期刊
NEURON
卷 109, 期 9, 页码 1513-+出版社
CELL PRESS
DOI: 10.1016/j.neuron.2021.03.007
关键词
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资金
- Inserm
- EU-FP7 (PAINCAGE) [HEALTH603191]
- European Research Council [ERC-2010-StG-260515, ERC2014PoC640923, ERC2017AdG786467]
- Fondation pour la Recherche Medicale [DRM20101220445, ARF20140129235]
- Human Frontiers Science Program
- Region Aquitaine
- French State/Agence Nationale de la Recherche [LABEX BRAIN ANR10LABX43]
- Marie Sk1odowskaCurie Actions Individual Fellowships (H2020MSCAIF2016) [ID747487]
- Basque Government [IT1211/19, IT123019]
- Fyssen Foundation
- CONACyT
- Ikerbasque
- MINECO (Ministerio de Economa y Competitividad)(MICIU/AEI/FEDER, UE) [PGC2018-093990-A-I00]
- NSERC [RGPIN-2019-06274]
- Red de Trastornos Adictivos, Instituto de Salud Carlos III
- European Regional Development Funds European Union (ERDFEU) [RD16/0017/0012]
- MINECO/FEDER, UE [SAF201565034R, BES2016076766]
- Ministry of Science and Innovation [PID2019107548RBI00]
- NSERC Discovery Grant [RGPIN201505880]
- CIHR [156238]
- Canada Research Chair program
- French State/Agence Nationale de la Recherche (JCJC MitoCB1fat)
Recent neuroscience advances have identified brain circuits as key players in controlling behavior, with evidence showing that activation of specific receptors at different subcellular locations can lead to distinct behavioral outcomes.
Recent advances in neuroscience have positioned brain circuits as key units in controlling behavior, implying that their positive or negative modulation necessarily leads to specific behavioral outcomes. However, emerging evidence suggests that the activation or inhibition of specific brain circuits can actually produce multimodal behavioral outcomes. This study shows that activation of a receptor at different subcellular locations in the same neuronal circuit can determine distinct behaviors. Pharmacological activation of type 1 cannabinoid (CB1) receptors in the striatonigral circuit elicits both antinociception and catalepsy in mice. The decrease in nociception depends on the activation of plasma membrane-residing CB1 receptors (pmCB1), leading to the inhibition of cytosolic PKA activity and substance P release. By contrast, mitochondrial-associated CB1 receptors (mtCB1) located at the same terminals mediate cannabinoid-induced catalepsy through the decrease in intra-mitochondrial PKA-dependent cellular respiration and synaptic transmission. Thus, subcellular-specific CB1 receptor signaling within striatonigral circuits determines multimodal control of behavior.
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