ArticleBiological psychiatry2015
Stress Impairs Prefrontal Cortical Function via D1 Dopamine Receptor Interactions With Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels.
Article in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021Pooled it
- Disrupted synapses: prefrontal cortex-reward circuit dysfunction in stress-induced depression-like behaviors.Frontiers in cellular neuroscience · 2026Review
- Central neural circuits and their associated mechanisms of inter-organ crosstalk.Frontiers in cell and developmental biology · 2026Review
- Multi-connectomics underpin emotional dysfunction in mouse exposed to simulated space composite environment.Translational psychiatry · 2025Article
- Higher dopamine D1 receptor expression in prefrontal parvalbumin neurons underlies higher distractibility in marmosets versus macaques.Communications biology · 2025Article
- Cortical VIP neurons as a critical node for dopamine actions.Science advances · 2025Article
- Inhibitory control is affected by reward in patients with alcohol use disorder.Frontiers in psychiatry · 2025Article
- Characterizing the Most Vulnerable Prefrontal Cortical Neurons in Schizophrenia.The American journal of psychiatry · 2024Article
- The meso-connectomes of mouse, marmoset, and macaque: network organization and the emergence of higher cognition.Cerebral cortex (New York, N.Y. : 1991) · 2024Review
- β1-adrenoceptor expression on GABAergic interneurons in primate dorsolateral prefrontal cortex: potential role in stress-induced cognitive dysfunction.Neurobiology of stress · 2024Review
- A Molecular Framework for Delirium.The Neurohospitalist · 2024Review
- Interaction Between HCN and Slack Channels Regulates mPFC Pyramidal Cell Excitability in Working Memory Circuits.Molecular neurobiology · 2024Article
- Inhibition of HCN1 currents by norquetiapine, an active metabolite of the atypical anti-psychotic drug quetiapine.Frontiers in pharmacology · 2024Article
- Dynamic Network Connectivity: from monkeys to humans.Frontiers in human neuroscience · 2024Review
- Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders.BMC neuroscience · 2023Review
- Localization of PDE4D, HCN1 channels, and mGluR3 in rhesus macaque entorhinal cortex may confer vulnerability in Alzheimer's disease.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Mind body medicine: a modern bio-psycho-social model forty-five years after Engel.BioPsychoSocial medicine · 2023Article
- The Aversive Lens: Stress effects on the prefrontal-cingulate cortical pathways that regulate emotion.Neuroscience and biobehavioral reviews · 2023Review
- Elevated prefrontal dopamine interferes with the stress-buffering properties of behavioral control in female rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Methylation pattern and mRNA expression of synapse-relevant genes in the MAM model of schizophrenia in the time-course of adolescence.Schizophrenia (Heidelberg, Germany) · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPsychiatric disorders such as schizophrenia are worsened by stress, and working memory deficits are often a central feature of illness. Working memory is mediated by the persistent firing of prefrontal cortical (PFC) pyramidal neurons. Stress impairs working memory via high levels of dopamine D1 receptor (D1R) activation of cyclic adenosine monophosphate signaling, which reduces PFC neuronal firing. The current study examined whether D1R-cyclic adenosine monophosphate signaling reduces neuronal firing and impairs working memory by increasing the open state of hyperpolarization-activated cyclic nucleotide-gated (HCN) cation channels, which are concentrated on dendritic spines where PFC pyramidal neurons interconnect.
methodsA variety of methods were employed to test this hypothesis: dual immunoelectron microscopy localized D1R and HCN channels, in vitro recordings tested for D1R actions on HCN channel current, while recordings in monkeys performing a working memory task tested for D1R-HCN channel interactions in vivo. Finally, cognitive assessments following intra-PFC infusions of drugs examined D1R-HCN channel interactions on working memory performance.
resultsImmunoelectron microscopy confirmed D1R colocalization with HCN channels near excitatory-like synapses on dendritic spines in primate PFC. Mouse PFC slice recordings demonstrated that D1R stimulation increased HCN channel current, while local HCN channel blockade in primate PFC protected task-related firing from D1R-mediated suppression. D1R stimulation in rat or monkey PFC impaired working memory performance, while HCN channel blockade in PFC prevented this impairment in rats exposed to either stress or D1R stimulation.
conclusionsThese findings suggest that D1R stimulation or stress weakens PFC function via opening of HCN channels at network synapses.
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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.