Obesity by cafeteria diet (highly palatable foods), is linked to behavioral disorders, such as, addiction-like deficits in the brain reward system and pain sensitivity.1–6 The wearing off of the hedonical rewarding properties of these foods may gradually lead negative reinforcement so that consumption becomes necessary to prevent or relieve negative states that would result from abstinence.7 Endocannabinoids play an important role in this scenario, also modulating opioid system. 8 In this study, we investigated whether the long-term exposure to a cafeteria diet could modify pain sensitivity, whether the pharmacological manipulation, by PF-3845, a FAAH inhibitor, can ameliorate this alteration and the mechanisms involved. Animals were subject to chow only (CO) or extended access (EA) with ad libitum access to cafeteria diet for 40 days and then EA rats were undergo an “abstinence” period of 28 days. Pain threshold was evaluated by hot plate and tail flick tests, at day 40, and at the end of the abstinence period (day 68). On day 40, EA showed a significant increase of threshold pain respect CO rats along with an upregulation of CB1 and MU receptors in brain. On day 68, no difference in pain sensitivity was found between groups. Finally, PF-3845 (10 mg/kg) induced a significant analgesic effect and up regulation of MU, but no CB1. In conclusion, long exposure to high-palatable food produces an increase of threshold of pain, due to up regulation of CB1 and MU receptor, and endocannabinoid manipulation during abstinence period through opioidergic system. Keywords: opioid, endocannabinoid, cafeteria diet; abstinence References: [1] Dong C. Int. J Obes Relat Metab Disord 2004, 28; 790–5. [2] Roberts RE Int. J Obes Relat Metab Disord 2003, 27; 514–21. [3] Simon GE Arch Gen Psychiatric 2006, 63; 824–30. [4] Iannitti T. Exp Physiol 2001, 97; 1236–45. [5] Davis JF Behav Neuroisci 2008, 122; 1257–63. [6] Geigev BM Neuroscience 2009, 159; 1193–9. [7] Parylak SL Physiol Behan. 2011, 25; 149–56. [8] Welch SP. Int Rev Psychiatry. 2009, 21;143–51.

Pain threshold evaluation after PF-3845, a FAAH inhibitor, administration in cafeteria-induced abstinence in rat: role of cannabinoid and opioid receptors

Cifani C;Micioni Di Bonaventura MV;
2018-01-01

Abstract

Obesity by cafeteria diet (highly palatable foods), is linked to behavioral disorders, such as, addiction-like deficits in the brain reward system and pain sensitivity.1–6 The wearing off of the hedonical rewarding properties of these foods may gradually lead negative reinforcement so that consumption becomes necessary to prevent or relieve negative states that would result from abstinence.7 Endocannabinoids play an important role in this scenario, also modulating opioid system. 8 In this study, we investigated whether the long-term exposure to a cafeteria diet could modify pain sensitivity, whether the pharmacological manipulation, by PF-3845, a FAAH inhibitor, can ameliorate this alteration and the mechanisms involved. Animals were subject to chow only (CO) or extended access (EA) with ad libitum access to cafeteria diet for 40 days and then EA rats were undergo an “abstinence” period of 28 days. Pain threshold was evaluated by hot plate and tail flick tests, at day 40, and at the end of the abstinence period (day 68). On day 40, EA showed a significant increase of threshold pain respect CO rats along with an upregulation of CB1 and MU receptors in brain. On day 68, no difference in pain sensitivity was found between groups. Finally, PF-3845 (10 mg/kg) induced a significant analgesic effect and up regulation of MU, but no CB1. In conclusion, long exposure to high-palatable food produces an increase of threshold of pain, due to up regulation of CB1 and MU receptor, and endocannabinoid manipulation during abstinence period through opioidergic system. Keywords: opioid, endocannabinoid, cafeteria diet; abstinence References: [1] Dong C. Int. J Obes Relat Metab Disord 2004, 28; 790–5. [2] Roberts RE Int. J Obes Relat Metab Disord 2003, 27; 514–21. [3] Simon GE Arch Gen Psychiatric 2006, 63; 824–30. [4] Iannitti T. Exp Physiol 2001, 97; 1236–45. [5] Davis JF Behav Neuroisci 2008, 122; 1257–63. [6] Geigev BM Neuroscience 2009, 159; 1193–9. [7] Parylak SL Physiol Behan. 2011, 25; 149–56. [8] Welch SP. Int Rev Psychiatry. 2009, 21;143–51.
2018
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11581/438951
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