ArticleMolecular psychiatry2023
Cholecystokinin B receptor antagonists for the treatment of depression via blocking long-term potentiation in the basolateral amygdala.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Standardized chronic restraint stress protocols reveal dynamic evolution of behavioral adaptations in male mice: implications for translational neuroscience.Molecular psychiatry · 2026Article
- mGluR5 in ECAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Translational reprogramming of dentate gyrus peptidergic circuitry gates antidepressant efficacy.Molecular psychiatry · 2026Article
- Not only gut feelings: pancreatic hormone, amylin, controls emotionality and sociability, in a sex divergent manner.Translational psychiatry · 2026Article
- Cellular Diversity Underpins Cortical Organization and Disease Vulnerability in the Human Brain.Neuroscience bulletin · 2026Article
- CCK2R regulates METH-induced CPP acquisition within VTA-BLA-BNST circuit in male mice.Translational psychiatry · 2026Article
- Cholecystokinin upregulation in mPFC leads to social defeat-induced anxiety susceptibility in neuroligin 3 R451C knockin mice.Molecular autism · 2026Article
- Role of Neuronal Cholecystokinin Receptor: An Emerging Therapeutic Target for Ameliorating Neurological Diseases.Molecular neurobiology · 2025Review
- Discovery of a β-arrestin-biased CCKBR agonist that blocks CCKBR-dependent long-term potentiation.Nature communications · 2025Article
- Central neuropeptides as key modulators of astrocyte function in neurodegenerative and neuropsychiatric disorders.Psychopharmacology · 2025Review
- The central signaling pathways related to metabolism-regulating hormones of the gut-brain axis: a review.Journal of translational medicine · 2025Review
- The primary somatosensory sensory cortex-basolateral amygdala pathway contributes to comorbid depression in spared nerve injury-induced neuropathic pain.Scientific reports · 2025Article
- Roles of KCNA2 in Neurological Diseases: from Physiology to Pathology.Molecular neurobiology · 2024Review
- Cholecystokinin-expressing interneurons mediated inhibitory transmission and plasticity in basolateral amygdala modulate stress-induced anxiety-like behaviors in mice.Neurobiology of stress · 2024Article
- Basolateral amygdala parvalbumin and cholecystokinin-expressing GABAergic neurons modulate depressive and anxiety-like behaviors.Translational psychiatry · 2024Article
- Netazepide, an Antagonist of Cholecystokinin Type 2 Receptor, Prevents Vincristine-Induced Sensory Neuropathy in Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Blue light at night produces stress-evoked heightened aggression by enhancing brain-derived neurotrophic factor in the basolateral amygdala.Neurobiology of stress · 2024Article
- Cholecystokinin neurotransmission in the central nervous system: Insights into its role in health and disease.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 3 countries.
Funding
Abstract
Depression is a common and severe mental disorder. Evidence suggested a substantial causal relationship between stressful life events and the onset of episodes of major depression. However, the stress-induced pathogenesis of depression and the related neural circuitry is poorly understood. Here, we investigated how cholecystokinin (CCK) and CCKBR in the basolateral amygdala (BLA) are implicated in stress-mediated depressive-like behavior. The BLA mediates emotional memories, and long-term potentiation (LTP) is widely considered a trace of memory. We identified that the cholecystokinin knockout (CCK-KO) mice impaired LTP in the BLA, while the application of CCK4 induced LTP after low-frequency stimulation (LFS). The entorhinal cortex (EC) CCK neurons project to the BLA and optogenetic activation of EC CCK afferents to BLA-promoted stress susceptibility through the release of CCK. We demonstrated that EC CCK neurons innervate CCKBR cells in the BLA and CCK-B receptor knockout (CCKBR-KO) mice impaired LTP in the BLA. Moreover, the CCKBR antagonists also blocked high-frequency stimulation (HFS) induced LTP formation in the BLA. Notably, CCKBR antagonists infusion into the BLA displayed an antidepressant-like effect in the chronic social defeat stress model. Together, these results indicate that CCKBR could be a potential target to treat depression.
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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.