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01 August 2005

Endocannabinoid Signaling in Stress, Medicine and Wellness

Tobias Esch

Med Sci Monit 2005; 11(8): ED3-5 :: ID: 199607

Abstract

Based on self-care and stress research, it is reasonable to propose thatour bodies contain naturally occurring properties, that is, tools that serve to maintain our health andintegrity for a passable period of time, even in times of stress: These processes, including endocannabinoidautoregulation, might in part determine our well-being and life span. Such properties would also manifestthemselves during times of stress, i.e, stress reduction. Stress potentially triggers endocannabinoidand NO synthesis and release. In fact, endocannabinoids exert stress-reducing functions by their potentialto modulate norepinephrine release, e.g., via constitutive NO activation, therefore suggesting a sympatho-inhibitorymechanism that effectively diminishes sympathetic tone. This stress-reducing and health-promoting potentialcan be detected not only in central but also peripheral pathways, again indicating general or systemicdown-regulation. In this process, signaling molecules such as the endocannabinoids may play a role inconnecting mind and body phenomena, and one could speculate that such evolutionarily old autoregulatorypathways, by using endocannabinoids as one type of their molecular messengers and constitutive NO asa possible converging point, are involved in natural or innate health promotion, including wellness,reward and pleasure. Consequently, endocannabinoid research has now become a focus not only of neurobiologicalbut also medical science: With this interdisciplinary approach, we will gather new insight on these fascinatingmolecules and their healing properties in the coming years ahead.

Keywords: Animals, Endocannabinoids - metabolism, Health, Medicine, Signal Transduction, Stress - metabolism, Animals, Cannabinoid Receptor Modulators - metabolism, Endocannabinoids, Health, Medicine, Signal Transduction, Stress, Physiological - metabolism

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Medical Science Monitor eISSN: 1643-3750
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