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Cited by 42Cannabis and Cannabinoid ResearchNeuroscience and Neuropharmacology ResearchPain Mechanisms and Treatments

Cannabinoid-induced presynaptic inhibition at the primary afferent trigeminal synapse of juvenile rat brainstem slices

Liang, Ying‐Ching, Huang, Chiung‐Chun, Hsu, Kuei‐Sen, Takahashi, Tomoyuki·2004·The Journal of Physiology
DOI 10.1113/jphysiol.2003.056986
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Abstract

Systemic or intraventricular administration of cannabinoids causes analgesic effects, but relatively little is known for their cellular mechanism. Using brainstem slices with the mandibular nerve attached, we examined the effect of cannabinoids on glutamatergic transmission in superficial trigeminal caudal nucleus of juvenile rats. The exogenous cannabinoid receptor agonist WIN 55,212-2 (WIN), as well as the endogenous agonist anandamide, hyperpolarized trigeminal caudal neurones and depressed the amplitude of excitatory postsynaptic potentials (EPSPs) or currents (EPSCs) monosynaptically evoked by stimulating mandibular nerves in a concentration-dependent manner. The inhibitory action of WIN was blocked or fully reversed by the CB1 receptor antagonist SR 141716A. WIN had no effect on the amplitude of miniature excitatory postsynaptic currents (mEPSCs) recorded in the presence of tetrodotoxin or cadmium. The inhibitory effect of WIN on EPSCs was greater for those with longer synaptic latency, suggesting that cannabinoids have a stronger effect on C-fibre EPSPs than on Adelta-fibre EPSPs. Ba2+ (100 microm) blocked the hyperpolarizing effect of cannabinoids, but did not affect their inhibitory effect on EPSPs. The N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTX) occluded the WIN-mediated presynaptic inhibition, whereas the P/Q-type Ca2+ channel blocker omega-agatoxin TK (omega-Aga) had no effect. These results suggest that cannabinoids preferentially activate CB1 receptors at the nerve terminal of small-diameter primary afferent fibres. Upon activation, CB1 receptors may selectively inhibit presynaptic N-type Ca2+ channels and exocytotic release machinery, thereby attenuating the transmitter release at the trigeminal nociceptive synapses.

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  • Cannabinoids are negative modulators of nociceptive transmission at the superficial layer of the trigeminal caudal subnucleus.

    “These and earlier findings from the same group95 indicate that cannabinoids are negative modulators of nociceptive transmission at the superficial layer of the trigeminal caudal subnucleus.”

    From Cannabinoids as Pharmacotherapies for Neuropathic Pain: From the Bench to the Bedside (2009) · cites this paper as [95]

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Authors
Liang, Y., Huang, C., Hsu, K., & Takahashi, T.
Affiliations
  • Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (CN)
  • National Cheng Kung University (TW)
  • The University of Tokyo (JP)
ORCID
Venue
The Journal of Physiology
Publisher
Wiley
Published
2004-02-15
Volume
555
Issue
1
Pages
85-96
ISSN
  • 0022-3751 (ISSN-L)
  • 1469-7793
DOI
10.1113/jphysiol.2003.056986
OpenAlex
W1663380562
Cited by
42
References
61
Citations by year
2023: 2 · 2021: 1 · 2020: 2 · 2018: 1 · 2017: 5 · 2016: 2 · 2015: 1 · 2014: 1 · 2013: 1 · 2012: 2
FWCI
1.71
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 3 d)
Locations
  • The Journal of Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords
cannabinoids, presynaptic inhibition, CB1 receptor, primary afferent fibers, N-type calcium channels, omega-conotoxin GVIA, glutamatergic neurotransmission, WIN 55,212-2, anandamide, synaptic depression, young rats
MeSH terms
Afferent Pathways, Aging, Animals, Brain Stem, Cannabinoids, Male, Neural Inhibition, Synapses, Trigeminal Nuclei, Rats, Sprague-Dawley, Presynaptic Terminals, Excitatory Postsynaptic Potentials, Rats, In Vitro Techniques

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