The endocannabinoid, endovanilloid and nitrergic systems could interact in the rat dorsolateral periaqueductal gray matter to control anxiety-like behaviors

Batista, Priscila A.; Fogaça, Manoela V.; Guimarães, Francisco Silveira

doi:10.1016/j.bbr.2015.07.019

Cited by 19 publications

(13 citation statements)

References 51 publications

(88 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Capsaicin, AEA, Tocrisolve TM , 6-IODO, and WIN were purchased from Tocris Cookson, Ballwin, MO, United States and AM251 from Sigma–Aldrich. The doses were based in pilot and previous studies (Maione et al, 2006; Moreira et al, 2007; Mascarenhas et al, 2013, 2015; Batista et al, 2015). The mass weight of each drug necessary for samples of 25 μL in the doses described were as follow: 50 nmol AEA = 2.12 mg; 10 nmol capsaicin = 3.75 mg; 50 nmol WIN = 3.25 mg; 10 nmol AM251 = 6.94 mg; and 3 nmol 6-IODO = 1.57 mg. Evidently, all drugs had to be diluted from this first solution to reach the proper doses.…”

Section: Methodsmentioning

confidence: 99%

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

et al. 2017

View full text Add to dashboard Cite

Divergent results in pain management account for the growing number of studies aiming at elucidating the pharmacology of the endocannabinoid/endovanilloid anandamide (AEA) within several pain-related brain structures. For instance, the stimulation of both Transient Receptor Potential Vanilloid type 1 (TRPV1) and Cannabinoid type 1 (CB1) receptors led to paradoxical effects on nociception. Here, we attempted to propose a clear and reproducible methodology to achieve the antinociceptive effect of exogenous AEA within the dorsal periaqueductal gray (dPAG) of mice exposed to the tail-flick test. Accordingly, male Swiss mice received intra-dPAG injection of AEA (CB1/TRPV1 agonist), capsaicin (TRPV1 agonist), WIN (CB1 agonist), AM251 (CB1 antagonist), and 6-iodonordihydrocapsaicin (6-IODO) (TRPV1 selective antagonist) and their nociceptive response was assessed with the tail-flick test. In order to assess AEA effects on nociception specifically at vanilloid or cannabinoid (CB) substrates into the dPAG, mice underwent an intrinsically inactive dose of AM251 or 6-IODO followed by local AEA injections and were subjected to the same test. While intra-dPAG AEA did not change acute pain, local injections of capsaicin or WIN induced a marked TRPV1- and CB1-dependent antinociceptive effect, respectively. Regarding the role of AEA specifically at CB/vanilloid substrates, while the blockade of TRPV1 did not change the lack of effects of intra-dPAG AEA on nociception, local pre-treatment of AM251, a CB1 antagonist, led to a clear AEA-induced antinociception. It seems that the exogenous AEA-induced antinociception is unmasked when it selectively binds to vanilloid substrates, which might be useful to address acute pain in basic and perhaps clinical trials.

show abstract

Section: Methodsmentioning

confidence: 99%

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Studies from the same group have reported that lack of anxiogenic effects of higher doses of AEA is due to NO (nitric oxide) synthesis (Batista et al, 2015). A NO scavenger (c-PTIO) restored the anxiolytic effect of a high dose of AEA in the EPM and VCT (Batista et al, 2015).…”

Section: Acute Painmentioning

confidence: 99%

“…High doses of AEA, ineffective doses of TRPV1 antagonist (capsazepine) or NMDA antagonist (AP7) failed to produce any changes in EPM alone, but the administration of capsazepine or AP7 prior to the higher dose of AEA produced an anxiolytic effect (Fogaça et al, 2013). Studies from the same group have reported that lack of anxiogenic effects of higher doses of AEA is due to NO (nitric oxide) synthesis (Batista et al, 2015). A NO scavenger (c-PTIO) restored the anxiolytic effect of a high dose of AEA in the EPM and VCT (Batista et al, 2015).…”

Section: Acute Painmentioning

confidence: 99%

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Madasu

Okine

Olango

et al. 2016

Pharmacological Research

View full text Add to dashboard Cite

“…In vitro and in vivo studies reported that the TRPV1 agonist capsaicin both facilitated LTP and prevented spatial memory retrieval deficit, while the selective antagonist capsazepine inhibited LTD (Li et al, 2008). Moreover, Batista et al (2015) reported that anandamide produced anxiolytic-like effect via TRPV1 receptor activation. Here we add to these observations the finding that TRPV1 receptors participate in the modulation of memory consolidation for emotional experiences exerted by cannabinoid compounds.…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid Modulation of Memory Consolidation in Rats: Beyond the Role of Cannabinoid Receptor Subtype 1

et al. 2017

View full text Add to dashboard Cite

The effects induced by exogenous manipulation of endocannabinoid neurotransmission on emotion and memory are often contradictory. Among the different factors involved, of particular interest is the binding affinity of endocannabinoids, and their analogs, for other receptor families beyond cannabinoid receptors, such as the peroxisome proliferator-activated receptors (PPARs), and the transient receptor potential cation channel subfamily V member 1 (TRPV1). The aim of this study was to investigate which receptor subtype mediates cannabinoid effects on memory consolidation for emotionally arousing experiences. We tested two cannabinoid compounds with different pharmacological properties in the inhibitory avoidance task, and evaluated whether the observed effects are mediated by cannabinoid, PPARα or TRPV1 receptor activation. We found that the synthetic cannabinoid agonist WIN55,212-2 and the FAAH inhibitor URB597 both enhanced memory consolidation for inhibitory avoidance training. WIN55,212-22 effects on memory consolidation were predominantly mediated by CB1 receptor activation but CB2 receptors were involved as well. The URB597-induced memory enhancement was dependent on the activation not only of CB1 and CB2 receptors but, notwithstanding, PPAR-α and TRPV1 receptors were involved as well. Our findings drive beyond the classical hypothesis centered on the unique role of CB1 receptor activation for cannabinoid effects on memory, and reveal new insights in the neural mechanisms of memory consolidation.

show abstract

The endocannabinoid, endovanilloid and nitrergic systems could interact in the rat dorsolateral periaqueductal gray matter to control anxiety-like behaviors

Cited by 19 publications

References 51 publications

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

Cannabinoid Modulation of Memory Consolidation in Rats: Beyond the Role of Cannabinoid Receptor Subtype 1

Contact Info

Product

Resources

About