ArticleNeuropharmacology2016
Stress increases GABAergic neurotransmission in CRF neurons of the central amygdala and bed nucleus stria terminalis.
Article in Neuropharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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Who cites it
59 citing papers in PubMed, 90 citations in OpenAlex.
- Regulation of amygdala and dopamine system in naïve and chronic alcohol states.Alcohol (Fayetteville, N.Y.) · 2026Article
- A comprehensive overview of the biological foundations of ADHD.Bioscience reports · 2026Review
- Chronic Stress Alters Dorsal Bed Nucleus of Stria Terminalis Synaptic Neurotransmission in a Dravet Syndrome Mouse Model.bioRxiv : the preprint server for biology · 2026Article
- Article
- Chloride homeostasis dysfunction drives hyperactivation of corticotropin-releasing factor-expressing neurons in the amygdala in stress-induced hypertension.The Journal of clinical investigation · 2026Article
- Stress History Modulates Corticotropin-Releasing Factor Neurons to Establish Resilience.Biological psychiatry global open science · 2026Article
- Alcohol Attenuates CRF-Induced Excitatory Effects from the Extended Amygdala to Dorsostriatal Cholinergic Interneurons.bioRxiv : the preprint server for biology · 2025Article
- Disentangling the effects of corticotrophin releasing factor and GABA release from the bed nucleus of the stria terminalis on ethanol self-administration in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Extended amygdala corticotropin-releasing hormone neurons regulate sexually dimorphic changes in pair bond formation following social defeat in prairie voles (Microtus ochrogaster).Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Article
- Disentangling the Neural Circuits of Arousal and Anxiety-Like Behavior.Current topics in behavioral neurosciences · 2025Review
- Extended amygdala corticotropin-releasing hormone neurons regulate sexually dimorphic changes in pair bond formation following social defeat in prairie voles (bioRxiv : the preprint server for biology · 2024Article
- Optimized ultrasound neuromodulation for non-invasive control of behavior and physiology.Neuron · 2024Article
- A dual-pathway architecture enables chronic stress to disrupt agency and promote habit formation.bioRxiv : the preprint server for biology · 2024Article
- Association between social dominance hierarchy and PACAP expression in the extended amygdala, corticosterone, and behavior in C57BL/6 male mice.Scientific reports · 2024Article
- Chemogenetic activation of corticotropin-releasing factor-expressing neurons in the anterior bed nucleus of the stria terminalis reduces effortful motivation behaviors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Article
- The role of genetically distinct central amygdala neurons in appetitive and aversive responding assayed with a novel dual valence operant conditioning paradigm.bioRxiv : the preprint server for biology · 2023Article
- Impact of social dominance hierarchy on PACAP expression in the extended amygdala, corticosterone, and behavior in C57BL/6 male mice.bioRxiv : the preprint server for biology · 2023Article
- Pharmacological Inactivation of the Bed Nucleus of the Stria Terminalis Increases Affiliative Social Behavior in Rhesus Macaques.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Corticotrophin Releasing Factor (CRF) is a critical stress-related neuropeptide in major output pathways of the amygdala, including the central nucleus (CeA), and in a key projection target of the CeA, the bed nucleus of the stria terminalis (BnST). While progress has been made in understanding the contributions and characteristics of CRF as a neuropeptide in rodent behavior, little attention has been committed to determine the properties and synaptic physiology of specific populations of CRF-expressing (CRF(+)) and non-expressing (CRF(-)) neurons in the CeA and BnST. Here, we fill this gap by electrophysiologically characterizing distinct neuronal subtypes in CeA and BnST. Crossing tdTomato or channelrhodopsin-2 (ChR2-YFP) reporter mice to those expressing Cre-recombinase under the CRF promoter allowed us to identify and manipulate CRF(+) and CRF(-) neurons in CeA and BnST, the two largest areas with fluorescently labeled neurons in these mice. We optogenetically activated CRF(+) neurons to elicit action potentials or synaptic responses in CRF(+) and CRF(-) neurons. We found that GABA is the predominant co-transmitter in CRF(+) neurons within the CeA and BnST. CRF(+) neurons are highly interconnected with CRF(-) neurons and to a lesser extent with CRF(+) neurons. CRF(+) and CRF(-) neurons differentially express tonic GABA currents. Chronic, unpredictable stress increase the amplitude of evoked IPSCs and connectivity between CRF(+) neurons, but not between CRF(+) and CRF(-) neurons in both regions. We propose that reciprocal inhibition of interconnected neurons controls CRF(+) output in these nuclei.
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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.