Protracted cannabinoid administration elicits antidepressant behavioral responses in rats: Role of gender and noradrenergic transmission

Morrish, Anna C.; Hill, Matthew N.; Riebe, Caitlin; Gorzalka, Boris B.

doi:10.1016/j.physbeh.2009.04.023

Cited by 48 publications

(32 citation statements)

References 30 publications

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“…In addition to the already mentioned possibility that CB 1 receptors participate in these effects via the modulation of fluoxetine-induced adaptations in cAMP cascade, recent data also suggest that up-regulated CB 1 receptor signaling in the PFC could also elicit antidepressant effects by enhancing the activity of 5-HT neurons in the DRN (Gobbi et al, 2005;Bambico et al, 2007). Consistent with the idea that enhanced signaling through CB 1 receptors may result in antidepressant effects, CB 1 receptor knockout mice exhibit enhanced depressive-like behaviors Mato et al, 2007), and low doses of cannabinoid agonists (Bambico et al, 2007;McLaughlin et al, 2007;Morrish et al, 2009) or inhibitors of EC degradation (Gobbi et al, 2005;Bortolato et al, 2007) produce antidepressant-like effects in rodents. Nevertheless, it should be noted that CB 1 receptor antagonists also behave as antidepressants in behavioral models (Griebel et al, 2005;Witkin et al, 2005;Steiner et al, 2008).…”

Section: Discussionmentioning

confidence: 72%

“…CB 1 receptor knockout mice exhibit enhanced "depressive-like" behaviors in animal models Mato et al, 2007). Pharmacological modulation of CB 1 receptors has led to more conflicting results, because both CB 1 receptor activation and blockade induce antidepressant-like responses in the same tasks (Griebel et al, 2005;Hill and Gorzalka, 2005;Witkin et al, 2005;Bambico et al, 2007;McLaughlin et al, 2007;Steiner et al, 2008;Morrish et al, 2009). These evidences strongly support the involvement of the brain endocannabinoid (EC) system in the modulation of mood, suggesting that CB 1 receptors could play a role in the cause of major depression (Vinod and Hungund, 2006).…”

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confidence: 99%

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Long-Term Fluoxetine Treatment Modulates Cannabinoid Type 1 Receptor-Mediated Inhibition of Adenylyl Cyclase in the Rat Prefrontal Cortex through 5-Hydroxytryptamine1A Receptor-Dependent Mechanisms

Mato

Vidal²,

Castro³

et al. 2010

Molecular Pharmacology

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Increasing data indicate that brain endocannabinoid system plays a role in the effects of antidepressant medications. Here we examined the effect of in vivo exposure to the selective serotonin uptake inhibitor fluoxetine on cannabinoid type 1 (CB 1 ) receptor density and functionality in the rat prefrontal cortex (PFC) and cerebellum. Long-term treatment with fluoxetine (10 mg/kg/day) enhanced CB 1 receptor inhibition of adenylyl cyclase (AC) in the PFC and reduced it in the cerebellum without altering receptor density and agonist stimulation of guanosine 5Ј-O-(3-[ oxetine-induced modulation of CB 1 receptor coupling to G␣ subunits and AC in the PFC but not in the cerebellum. These results indicate that increased CB 1 receptor signaling at the G␣ i -AC transduction level is a long-term adaptation induced by fluoxetine in the PFC and point to a role for 5-HT 1A receptors in this effect. Basal AC activity, protein kinase A (PKA) catalytic subunit expression, and phospho-cAMP response element-binding protein (pCREB)/CREB ratio were also up-regulated in the PFC of fluoxetine-treated animals, whereas no differences were detected in the cerebellum. It is interesting that long-term ⌬ 9 -tetrahydrocannabinol treatment did not elicit antidepressant-like effects or modulated behavioral responses of fluoxetine in an animal model of depression (olfactory bulbectomy). These data suggest that altered signal transduction through CB 1 receptors in the PFC may participate in the regulation of the AC-PKA-CREB cascade induced by fluoxetine in this brain area.

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Section: Discussionmentioning

confidence: 72%

mentioning

confidence: 99%

Long-Term Fluoxetine Treatment Modulates Cannabinoid Type 1 Receptor-Mediated Inhibition of Adenylyl Cyclase in the Rat Prefrontal Cortex through 5-Hydroxytryptamine1A Receptor-Dependent Mechanisms

Mato

Vidal²,

Castro³

et al. 2010

Molecular Pharmacology

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“…Preclinical studies have indicated that adolescent THC exposure elevates depressive-like behavior in adulthood in female rats [61, 164] but not male rats [61]. Cannabinoid exposure in males, in contrast, has been shown to decrease depressive-like behavior [149, 165]. Conflicting evidence does exist, however, as elevated depressive symptoms in both sexes [41], or no effects in males [69], have been reported.…”

