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Caffeine promotes dopamine D1 receptor-mediated body temperature, heart rate and behavioural responses to MDMA (‘ecstasy’).

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Title: Caffeine promotes dopamine D1 receptor-mediated body temperature, heart rate and behavioural responses to MDMA (‘ecstasy’).
Authors: Vanattou-Saïfoudine, Natacha, McNamara, Ruth, Harkin, Andrew
Source: Psychopharmacology. Aug2010, Vol. 211 Issue 1, p15-25. 11p. 3 Graphs.
Subjects: Physiological effects of caffeine, Dopamine receptors, Body temperature, Locomotion, Laboratory rats, Heart rate monitoring, Ecstasy (Drug), Psychology, Physiology, Animal behavior
Abstract: Caffeine exacerbates the acute toxicity of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) in rats characterised by hyperthermia, tachycardia and lethality. Depletion of central catecholamine stores and dopamine D1 receptor blockade have been reported to attenuate the ability of caffeine to exacerbate MDMA-induced hyperthermia. Here, we investigate whether dopamine D1 and D2 receptors mediate the effects of caffeine on MDMA-induced changes in body temperature, heart rate and locomotor activity. All parameters were recorded continuously in individually housed rats using bioradiotelemetry from 1 h prior to 4 h following caffeine (10 mg/kg, s.c.) and/or MDMA (10 mg/kg, s.c.) administration. Co-administration of caffeine with MDMA provoked a switch from MDMA-induced hypothermia and bradycardia to hyperthermia and tachycardia without influencing MDMA-induced hyperlocomotion. Pre-treatment with a specific dopamine D1/5 antagonist SCH 23390 (1 mg/kg) enhanced MDMA-induced hypothermia and blocked the ability of caffeine to provoke a switch from MDMA-induced hypothermia to hyperthermia. Furthermore, SCH 23390 blocked MDMA-induced hyperactivity and the ability of caffeine to promote a tachycardic response to MDMA. By contrast, pre-treatment with the selective D2 antagonist, sulpiride (100 mg/kg) blocked MDMA-induced hypothermia, failed to influence the ability of caffeine to promote tachycardia whilst enhancing MDMA-induced hyperactivity. Our results highlight the importance of dopamine D1 and D2 receptors in shaping the behavioural and physiological response to MDMA and suggest that the ability of caffeine to provoke MDMA-induced toxicity is associated with the promotion of dopamine D1 over D2 receptor-related responses. [ABSTRACT FROM AUTHOR]
Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Caffeine exacerbates the acute toxicity of 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) in rats characterised by hyperthermia, tachycardia and lethality. Depletion of central catecholamine stores and dopamine D1 receptor blockade have been reported to attenuate the ability of caffeine to exacerbate MDMA-induced hyperthermia. Here, we investigate whether dopamine D1 and D2 receptors mediate the effects of caffeine on MDMA-induced changes in body temperature, heart rate and locomotor activity. All parameters were recorded continuously in individually housed rats using bioradiotelemetry from 1 h prior to 4 h following caffeine (10 mg/kg, s.c.) and/or MDMA (10 mg/kg, s.c.) administration. Co-administration of caffeine with MDMA provoked a switch from MDMA-induced hypothermia and bradycardia to hyperthermia and tachycardia without influencing MDMA-induced hyperlocomotion. Pre-treatment with a specific dopamine D1/5 antagonist SCH 23390 (1 mg/kg) enhanced MDMA-induced hypothermia and blocked the ability of caffeine to provoke a switch from MDMA-induced hypothermia to hyperthermia. Furthermore, SCH 23390 blocked MDMA-induced hyperactivity and the ability of caffeine to promote a tachycardic response to MDMA. By contrast, pre-treatment with the selective D2 antagonist, sulpiride (100 mg/kg) blocked MDMA-induced hypothermia, failed to influence the ability of caffeine to promote tachycardia whilst enhancing MDMA-induced hyperactivity. Our results highlight the importance of dopamine D1 and D2 receptors in shaping the behavioural and physiological response to MDMA and suggest that the ability of caffeine to provoke MDMA-induced toxicity is associated with the promotion of dopamine D1 over D2 receptor-related responses. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Psychopharmacology is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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      – TitleFull: Caffeine promotes dopamine D1 receptor-mediated body temperature, heart rate and behavioural responses to MDMA (‘ecstasy’).
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