ArticleMolecular neurobiology2018
Long-Term Plasticity in Amygdala Circuits: Implication of CB1-Dependent LTD in Stress.
Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Article
- Fear conditioning and extinction distinctively alter bidirectional synaptic plasticity within the amygdala of an animal model of post-traumatic stress disorder.Neurobiology of stress · 2024Article
- Amygdalo-nigral circuit mediates stress-induced vulnerability to the parkinsonian toxin MPTP.CNS neuroscience & therapeutics · 2023Article
- Fatty acid amide hydrolase levels in brain linked with threat-related amygdala activation.Neuroimage. Reports · 2022Article
- Effect of caloric restriction on depression.Journal of cellular and molecular medicine · 2018Review
- Stress in Regulation of GABA Amygdala System and Relevance to Neuropsychiatric Diseases.Frontiers in neuroscience · 2018Review
- Stress-Induced Functional Alterations in Amygdala: Implications for Neuropsychiatric Diseases.Frontiers in neuroscience · 2018Review
- Affective Processing in Non-invasive Brain Stimulation Over Prefrontal Cortex.Frontiers in human neuroscience · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The amygdala mediates many forms of emotional learning, during which the central nucleus of amygdala (CeA) functions as a major output of the amygdala by converging inputs from the basolateral nucleus (BLA) and other amygdalar subregions. However, the contribution of BLA-CeA synaptic transmission and plasticity of this transmission after exposure to emotional stimuli remains to be completely understood. Using paired recording, we simultaneously recorded BLA and CeA neurons, and observed that BLA-CeA transmission was glutamatergic. In this transmission, high-frequency stimulation induced NMDA receptor (NMDAR)-dependent LTP, low-frequency stimulation induced NMDAR-dependent LTD, whereas modest-frequency stimulation induced cannabinoid receptor1 (CB1)-dependent LTD. After acute stress, CB1-dependent LTD of this transmission was selectively abolished. This effect of stress was mimicked by intra-CeA administration of CB1-selective agonists and prevented by CB1-selective antagonists. Furthermore, intra-CeA administration of CB1 antagonists prevented stress-induced reduction of explorative behaviors. These results indicate that CB1 signaling-mediated plasticity in local circuits of the amygdala plays a critical role in emotional responses.
Indexed as
Identifiers
28593436What OpenQuestion holds
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.