cotransporter Stoichiometry.The European journal of neuroscience · 2026Article
- Chloride Homeostasis Failure in Human Disease: KCC2/NKCC1 Microdomain Dysfunction as a Driver of Cortical Network Collapse.International journal of molecular sciences · 2026Review
- Direct energy consumption by inhibitory GABAFrontiers in neuroscience · 2026Article
- Article
- Chloride Homeostasis in Neuronal Disorders: Bridging Measurement to Therapy.Life (Basel, Switzerland) · 2025Review
- Sleep-wake-related changes in intracellular chloride regulate plasticity at glutamatergic cortical synapses.Current biology : CB · 2025Article
- Optogenetic Determination of Dynamic and Cell-Type-Specific Inhibitory Reversal Potentials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Article
- Neural ensembles: role of intrinsic excitability and its plasticity.Frontiers in cellular neuroscience · 2024Review
- How Merkel cells transduce mechanical stimuli: A biophysical model of Merkel cells.PLoS computational biology · 2023Article
- Electromechanical model for object roughness perception during finger sliding.Biophysical journal · 2022Article
- Thalamocortical bistable switch as a theoretical model of fibromyalgia pathogenesis inferred from a literature survey.Journal of computational neuroscience · 2022Article
- Computational models reveal how chloride dynamics determine the optimal distribution of inhibitory synapses to minimise dendritic excitability.PLoS computational biology · 2022Article
- Non-monotonic effects of GABAergic synaptic inputs on neuronal firing.PLoS computational biology · 2022Article
- Dynamics of ramping bursts in a respiratory neuron model.Journal of computational neuroscience · 2022Article
- Chloride channels with ClC-1-like properties differentially regulate the excitability of dopamine receptor D1- and D2-expressing striatal medium spiny neurons.American journal of physiology. Cell physiology · 2022Article
- NKCC1 and KCC2: Structural insights into phospho-regulation.Frontiers in molecular neuroscience · 2022Review
- Modelling the spatial and temporal constrains of the GABAergic influence on neuronal excitability.PLoS computational biology · 2021Article
- Intricacies of GABAInternational journal of molecular sciences · 2021Review
- When Are Depolarizing GABAergic Responses Excitatory?Frontiers in molecular neuroscience · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Fast synaptic inhibition is a critical determinant of neuronal output, with subcellular targeting of synaptic inhibition able to exert different transformations of the neuronal input-output function. At the receptor level, synaptic inhibition is primarily mediated by chloride-permeable Type A GABA receptors. Consequently, dynamics in the neuronal chloride concentration can alter the functional properties of inhibitory synapses. How differences in the spatial targeting of inhibitory synapses interact with intracellular chloride dynamics to modulate the input-output function of neurons is not well understood. To address this, we developed computational models of multi-compartment neurons that incorporate experimentally parametrised mechanisms to account for neuronal chloride influx, diffusion, and extrusion. We found that synaptic input (either excitatory, inhibitory, or both) can lead to subcellular variations in chloride concentration, despite a uniform distribution of chloride extrusion mechanisms. Accounting for chloride changes resulted in substantial alterations in the neuronal input-output function. This was particularly the case for peripherally targeted dendritic inhibition where dynamic chloride compromised the ability of inhibition to offset neuronal input-output curves. Our simulations revealed that progressive changes in chloride concentration mean that the neuronal input-output function is not static but varies significantly as a function of the duration of synaptic drive. Finally, we found that the observed effects of dynamic chloride on neuronal output were mediated by changes in the dendritic reversal potential for GABA. Our findings provide a framework for understanding the computational effects of chloride dynamics on dendritically targeted synaptic inhibition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.