Objective: Previous reports have shown that the Δ9-tetrahydrocannabinol (Δ9TCH), the major psychoactive cannabinoid components of marijuana, is unable to inhibit thyroid hormonal activity. The aim of this study was to characterize the CB1 functional expression in the rat thyroid by a multi-methods approach. Methods and Results: RT-PCR was used to detect the mRNA expression of the CB1 cannabinoid receptor (17.8 2±4.0% of the normalizing reference gene β2 microglobulin), as well as the expression of the endocannabinoid hydrolyzing enzyme, fatty acid amide hydrolase (46.9±4.3% of β2 microglobulin), in the rat thyroid gland. The CB1-encoded protein was detected in its glycosylated form (63 kDa) by Western blot, employing a polyclonal antibody, while CB1 immunohistochemical localization showed an intracellular positive staining in both follicular and parafollicular cells. In addition, a 30% decrease in serum levels of both 3,5,3′ tri-iodothyronine (T3) and thyroxine (T4) was detected 4 h after the administration of the synthetic cannabinoid receptor agonist, WIN 55,212-2 (10mg/kg i.p.). These effects were antagonized by pretreatment with the CB1 antagonist SR 141716A (3 mg/kg i.p.); thyrotrophin levels were unaffected by both treatments. Conclusion: These data indicate that functional CB1 receptors which are able to modulate the release of T3 and T4 are expressed in the rat thyroid, and suggest a possible role of cannabinoids in the regulation of rat thyroid hormonal activity.

Evidence for functional CB1 cannabinoid receptor expressed in the rat thyroid / Porcella, A.; Marchese, G.; Casu, M. A.; Rocchitta, A.; Lai, M. L.; Luigi, G.; Pani, L.. - In: EUROPEAN JOURNAL OF ENDOCRINOLOGY. - ISSN 0804-4643. - 147:2(2002), pp. 255-261. [10.1530/eje.0.1470255]

Evidence for functional CB1 cannabinoid receptor expressed in the rat thyroid

Pani L.
2002

Abstract

Objective: Previous reports have shown that the Δ9-tetrahydrocannabinol (Δ9TCH), the major psychoactive cannabinoid components of marijuana, is unable to inhibit thyroid hormonal activity. The aim of this study was to characterize the CB1 functional expression in the rat thyroid by a multi-methods approach. Methods and Results: RT-PCR was used to detect the mRNA expression of the CB1 cannabinoid receptor (17.8 2±4.0% of the normalizing reference gene β2 microglobulin), as well as the expression of the endocannabinoid hydrolyzing enzyme, fatty acid amide hydrolase (46.9±4.3% of β2 microglobulin), in the rat thyroid gland. The CB1-encoded protein was detected in its glycosylated form (63 kDa) by Western blot, employing a polyclonal antibody, while CB1 immunohistochemical localization showed an intracellular positive staining in both follicular and parafollicular cells. In addition, a 30% decrease in serum levels of both 3,5,3′ tri-iodothyronine (T3) and thyroxine (T4) was detected 4 h after the administration of the synthetic cannabinoid receptor agonist, WIN 55,212-2 (10mg/kg i.p.). These effects were antagonized by pretreatment with the CB1 antagonist SR 141716A (3 mg/kg i.p.); thyrotrophin levels were unaffected by both treatments. Conclusion: These data indicate that functional CB1 receptors which are able to modulate the release of T3 and T4 are expressed in the rat thyroid, and suggest a possible role of cannabinoids in the regulation of rat thyroid hormonal activity.
147
2
255
261
Evidence for functional CB1 cannabinoid receptor expressed in the rat thyroid / Porcella, A.; Marchese, G.; Casu, M. A.; Rocchitta, A.; Lai, M. L.; Luigi, G.; Pani, L.. - In: EUROPEAN JOURNAL OF ENDOCRINOLOGY. - ISSN 0804-4643. - 147:2(2002), pp. 255-261. [10.1530/eje.0.1470255]
Porcella, A.; Marchese, G.; Casu, M. A.; Rocchitta, A.; Lai, M. L.; Luigi, G.; Pani, L.
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

Caricamento pubblicazioni consigliate

Licenza Creative Commons
I metadati presenti in IRIS UNIMORE sono rilasciati con licenza Creative Commons CC0 1.0 Universal, mentre i file delle pubblicazioni sono rilasciati con licenza Attribuzione 4.0 Internazionale (CC BY 4.0), salvo diversa indicazione.
In caso di violazione di copyright, contattare Supporto Iris

Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11380/1212056
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 42
  • ???jsp.display-item.citation.isi??? 39
social impact