ArticleThe European journal of neuroscience2017
Essential role of endogenous calcitonin gene-related peptide in pain-associated plasticity in the central amygdala.
Article in The European journal of neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Article
- Calcitonin Gene-Related Peptide (CGRP)-Containing Terminals in the Central Amygdala of Mice and Monkeys: Ultrastructural Analysis and Subsynaptic Expression of GluD1.The European journal of neuroscience · 2026Article
- Sex-dependent central amygdala physiology after supradural CGRP exposure is associated with migraine-like behaviors.The journal of headache and pain · 2026Article
- Optogenetic LTP Manipulation and Mathematical Modeling to Investigate Value Plasticity of the Instructive Signal in Mice.Bio-protocol · 2026Article
- Article
- Elevated TRPV1 expression in the central nucleus of the amygdala participates in initial pain and subsequent anxiety-related behaviors in mice undergoing orthodontic tooth movement.BMC oral health · 2026Article
- Amygdalar calcitonin gene-related peptide driven effects of cold sensitivity induced by peripheral neuropathy in mice.The journal of pain · 2026Article
- Ex Vivo Modulation of the BNST by Parabrachial CGRP Projections Is Decreased After a History of Stress-Induced Anxiety.The European journal of neuroscience · 2025Article
- The posterior capsular central amygdala showing synaptic coactivation with nociplastic pain-associated parabrachial neurons in mice.iScience · 2025Article
- A nociceptive amygdala-striatal pathway modulating affective-motivational pain.Science advances · 2025Article
- Aversive experiences induce valence plasticity of instructive signals to change future learning rules in mice.Communications biology · 2025Article
- Calcitonin Gene-Related Peptide-Induced Central Sensitization: A Hypothesis for Long COVID Symptoms.Medical hypotheses · 2025Article
- Sex Differences in Central Amygdala Glutamate Responses to Calcitonin Gene-Related Peptide.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Sex differences in central amygdala glutamate responses to calcitonin gene-related peptide.bioRxiv : the preprint server for biology · 2024Article
- Cells and circuits for amygdala neuroplasticity in the transition to chronic pain.Cell reports · 2024Article
- Parabrachial Calca neurons drive nociplasticity.Cell reports · 2024Article
- Bridging the Mind and Gut: Uncovering the Intricacies of Neurotransmitters, Neuropeptides, and their Influence on Neuropsychiatric Disorders.Central nervous system agents in medicinal chemistry · 2024Review
- Divergent changes in PBN excitability in a mouse model of neuropathic pain.bioRxiv : the preprint server for biology · 2023Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- A Parabrachial-to-Amygdala Circuit That Determines Hemispheric Lateralization of Somatosensory Processing.Biological psychiatry · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of the neuropeptide calcitonin gene-related peptide (CGRP) is well established in nociceptive behaviors. CGRP is highly expressed in the projection pathway from the parabrachial nucleus to the laterocapsular region of the central amygdala (CeC), which plays a critical role in relaying nociceptive information. The CeC is a key structure in pain behavior because it integrates and modulates nociceptive information along with other sensory signals. Previous studies have demonstrated that blockade of the amygdalar CGRP-signaling cascade attenuates nociceptive behaviors in pain models, while CGRP application facilitates amygdalar synaptic transmission and induces pain behaviors. Despite these lines of evidence, it remains unclear whether endogenous CGRP is involved in the development of nociceptive behaviors accompanied with amygdalar plasticity in a peripheral inflammation model in vivo. To directly address this, we utilized a previously generated CGRP knockout (KO) mouse to longitudinally study formalin-induced plasticity and nociceptive behavior. We found that synaptic potentiation in the right PB-CeC pathway that was observed in wild-type mice was drastically attenuated in the CGRP KO mice 6 h post-inflammation, when acute nociceptive behavior was no longer observed. Furthermore, the bilateral tactile allodynia 6 h post-inflammation was significantly decreased in the CGRP KO mice. In contrast, the acute nociceptive behavior immediately after the formalin injection was reduced only at 20-25 min post-injection in the CGRP KO mice. These results suggest that endogenous CGRP contributes to peripheral inflammation-induced synaptic plasticity in the amygdala, and this plasticity may underlie the exaggerated nociception-emotion linkage in pain chronification.
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