This article is a correction to:
Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington’s Disease
Melissa Serranilla
Melanie A. WoodinA Corrigendum on
Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington's Disease
Serranilla, M., and Woodin, M. A. (2022). Front. Cell. Neurosci. 15:817013. doi: 10.3389/fncel.2021.817013
In the original article, there was a mistake in the legend for Figures 3, 4 as published. The legends for those figures were swapped. The corrected legends appear below.
FIGURE 3 | Underlying network connection can render some neurons more susceptible to GABAergic disinhibition. Excitatory neuron A is reciprocally connected with inhibitory neuron B to form a small feedback loop. With a reduction in KCC2 function (or increase in NKCC1, not shown here), in excitatory neuron A (below), Cl− will accumulate leading to a faster rate of collapse in the Cl− driving force subsequently weakening GABAergic inhibition. As neuron A experiences less inhibition, it will fire more, leading to greater excitation of the inhibitory neuron B. As a result of increased excitatory input, the inhibitory neuron will then increase inhibitory input back onto the excitatory neuron A, which will further enhance the Cl− load in the excitatory neuron to create a deleterious loop. Created with BioRender.com.
FIGURE 4 | Synaptic changes in the basal ganglia circuitry in HD. In the healthy brain, activation of D1-MSNs of the direct pathway (blue) leads to disinhibition of the thalamus, which increases excitatory feedback to the motor cortex. Activation of the D2-MSNs of the indirect pathway (purple) leads to inhibition of the thalamus, which decreases excitatory feedback to the motor cortex. Dopaminergic inputs from the SNc produces different outcomes in D1- and D2- MSNs; inhibiting D2-MSNs, while exciting D1-MSNs. Early in HD, there is a preferential loss of D2-MSNs leading to increased output along the direct pathway, mediated by D1- MSNs. The decreased inhibitory output through the indirect pathway and increased output through the direct pathway, lead to the development of unwanted, hyperkinetic movements called chorea (GPe, Globus pallidus externa; GPi, Globus pallidus interna; STN, Subthalamic Nucleus; SNc, Substantia Nigra pars compacta). Template taken and modified with BioRender.com.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
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Keywords: KCC2, chloride regulation, GABA, synaptic inhibition, striatum, Huntington's disease
Citation: Serranilla M and Woodin MA (2022) Corrigendum: Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington's Disease. Front. Cell. Neurosci. 16:876821. doi: 10.3389/fncel.2022.876821
Received: 15 February 2022; Accepted: 17 February 2022;
Published: 11 March 2022.
Approved by:
Frontiers Editorial Office, Frontiers Media SA, SwitzerlandCopyright © 2022 Serranilla and Woodin. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Melanie A. Woodin, bS53b29kaW4mI3gwMDA0MDt1dG9yb250by5jYQ==