Role of KCNQ potassium channels in stress-induced deficit of working memory
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The prefrontal cortex (PFC) mediates higher cognition but is impaired by stress exposure when high levels of catecholamines activate calcium-cAMP-protein kinase A (PKA) signaling. The current study examined whether stress and increased cAMP-PKA signaling in rat medial PFC (mPFC) reduce pyramidal cell firing and impair working memory by activating KCNQ potassium channels. KCNQ2 channels were found in mPFC layers II/III and V pyramidal cells, and patch-clamp recordings demonstrated KCNQ currents that were increased by forskolin or by chronic stress exposure, and which were associated with reduced neuronal firing. Low dose of KCNQ blockers infused into rat mPFC improved cognitive performance and prevented acute pharmacological stress-induced deficits. Systemic administration of low doses of KCNQ blocker also improved performance in young and aged rats, but higher doses impaired performance and occasionally induced seizures. Taken together, these data demonstrate that KCNQ channels have powerful influences on mPFC neuronal firing and cognitive function, contributing to stress-induced PFC dysfunction.
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Under conditions of uncontrollable stress, high levels of NE and DA release in PFC engage α1-AR and D1R to drive Ca2+-PKC and cAMP-PKA signaling, rapidly opening nearby K+ channels to weaken PFC network connectivity and impair working memory and top-down control.
“However, under conditions of uncontrollable stress, there are high levels of NE and DA release in the PFC (Finlay et al., 1995, Murphy et al., 1996), which engage α1-AR and D1R to drive Ca2+-PKC and cAMP-PKA signaling, rapidly opening nearby K+ channels to weaken PFC network connectivity and impair working memory and top-down control (Fig. 4B); (Arnsten et al., 2019, Birnbaum et al., 2004, Gamo et”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Arnsten et al., 2019
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Experimental — accuracy not yet measuredKCNQ2 channels are localized on spines near synapse and spine apparatus.
“Later studies showed that KCNQ2 channels, which are opened by PKA signaling, are also localized on spines near the synapse and the spine apparatus (Arnsten et al., 2019).”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Arnsten et al., 2019
The Results (Anatomy; page unavailable) say that punctate labeling likely reflects KCNQ2 expression in dendritic spines, but do not locate the channels near synapses or the spine apparatus. The Introduction also says PKA phosphorylation increases the open state of KCNQ2 channels. (LLM, conf=0.86)
Experimental — accuracy not yet measuredHCN channels are co-localized with α2A-AR on dlPFC dendritic spines.
“ImmunoEM demonstrated the physical substrate for these physiological interactions, showing that HCN channels are co-localized with α2A-AR on dlPFC dendritic spines, e.g. on the spine head (Fig. 5B) and in the spine neck.”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Arnsten et al., 2019
The Results > Anatomy section describes KCNQ2 labeling in rat medial PFC, not HCN channels co-localized with α2A-AR in dlPFC spines. The Introduction discusses HCN-channel signaling, but the copy contains no passage establishing the claimed co-localization or reporting the stated immunoEM finding (searched: α2A-AR, HCN, immunoEM, spine head and neck). No page numbers were available in the copy. (LLM, conf=0.76)
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Bothe, M. S., Kohl, T., Felmy, F., Gallant, J. R., & Chagnaud, B. P. (2023) · Current Biology · doi:10.1016/j.cub.2023.11.062 · Cited by 7 · see citing works
Martin, M., & Pedersen, M. G. (2024) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1011559 · Cited by 6 · see citing works
Fan, L., Li, Q., Shi, Y., Li, X. O., Liu, Y., Chen, J., Sun, Y., Chen, A., Yang, Y., Zhang, X., et al. (2024) · BMC Medicine · doi:10.1186/s12916-024-03722-3 · Cited by 3 · see citing works
Datta, D. (2023) · The Journals of Gerontology Series A · doi:10.1093/gerona/glad134 · Cited by 3 · see citing works
Liu, E., Hang, Z., Liu, M., Mu, S., Han, W., Fan, S., Shi, Z. S., Yue, Q., & Sun, J. (2025) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2025.111483 · Cited by 1 · see citing works
Arnsten, A. F. T. (2020) · Oxford University Press eBooks · doi:10.1093/oxfordhb/9780190069162.013.4
Self-citationLos peregrinos noruegos también se dirigieron a Santiago
Njerve, E. (1996) · Peregrino: revista del Camino de Santiago
The circuit mechanisms of working memory: Key roles of the dorsolateral prefrontal cortex
Arnsten, A. F. T., & Martínez-Trujillo, J. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-15754-7.00038-9
Self-citationLindquist, K. L., Nimitvilai, S., Gonzalez, H. C., Hartman, J. H., Woodward, J. J., Zweifel, L. S., Rinker, J. A., & Mulholland, P. J. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.07.687180
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- Authors
- Arnsten, A. F. T., Jin, L. E., Gamo, N. J., Ramos, B., Paspalas, C. D., Morozov, Y. M., Kata, A., Bamford, N. S., Yeckel, M. F., Kaczmarek, L. K., & El-Hassar, L.
- Affiliations
- Yale University (US)
- Venue
- Neurobiology of Stress
- Publisher
- Elsevier BV
- Published
- 2019-11
- Volume
- 11
- Pages
- 100187
- ISSN
- 2352-2895 (ISSN-L)
- PMC
- PMC6889760
- OpenAlex
- W2964865062
- Cited by
- 27
- References
- 72
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 5 · 2023: 3 · 2022: 4 · 2021: 5 · 2020: 5
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neurobiology of Stress (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (DP1AG047744-01, DC0191 9)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- KCNQ potassium channels, KCNQ2, working memory, chronic stress, medial prefrontal cortex, cAMP/PKA signaling, pyramidal neurons, neuronal firing, cognitive impairment, age-related cognitive impairment, seizures
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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