ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2023
Peripheral CB1 receptor blockade acts as a memory enhancer through a noradrenergic mechanism.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 13 citations in OpenAlex.
- Dissociable control of depression and visceral pain by the pICNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Short Communication: The Peripheral Cannabinoid CBInternational journal of molecular sciences · 2026Article
- Enhancement of peripheral fatty acyl ethanolamide signaling prevents stress-induced social avoidance and anxiety-like behaviors in male rats.Psychopharmacology · 2025Article
- Sex differences in endocannabinoid tone in a pilot study of cannabis use disorder and acute cannabis abstinence.Addiction biology · 2023Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
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Abstract
Peripheral inputs continuously shape brain function and can influence memory acquisition, but the underlying mechanisms have not been fully understood. Cannabinoid type-1 receptor (CB1R) is a well-recognized player in memory performance, and its systemic modulation significantly influences memory function. By assessing low arousal/non-emotional recognition memory in mice, we found a relevant role of peripheral CB1R in memory persistence. Indeed, the peripherally-restricted CB1R specific antagonist AM6545 showed significant mnemonic effects that were occluded in adrenalectomized mice, and after peripheral adrenergic blockade. AM6545 also transiently impaired contextual fear memory extinction. Vagus nerve chemogenetic inhibition reduced AM6545-induced mnemonic effect. Genetic CB1R deletion in dopamine β-hydroxylase-expressing cells enhanced recognition memory persistence. These observations support a role of peripheral CB1R modulating adrenergic tone relevant for cognition. Furthermore, AM6545 acutely improved brain connectivity and enhanced extracellular hippocampal norepinephrine. In agreement, intra-hippocampal β-adrenergic blockade prevented AM6545 mnemonic effects. Altogether, we disclose a novel CB1R-dependent peripheral mechanism with implications relevant for lengthening the duration of non-emotional memory.
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