Cannabinoid Receptors: Which Cells, Where, How, and Why?

La, Matsuda; Ti, Bonner; Sj, Lolait

doi:10.1037/e496112006-007

Cited by 13 publications

(11 citation statements)

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“…It is known, however, that active compounds in phytocannabinoids, such as tetrahydrocannabinol (THC) and cannabidiol (CBD), bind to cannabinoid receptors (CB1 and CB2) in many human organs, including the testes (26, 27). Experimental animal studies have shown that by binding to CB1 and CB2 in Leydig cells and Sertoli cells of the testes, levels of testosterone, follicle-stimulating hormone and luteinizing hormone are affected, as is the survival of Sertoli cells (28–31).…”

Section: Discussionmentioning

confidence: 99%

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Callaghan

Allebeck

Akre

et al. 2017

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background Given current drug-policy reforms to decriminalize or legalize cannabis in numerous countries worldwide, it is critically important to understand the potential impacts of cannabis use on the development of cancer. The current study aims to assess the relation between cannabis use and the development of testicular cancer. Method The current study relied on a population-based sample (n = 49 343) of young men aged 18–21 years who underwent conscription assessment for Swedish military service in 1969–1970. The conscription process included a non-anonymous questionnaire eliciting information about drug use. Individual-level conscription information was linked to Swedish health and social registry data. Testicular cancers diagnosed between 1970 and 2011 were identified by ICD-7/8/9/10 testicular cancer codes in the Swedish National Patient Register, the Cancer Register, or the Cause of Death Register. Cox regression modeling was used to estimate the hazards associated with cannabis use and time to diagnosis of testicular cancer. Results No evidence was found of a significant relation between lifetime “ever” cannabis use and the subsequent development of testicular cancer [n = 45 250; 119 testicular cancer cases; adjusted hazard ratio (AHR) 1.42, 95% CI, 0.83, 2.45]. “Heavy” cannabis use (defined as usage of more than 50 times in lifetime, as measured at conscription) was associated with the incidence of testicular cancer (n = 45 250; 119 testicular cancer cases; AHR 2.57, 95% CI, 1.02, 6.50). Conclusion The current study provides additional evidence to the limited prior literature suggesting cannabis use may contribute to the development of testicular cancer.

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Section: Discussionmentioning

confidence: 99%

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Callaghan

Allebeck

Akre

et al. 2017

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…;18-20 Two cannabinoid receptors exist in humans, the brain-type receptors (CB1) and the spleen-type receptors (CB2) 21-23. These two major sub-types of cannabinoid receptors are part of the G-protein-coupled receptor family and influence a variety of biologic responses.…”

Section: Discussionmentioning

confidence: 99%

“…13,[18][19][20] Two cannabinoid receptor subtypes exist in humans: the brain-type receptors (CB1) and the spleen-type receptors (CB2). [21][22][23] These two subtypes are part of the G protein-coupled receptor family and influence a variety of biological responses. CB1 and CB2 are expressed in the testes and sperm as well as in the brain, heart, uterus, embryo, spleen, and immune cells.…”

Section: Discussionmentioning

confidence: 99%

Marijuana use and testicular germ cell tumors

Trabert

Sigurdson

Sweeney

et al. 2010

Cancer

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BACKGROUND: Since the early 1970s, the incidence of testicular germ cell tumors (TGCTs) in the United States has been increasing; however, potential environmental exposures accounting for this increase have not been identified. A previous study reported a significant association between frequent and long-term current marijuana users and TGCT risk. The purpose of this study was to evaluate the relation between marijuana use and TGCTs in a hospital-based case-control study. METHODS: TGCT patients diagnosed between January 1990 and October 1996 (n ¼ 187) and male friend controls (n ¼ 148) were enrolled in the study. All participants were between the ages of 18 and 50 at the time of diagnosis and resided in Texas, Louisiana, Arkansas, or Oklahoma. Associations of marijuana use and TGCTs were estimated using unconditional logistic regression, adjusting for age, race, prior cryptorchidism, cigarette smoking, and alcohol intake. RESULTS: Overall, patients with TGCTs were more likely to be frequent marijuana users (daily or greater) compared with controls (odds ratio [OR], 2.2; 95% confidence interval [CI], 1.0-5.1). Histological-specific analyses revealed that patients with nonseminoma were significantly more likely than controls to be frequent users (OR, 3.1; 95% CI, 1.2-8.2) and long-term (10 years) users (OR, 2.4; 95% CI, 1.0-6.1). CONCLUSIONS: The finding of an association between frequent marijuana use and TGCTs, particularly among men with nonseminoma, was consistent with the findings of a previous report. Additional studies of marijuana use and TGCTs are warranted, especially studies evaluating the role of endocannabinoid signaling and cannabinoid receptors in TGCTs. Cancer 2011;117:848-53.