Section: Sex Differences In Cannabis Use Comorbidity With Psychiatricmentioning

confidence: 99%

Mechanisms Underlying Sex Differences in Cannabis Use

et al. 2017

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Purpose of the Review Cannabis is the most commonly used illicit substance worldwide. In recent decades, highly concentrated products have flooded the market, and prevalence rates have increased. Gender differences exist in cannabis use, as men have higher prevalence of both cannabis use and cannabis use disorder (CUD), while women progress more rapidly from first use to CUD. This paper reviews findings from preclinical and human studies examining the sex-specific neurobiological underpinnings of cannabis use and CUD, and associations with psychiatric symptoms. Recent Findings Sex differences exist in the endocannabinoid system, in cannabis exposure effects on brain structure and function, and in the co-occurrence of cannabis use with symptoms of anxiety, depression and schizophrenia. In female cannabis users, anxiety symptoms correlate with larger amygdala volume and social anxiety disorder symptoms correlate with CUD symptoms. Female cannabis users are reported to be especially vulnerable to earlier onset of schizophrenia, and mixed trends emerge in the correlation of depressive symptoms with cannabis exposure in females and males. Summary As prevalence of cannabis use may continue to increase given the shifting policy landscape regarding marijuana laws, understanding the neurobiological mechanisms of cannabis exposure in females and males is key. Examining these mechanisms may help inform future research on sex-specific pharmacological and behavioral interventions for women and men with high-risk cannabis use, comorbid psychiatric disease, and CUD.

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“…5.1) to endocannabinoid enhancers have been evaluated in several in vitro and in vivo studies to assess their therapeutic potential in stress-related neuropsychiatric disorders [23] (Table 5.4). Based on the hypothesis that a reduction of endocannabinoid signaling could underlie depressive disorders, it has been seen that acute or repeated treatment with different compounds which activate directly cannabinoid receptors, such as the main pharmacologically active principle of Cannabis sativa ∆9-THC [98,[127][128][129][130], the endogenous cannabinoid AEA [131,132], the synthetic nonspecific CB1/CB2 receptor agonists CP55,940 [133], WIN55,212-2 [134,135] and HU-210 [136][137][138][139] or the selective CB1 receptor agonist arachidonoyl 2'-chloroethylamide (ACEA) [140,141] elicited antidepressant-like effects through CB1 and 5-HTergic or NEergic receptor-mediated mechanisms.…”

Section: Effects Of Pharmacological Manipulation Of the Endocannabinomentioning

confidence: 99%

Role of the Endocannabinoid System in Depression: from Preclinical to Clinical Evidence

Micale

Tabiová

Kučerová

et al. 2015

Cannabinoid Modulation of Emotion, Memory, and Motivation

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The endogenous cannabinoid system (ECS) works as pro-homeostatic and pleiotropic signaling system activated in a time-and tissue-specific way during physiological conditions, which include cognitive, emotional and motivational processes. It is composed of two G protein-coupled receptors (the cannabinoid receptors types 1 and 2 [CB1 and CB2] for marijuana's psychoactive ingredient Δ9-tetrahydrocannabinol [Δ9-THC]), their endogenous small lipid ligands (anandamide [AEA] and 2-arachidonoylglycerol [2-AG], also known as endocannabinoids), and the proteins for endocannabinoid biosynthesis and deactivation. Data from preclinical and clinical studies have reported that a hypofunction of the endocannabinoid signaling could induce a depressive-like phenotype; consequently, enhancement of endocannabinoid signaling could be a novel therapeutic avenue for the treatment of depression. To this aim there have been proposed cannabinoid receptor agonists or synthetic molecules that inhibit endocannabinoid degradation. The latter ones do not induce the psychotropic side effects by direct CB1 receptor activation, but rather elicit antidepressant-like effects by enhancing the monoaminergic neurotransmission, promoting hippocampal neurogenesis and normalizing the hyperactivity of hypothalamic-pituitary-adrenal axis, similarly as the standard antidepressants. The dysfunction of elements belonging to the ECS and the possible therapeutic use of endocannabinoid deactivation inhibitors and phytocannabinoids in depression is discussed in this chapter.

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Protracted cannabinoid administration elicits antidepressant behavioral responses in rats: Role of gender and noradrenergic transmission

Cited by 48 publications

References 30 publications

Long-Term Fluoxetine Treatment Modulates Cannabinoid Type 1 Receptor-Mediated Inhibition of Adenylyl Cyclase in the Rat Prefrontal Cortex through 5-Hydroxytryptamine1A Receptor-Dependent Mechanisms

Long-Term Fluoxetine Treatment Modulates Cannabinoid Type 1 Receptor-Mediated Inhibition of Adenylyl Cyclase in the Rat Prefrontal Cortex through 5-Hydroxytryptamine1A Receptor-Dependent Mechanisms

Mechanisms Underlying Sex Differences in Cannabis Use

Role of the Endocannabinoid System in Depression: from Preclinical to Clinical Evidence

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