Modulation by female sex hormones of the cannabinoid-induced catalepsy and analgesia in ovariectomized mice

Anaraki, Dina Kalbasi; Sianati, Setareh; Sadeghi, Mahsa; Ghasemi, Mehdi; Javadi, Parvin; Mehr, Shahram Ejtemaei; Dehpour, Ahmad Reza

doi:10.1016/j.ejphar.2008.02.055

Cited by 19 publications

(10 citation statements)

References 58 publications

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“…For example, similar to the present study, two previous studies found that in male rats gonadectomized as adults, T decreased THC-induced motoric effects but did not significantly alter THC's antinociceptive effects (Craft & Leitl, 2008; Wakley et al, 2015). Also similar to the present study, two previous studies reported no significant E2 modulation of cannabinoid-induced motor suppression in GDX female rats or mice (Craft & Leitl, 2008; Kalbasi Anaraki et al, 2008). However, in regard to E2 modulation of THC-induced antinociception, two previous studies reported that E2 increased THC's antinociceptive effect in female rats gonadectomized as adults (Craft & Leitl, 2008; Wakley et al, 2014), one reported that E2 decreased the antinociceptive effect of WIN55,212-2 in GDX female mice (Kalbasi Anaraki et al, 2008), and yet another reported no E2 modulation of THC antinociceptive potency in GDX female rats (Wakley et al, 2015).…”

Section: Discussionsupporting

confidence: 92%

“…Also similar to the present study, two previous studies reported no significant E2 modulation of cannabinoid-induced motor suppression in GDX female rats or mice (Craft & Leitl, 2008; Kalbasi Anaraki et al, 2008). However, in regard to E2 modulation of THC-induced antinociception, two previous studies reported that E2 increased THC's antinociceptive effect in female rats gonadectomized as adults (Craft & Leitl, 2008; Wakley et al, 2014), one reported that E2 decreased the antinociceptive effect of WIN55,212-2 in GDX female mice (Kalbasi Anaraki et al, 2008), and yet another reported no E2 modulation of THC antinociceptive potency in GDX female rats (Wakley et al, 2015). Thus, the lack of E2 modulation of THC effects in GDX females observed in the present study agrees only with the results reported in Wakley et al (2015).…”

Section: Discussionsupporting

confidence: 92%

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Gonadal hormone modulation of ∆9-tetrahydrocannabinol-induced antinociception and metabolism in female versus male rats

Craft

Haas

Wiley

et al. 2017

Pharmacology Biochemistry and Behavior

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The gonadal hormones testosterone (T) in adult males and estradiol (E2) in adult females have been reported to modulate behavioral effects of Δ9-tetrahydrocannabinol (THC). This study determined whether activational effects of T and E2 are sex-specific, and whether hormones modulate production of the active metabolite 11-hydroxy-THC (11-OH-THC) and the inactive metabolite 11-nor-9-carboxy-THC (THC-COOH). Adult male and female rats were gonadectomized (GDX) and treated with nothing (0), T (10-mm Silastic capsule/100 g body weight), or E2 (1-mm Silastic capsule/rat). Three weeks later, saline or the cytochrome P450 inhibitor proadifen (25 mg/kg; to block THC metabolism and boost THC's effects) was injected i.p.; one h later, vehicle or THC (3 mg/kg females, 5 mg/kg males) was injected i.p., and rats were tested for antinociceptive and motoric effects 15-240 min post-injection. T did not consistently alter THC-induced antinociception in males, but decreased it in females (tail withdrawal test). Conversely, T decreased THC-induced catalepsy in males, but had no effect in females. E2 did not alter THC-induced antinociception in females, but enhanced it in males. The discrepant effects of T and E2 on males’ and females’ behavioral responses to THC suggests that sexual differentiation of THC sensitivity is not simply due to activational effects of hormones, but also occurs via organizational hormone or sex chromosome effects. Analysis of serum showed that proadifen increased THC levels, E2 increased 11-OH-THC in GDX males, and T decreased 11-OH-THC (and to a lesser extent, THC) in GDX females. Thus, hormone modulation of THC's behavioral effects is caused in part by hormone modulation of THC oxidation to its active metabolite. However, the fact that hormone modulation of metabolism did not alter THC sensitivity similarly on all behavioral measures within each sex suggests that other mechanisms also play a role in gonadal hormone modulation of THC sensitivity in adult rats.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 92%

Gonadal hormone modulation of ∆9-tetrahydrocannabinol-induced antinociception and metabolism in female versus male rats

Craft

Haas

Wiley

et al. 2017

Pharmacology Biochemistry and Behavior

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“…A previous study also reported that P4 decreased antinociception produced by a moderate (but not low) dose of WIN55,212-2 in GDX female mice (Kalbasi Anaraki et al, 2008). In rats, P4 decreased i.c.v.…”