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“…The effects of THC on motor activity are complex although it is believed that one mechanism of action may be a decrease in dopamine release in the dorsolateral striatum (Fernandez‐Ruiz and Gonzales 2005). The CB receptor family consists of CB 1 and CB 2 receptors which are members of the seven‐helix transmembrane, G‐protein‐linked‐receptor super family (Matsuda et al. 1992; Matsuda 1997).…”

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confidence: 99%

D₂ receptor‐mediated inhibition of dopamine release in the rat striatum in vitro is modulated by CB₁ receptors: studies using fast cyclic voltammetry

O’Neill

Evers-Donnelly

Nicholson

et al. 2009

Journal of Neurochemistry

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Cannabinoid CB1 receptors are highly expressed in the striatum where they are known to be co‐localized with dopamine D2 receptors. There is now strong evidence that cannabinoids modulate dopamine release in the brain. Using fast cyclic voltammetry, single pulse stimulation (0.1 ms; 10 V) was applied every 5 min and peak dopamine release was measured with a carbon fibre microelectrode. Application of the D2 receptor agonist, quinpirole, inhibited single pulse dopamine overflow in a concentration‐dependent manner (IC50: 3.25 × 10−8 M). The CB1 receptor agonist WIN55212‐2 (WIN; 1 μM) had no effect on single pulse dopamine release (93.9 ± 6.6% at 60 min, n = 5) but attenuated the inhibitory effect of quinpirole (30 nM; quinpirole 39.0 ± 4.2% vs. quinpirole + WIN, 48.2 ± 3.7%, n = 5, p < 0.05). This affect was antagonized by the CB1 receptor anatgonist [N‐(Piperidin‐1‐yl)‐5‐(4‐iodophenyl)‐1‐(2,4‐dichlorophenyl)‐4‐methyl‐1H‐pyrazole‐3‐carboxamide] (AM‐251, 1 μM). Dopamine release evoked by four pulses delivered at 1 Hz (4P1Hz) and 10 pulses delivered at 5 Hz (10P5Hz) was significantly inhibited by WIN [72.3 ± 7.9% control (peak 4 to 1 ratio measurement) and 66.9 ± 3.8% control (area under the curve measurement), respectively, p < 0.05; n = 6 for both]. Prior perfusion of WIN significantly attenuated the effects of quinpirole on multiple pulse‐evoked dopamine release (4P1Hz: quinpirole, 28.4 ± 4.8% vs. WIN + quinpirole, 52.3 ± 1.2%; 10P5Hz: quinpirole, 29.5 ± 1.3% vs. WIN + quinpirole, 59.4 ±7.1%; p < 0.05 for both; n = 6). These effects were also antagonized by AM‐251 (1 μM). This is the first report demonstrating a functional, antagonistic interaction between CB1 receptors and D2 autoreceptors in regulating rat striatal dopamine release.

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Cannabinoid Receptors: Which Cells, Where, How, and Why?

Cited by 13 publications

References 0 publications

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Marijuana use and testicular germ cell tumors

D₂ receptor‐mediated inhibition of dopamine release in the rat striatum in vitro is modulated by CB₁ receptors: studies using fast cyclic voltammetry

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Cannabinoid Receptors: Which Cells, Where, How, and Why?

Cited by 13 publications

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Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Cannabis Use and Incidence of Testicular Cancer: A 42-Year Follow-up of Swedish Men between 1970 and 2011

Marijuana use and testicular germ cell tumors

D2 receptor‐mediated inhibition of dopamine release in the rat striatum in vitro is modulated by CB1 receptors: studies using fast cyclic voltammetry

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D₂ receptor‐mediated inhibition of dopamine release in the rat striatum in vitro is modulated by CB₁ receptors: studies using fast cyclic voltammetry