The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Activation of the Cannabinoid Receptor Type 1 Decreases Glutamatergic and GABAergic Synaptic Transmission in the Lateral Amygdala of the Mouse
Open accessAbstract
The endogenous cannabinoid system has been shown recently to play a crucial role in the extinction of aversive memories. As the amygdala is presumably involved in this process, we investigated the effects of the cannabinoid receptor agonist WIN 55,212-2 (WIN-2) on synaptic transmission in the lateral amygdala (LA) of wild-type and cannabinoid receptor type 1 (CB1)-deficient mice. Extracellular field potential recordings and patch-clamp experiments were performed in an in vitro slice preparation. We found that WIN-2 reduces basal synaptic transmission and pharmacologically isolated AMPA receptor- and GABA(A) receptor-mediated postsynaptic currents in wild-type, but not in CB1-deficient mice. These results indicate that, in the LA, cannabinoids modulate both excitatory and inhibitory synaptic transmission via CB1. WIN-2-induced changes of paired-pulse ratio and of spontaneous and miniature postsynaptic currents suggest a presynaptic site of action. Inhibition of G(i/o) proteins and blockade of voltage-dependent and G protein-gated inwardly rectifying K(+) channels inhibited WIN-2 action on basal synaptic transmission. In contrast, modulation of the adenylyl cyclase-protein kinase A pathway, and blockade of presynaptic N- and P/Q- or of postsynaptic L- and R/T-type voltage-gated Ca(2+) channels did not affect WIN-2 effects. Our results indicate that the mechanisms underlying cannabinoid action in the LA partly resemble those observed in the nucleus accumbens and differ from those described for the hippocampus.
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“Although activation of CB1R in the BLA causes a decrease in both glutamatergic and GABAergic transmission, there is typically a net reduction in neuronal excitability on application of CB1R agonists, probably due to CB1R-mediated presynaptic inhibition of glutamate release [48,49].”
From Amygdala FAAH and anandamide: mediating protection and recovery from stress (2013) · cites this paper as [48]
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Metadata
- Authors
- Azad, S. C., Eder, M., Marsicano, G., Lutz, B., Zieglgänsberger, W., & Rammes, G.
- Affiliations
- LMU Klinikum (DE)
- Venue
- Learning & Memory
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2003-03-01
- Volume
- 10
- Issue
- 2
- Pages
- 116-128
- ISSN
- 1072-0502 (ISSN-L)
- 1549-5485
- PMC
- PMC196665
- OpenAlex
- W2134429437
- Cited by
- 220
- References
- 51
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 3 · 2023: 1 · 2022: 7 · 2021: 5 · 2020: 11 · 2019: 6 · 2018: 10 · 2017: 10 · 2016: 10 · 2015: 9 · 2014: 12 · 2013: 9 · 2012: 7
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Learning & Memory (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pharmacology (medical) › Cannabis and Cannabinoid Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- cannabinoid receptor type 1, WIN 55,212-2, lateral amygdala, synaptic transmission, AMPA receptors, GABAA receptor, presynaptic modulation, G protein signaling, inwardly rectifying potassium channels, voltage-gated calcium channels, endocannabinoid system
- MeSH terms
- Amygdala, Analgesics, Animals, Electrophysiology, gamma-Aminobutyric Acid, Male, Mice, Inbred C57BL, Mice, Transgenic, Morpholines, Naphthalenes, Neural Inhibition, Synaptic Transmission, Receptors, Drug, Receptors, GABA-A, Calcium Channels, Potassium Channels, Receptors, AMPA, Patch-Clamp Techniques, Glutamic Acid, Excitatory Postsynaptic Potentials, Receptors, Cannabinoid, Benzoxazines, Mice
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