Section: Discussionmentioning

confidence: 67%

“…It should be noted that when all dose-effect curves were included in the analysis (pre- and post-chronic), E2 did significantly increase THC effect on the tail withdrawal test, which may suggest that the E2 effect is small in this population and may only be evident when sample size is very large. The only other study of ovarian hormone modulation of cannabinoid antinociception, conducted in female mice, showed that gonadectomy increased antinociception produced by WIN55,212-2, and this increase was reversed by E2 given in a single large dose approximately 4 h before testing (Kalbasi Anaraki et al, 2008). Thus, E2 modulation of cannabinoid antinociception may depend on species, strain, and other variables, and should be investigated further.…”

Section: Discussionmentioning

confidence: 99%

Gonadal hormones do not alter the development of antinociceptive tolerance to delta-9-tetrahydrocannabinol in adult rats

Wakley¹,

Wiley

Craft³

2015

Pharmacology Biochemistry and Behavior

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The purpose of this study was to determine whether sex differences in the development of antinociceptive tolerance to delta-9-tetrahydrocannabinol (THC) are due to activational effects of gonadal hormones. Rats were sham-gonadectomized (sham-GDX) or gonadectomized (GDX). GDX females received no hormone replacement (GDX+0), estradiol (GDX+E2), progesterone (GDX+P4), or both (GDX+E2/P4). GDX male rats received no hormone (GDX+0) or testosterone (GDX+T). Two weeks later, antinociceptive potency of THC was determined (pre-chronic test) on the warm water tail withdrawal and paw pressure assays. Vehicle or a sex-specific THC dose (females, 5.7 mg/kg, males, 9.9 mg/kg) was administered twice-daily for 9 days, then the THC dose-effect curves were re-determined (post-chronic test). On the pre-chronic test (both assays), THC was more potent in sham-GDX females than males, and gonadectomy did not alter this sex difference. In GDX females, P4 significantly decreased THC’s antinociceptive potency, whereas E2 had no effect. In GDX males, T did not alter THC’s antinociceptive potency. After chronic THC treatment, THC’s antinociceptive potency was decreased more in sham-GDX females than males, on the tail withdrawal test; this sex difference in tolerance was not altered in GDX or hormone-treated groups. These results suggest that greater antinociceptive tolerance in females, which occurred despite females receiving 40% less THC than males, is not due to activational effects of gonadal hormones.

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“…On the other hand, data from the orofacial myositis pain model indicate that testosterone promotes cytokine-induced upregulation of CB1 receptor expression in the trigeminal ganglia of male rats (Niu et al, 2012). By contrast, ovariectomy enhances cannabinoid-induced antinociception in mice, which is completely reversed by estradiol replacement (Anaraki et al, 2008). This discrepancy is indicative of a species difference in the cannabinoid regulation of pain processing, which has implications as to whether or how these data pertain to the human condition.…”

Section: Sex Differences In Cannabinoid-induced Antinociceptionmentioning

confidence: 99%

Sex differences in cannabinoid-regulated biology: A focus on energy homeostasis

Wagner

2016

Frontiers in Neuroendocrinology

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Considerable strides have been made over the past 20 years in our understanding of the ligands, receptor subtypes, signal transduction mechanisms and biological actions comprising the endocannabinoid system. From the ever-expanding number of studies that have been conducted during this time, it has become increasingly clear that sex differences are the cornerstone of cannabinoid-regulated biology. Available evidence has demonstrated that these sex differences endure in the absence of gonadal steroids, and are modulated by the acute, activational effects of these hormones. This review focuses on select aspects of sexually differentiated, cannabinoid-regulated biology, with a particular emphasis on the control of energy balance. It is anticipated that it will lend impactful insight into the pervasive and diverse disparities in how males and females respond to cannabinoids – from the organismal level down to the molecular level. Additionally, it will furnish a newfound appreciation for the need to recalibrate our thinking in terms of how cannabinoids are used as therapeutic adjuvants for a broad range of clinical disorders and associated comorbidities, including body wasting and obesity.

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Modulation by female sex hormones of the cannabinoid-induced catalepsy and analgesia in ovariectomized mice

Cited by 19 publications

References 58 publications

Gonadal hormone modulation of ∆9-tetrahydrocannabinol-induced antinociception and metabolism in female versus male rats

Gonadal hormone modulation of ∆9-tetrahydrocannabinol-induced antinociception and metabolism in female versus male rats

Gonadal hormones do not alter the development of antinociceptive tolerance to delta-9-tetrahydrocannabinol in adult rats

Sex differences in cannabinoid-regulated biology: A focus on energy homeostasis

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