ArticleFrontiers in cellular neuroscience2013
Activation of CRH receptor type 1 expressed on glutamatergic neurons increases excitability of CA1 pyramidal neurons by the modulation of voltage-gated ion channels.
Article in Frontiers in cellular neuroscience, 2013. 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, 41 citations in OpenAlex.
- Temporal coding expands the bandwidth of GPCR-mediated neuromodulation.bioRxiv : the preprint server for biology · 2026Article
- Targeting corticotropin-releasing hormone receptor type 1 (Crhr1) neurons: validating the specificity of a novel transgenic Crhr1-FlpO mouse.Brain structure & function · 2024Article
- Restoring social deficits in IRSp53-deleted mice: chemogenetic inhibition of ventral dentate gyrus Emx1-expressing cells.Translational psychiatry · 2024Article
- Oxytocin and corticotropin-releasing hormone exaggerate nucleus tractus solitarii neuronal and synaptic activity following chronic intermittent hypoxia.The Journal of physiology · 2024Article
- A dietary polyphenol metabolite alters CA1 excitability ex vivo and mildly affects cortico-hippocampal field potential generators in anesthetized animals.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Article
- Local production of corticotropin-releasing hormone in prefrontal cortex modulates male-specific novelty exploration.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Central AT1 receptor signaling by circulating angiotensin II is permissive to acute intermittent hypoxia-induced sympathetic neuroplasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Repeated Exposure to Multiple Concurrent Stresses Induce Circuit Specific Loss of Inputs to the Posterior Parietal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Activation of the hypothalamic paraventricular nucleus by acute intermittent hypoxia: Implications for sympathetic long-term facilitation neuroplasticity.Experimental neurology · 2019Article
- Hyper-diversity of CRH interneurons in mouse hippocampus.Brain structure & function · 2019Article
- Deletion of CRH From GABAergic Forebrain Neurons Promotes Stress Resilience and Dampens Stress-Induced Changes in Neuronal Activity.Frontiers in neuroscience · 2019Article
- Cross-disorder risk gene CACNA1C differentially modulates susceptibility to psychiatric disorders during development and adulthood.Molecular psychiatry · 2018Article
- Deciphering the Contributions of CRH Receptors in the Brain and Pituitary to Stress-Induced Inhibition of the Reproductive Axis.Frontiers in molecular neuroscience · 2018Article
- The CRF Family of Neuropeptides and their Receptors - Mediators of the Central Stress Response.Current molecular pharmacology · 2018Review
- Estradiol-Dependent Stimulation and Suppression of Gonadotropin-Releasing Hormone Neuron Firing Activity by Corticotropin-Releasing Hormone in Female Mice.Endocrinology · 2018Article
- Single-cell analysis of experience-dependent transcriptomic states in the mouse visual cortex.Nature neuroscience · 2018Article
- Persistent Stress-Induced Neuroplastic Changes in the Locus Coeruleus/Norepinephrine System.Neural plasticity · 2018Review
- Stress and Seizures: Space, Time and Hippocampal Circuits.Trends in neurosciences · 2017Review
- The Endogenous Stress Hormone CRH Modulates Excitatory Transmission and Network Physiology in Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
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11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Corticotropin-releasing hormone (CRH) plays an important role in a substantial number of patients with stress-related mental disorders, such as anxiety disorders and depression. CRH has been shown to increase neuronal excitability in the hippocampus, but the underlying mechanisms are poorly understood. The effects of CRH on neuronal excitability were investigated in acute hippocampal brain slices. Population spikes (PS) and field excitatory postsynaptic potentials (fEPSP) were evoked by stimulating Schaffer-collaterals and recorded simultaneously from the somatic and dendritic region of CA1 pyramidal neurons. CRH was found to increase PS amplitudes (mean ± Standard error of the mean; 231.8 ± 31.2% of control; n = 10) while neither affecting fEPSPs (104.3 ± 4.2%; n = 10) nor long-term potentiation (LTP). However, when Schaffer-collaterals were excited via action potentials (APs) generated by stimulation of CA3 pyramidal neurons, CRH increased fEPSP amplitudes (119.8 ± 3.6%; n = 8) and the magnitude of LTP in the CA1 region. Experiments in slices from transgenic mice revealed that the effect on PS amplitude is mediated exclusively by CRH receptor 1 (CRHR1) expressed on glutamatergic neurons. The effects of CRH on PS were dependent on phosphatase-2B, L- and T-type calcium channels and voltage-gated potassium channels but independent on intracellular Ca(2+)-elevation. In patch-clamp experiments, CRH increased the frequency and decay times of APs and decreased currents through A-type and delayed-rectifier potassium channels. These results suggest that CRH does not affect synaptic transmission per se, but modulates voltage-gated ion currents important for the generation of APs and hence elevates by this route overall neuronal activity.
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