2. Academic Validation
  3. The CB1 Receptor as the Cornerstone of Exostasis

The CB1 Receptor as the Cornerstone of Exostasis

  • Neuron. 2017 Mar 22;93(6):1252-1274. doi: 10.1016/j.neuron.2017.02.002.
Pier Vincenzo Piazza 1,  Daniela Cota 2,  Giovanni Marsicano 3
Affiliations

Affiliations

  • 1 INSERM, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France; University of Bordeaux, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France. Electronic address: [email protected].
  • 2 INSERM, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France; University of Bordeaux, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France.
  • 3 INSERM, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France; University of Bordeaux, NeuroCentre Magendie, Physiopathologie de la Plasticité Neuronale, U1215, F-33077 Bordeaux, France. Electronic address: [email protected].
PMID: 28334603 DOI: 10.1016/j.neuron.2017.02.002
Abstract

The type-1 Cannabinoid Receptor (CB1) is the main effector of the endocannabinoid system (ECS), which is involved in most brain and body functions. In this Perspective, we provide evidence indicating that CB1 receptor functions are key determinants of bodily coordinated exostatic processes. First, we will introduce the concepts of endostasis and exostasis as compensation or accumulation for immediate or future energy needs and discuss how exostasis has been necessary for the survival of species during evolution. Then, we will argue how different specific biological functions of the CB1 receptor in the body converge to provide physiological exostatic processes. Finally, we will introduce the concept of proactive evolution-induced diseases (PEIDs), which helps explain the seeming paradox that an evolutionary-selected physiological function can become the cause of epidemic pathological conditions, such as obesity. We propose here a possible unifying theory of CB1 receptor functions that can be tested by future experimental studies.

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