Suppression of noxious stimulus-evoked expression of fos protein-like immunoreactivity in rat spinal cord by a selective cannabinoid agonist

Tsou, Kang; Lowitz, Karen; Hohmann, Andrea G.; Martin, William J.; Hathaway, Charles B.; Bereiter, David A.; Walker, J. Michael

doi:10.1016/s0306-4522(96)83015-6

Cited by 107 publications

(54 citation statements)

References 27 publications

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“…In acute pain, anandamide, THC, cannabidiol, and synthetic cannabinoids such as CP55,940 and WIN 55,212-2 are effective against chemical ( Sofia et al, 1973;Formukong et al, 1988;Calignano et al, 1998;Costa et al, 2004a,b;Ulugol et al, 2006), mechanical (Sofia et al, 1973;Martin et al, 1996;Smith et al, 1998;, and thermal pain stimuli (Buxbaum, 1972;Bloom et al, 1977;Lichtman and Martin, 1991a,b;Fride and Mechoulam, 1993;. Recent animal studies indicate that anandamide and cannabinoid ligands are also very effective against chronic pain of both neuropathic (Herzberg et al, 1997;Bridges et al, 2001;Fox et al, 2001;) and inflammatory origin (Tsou et al, 1996;Richardson et al, 1998a,b,c;Li et al, 1999;Martin et al, 1999b;. Moreover, endocannabinoids and synthetic cannabinoids exert synergistic antinociceptive effects when combined with commonly used nonsteroid anti-inflammatory drugs, which may have utility in the pharmacotherapy of pain Ulugol et al, 2006).…”

Section: B Pain and Inflammationmentioning

confidence: 99%

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

2006

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Section: B Pain and Inflammationmentioning

confidence: 99%

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

2006

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“…Similarly, intrathecal administration of another non-selective cannabinoid receptor agonist, WIN55,212-2, reverses the mechanical allodynia or hyperalgesia induced by injection of complete Freund's adjuvant into the rat hindpaw (Martin et al, 1999) or partial ligation of the sciatic nerve (Fox et al, 2001). Systemic administration of WIN55,212-2 suppresses nociceptive behaviors in the formalin test (Tsou et al, 1996) and thermal and mechanical hyperalgesia induced by intradermal injection of capsaicin, an agonist of nociceptive TRPV1 receptors, through CB1 receptors (Li et al, 1999). WIN55,212-2 also produces antihyperalgesic and antiallodynic effects in chronic pain caused by peripheral nerve injury (Herzberg et al, 1997;Bridges et al, 2001).…”

Section: Antinociceptive Effect Of Cannabinoid Receptor Agonistsmentioning

confidence: 99%

Modulation of pain transmission by G-protein-coupled receptors

Pan

Zhou

et al. 2008

Pharmacology & Therapeutics

169

116

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The heterotrimeric G protein-coupled receptors (GPCRs) represent the largest and most diverse family of cell surface receptors and proteins. GPCRs are widely distributed in the peripheral and central nervous systems and are one of the most important therapeutic targets in pain medicine. GPCRs are present on the plasma membrane of neurons and their terminals along the nociceptive pathways and are closely associated with the modulation of pain transmission. GPCRs that can produce analgesia upon activation include opioid, cannabinoid, α 2 -adrenergic, muscarinic acetylcholine, γ-aminobutyric acid B (GABA B ), group II and III metabotropic glutamate, and somatostatin receptors. Recent studies have led to a better understanding of the role of these GPCRs in the regulation of pain transmission. Here, we review the current knowledge about the cellular and molecular mechanisms that underlie the analgesic actions of GPCR agonists, with a focus on their effects on ion channels expressed on nociceptive sensory neurons and on synaptic transmission at the spinal cord level.

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“…The administration of 5 mg/kg WIN prior to extinction training did not enhance extinction; in contrast, WINtreated animals actually showed a nonsignificant, but slightly higher, level of conditioned fear 24 h following extinction training (Figure 2d). Notably, the well-documented emergence of prominent locomotor and analgesic effects following administration of higher doses of WIN (eg Tsou et al, 1996;Herzberg et al, 1997) limited our ability to test the effects of doses of WIN greater than 5 mg/kg.…”

Section: A Direct Cb1 Agonist Has No Effect On Extinctionmentioning

confidence: 99%

Enhancing Cannabinoid Neurotransmission Augments the Extinction of Conditioned Fear

Chhatwal

Davis

Maguschak

et al. 2004

Neuropsychopharmacol

329

253

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The endogenous cannabinoid (eCB) system represents a major therapeutic target for the treatment of a variety of anxiety-related disorders. A recent study has demonstrated that pharmacologic or genetic disruption of CB1-receptor-mediated neurotransmission decreases the extinction of conditioned fear in mice. Here, we examined whether CB1 blockade would similarly disrupt extinction in rats, using fear-potentiated startle as a measure of conditioned fear. We also examined whether pharmacologic enhancement of CB1 activation would lead to enhancements in extinction. Our results indicate that systemic administration of the CB1 antagonist rimonabant (SR141716A) prior to extinction training led to significant, dose-dependent decreases in extinction. While the administration of the CB1 agonist WIN 55,212-2 did not appear to affect extinction, administration of AM404, an inhibitor of eCB breakdown and reuptake, led to dose-dependent enhancements in extinction. In addition to showing decreased fear 1 and 24 h after extinction training, AM404-treated animals showed decreased shock-induced reinstatement of fear. Control experiments demonstrated that the effects of AM404 could not be attributed to alterations in the expression of conditioned fear, locomotion, shock reactivity, or baseline startle, as these parameters seemed unchanged by AM404. Furthermore, coadministration of rimonabant with AM404 blocked this enhancement of extinction, suggesting that AM404 was acting to increase CB1 receptor activation during extinction training. These results demonstrate that the eCB system can be modulated to enhance emotional learning, and suggest that eCB modulators may be therapeutically useful as adjuncts for exposure-based psychotherapies such as those used to treat Post-Traumatic Stress Disorder and other anxiety disorders.

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Suppression of noxious stimulus-evoked expression of fos protein-like immunoreactivity in rat spinal cord by a selective cannabinoid agonist

Cited by 107 publications

References 27 publications

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

Modulation of pain transmission by G-protein-coupled receptors

Enhancing Cannabinoid Neurotransmission Augments the Extinction of Conditioned Fear

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