Abstract
Endocannabinoids act as retrograde messengers that, by inhibiting neurotransmitter release via presynaptic CB1 cannabinoid receptors, regulate the functionality of many synapses. In addition, the endocannabinoid system participates in the control of neuron survival. Thus, CB1 receptor activation has been shown to protect neurons from acute brain injury as well as in neuroinflammatory conditions and neurodegenerative diseases. Nonetheless, some studies have reported that cannabinoids can also exert neurotoxic actions. Cannabinoid neuroprotective activity relies on the inhibition of glutamatergic neurotransmission and on other various mechanisms, and is supported by the observation that the brain overproduces endocannabinoids upon damage. Coupling of neuronal CB1 receptors to cell survival routes such as the phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase pathways may contribute to cannabinoid neuroprotective action. These pro-survival signals occur, at least in part, by the cross-talk between CB1 receptors and growth factor tyrosine kinase receptors. Besides promoting neuroprotection, a role for the endocannabinoid system in the control of neurogenesis from neural progenitors has been put forward. In addition, activation of CB2 cannabinoid receptors on glial cells may also participate in neuroprotection by limiting the extent of neuroinflammation. Altogether, these findings support that endocannabinoids constitute a new family of lipid mediators that act as instructive signals in the control of neuron survival.
Keywords: Cannabinoid, endocannabinoid system, neuron, neuroprotection, neurodegeneration, neurogenesis, neuroinflammation
Current Pharmaceutical Design
Title: Mechanisms of Control of Neuron Survival by the Endocannabinoid System
Volume: 14 Issue: 23
Author(s): Ismael Galve-Roperh, Tania Aguado, Javier Palazuelos and Manuel Guzman
Affiliation:
Keywords: Cannabinoid, endocannabinoid system, neuron, neuroprotection, neurodegeneration, neurogenesis, neuroinflammation
Abstract: Endocannabinoids act as retrograde messengers that, by inhibiting neurotransmitter release via presynaptic CB1 cannabinoid receptors, regulate the functionality of many synapses. In addition, the endocannabinoid system participates in the control of neuron survival. Thus, CB1 receptor activation has been shown to protect neurons from acute brain injury as well as in neuroinflammatory conditions and neurodegenerative diseases. Nonetheless, some studies have reported that cannabinoids can also exert neurotoxic actions. Cannabinoid neuroprotective activity relies on the inhibition of glutamatergic neurotransmission and on other various mechanisms, and is supported by the observation that the brain overproduces endocannabinoids upon damage. Coupling of neuronal CB1 receptors to cell survival routes such as the phosphatidylinositol 3-kinase/Akt and extracellular signal-regulated kinase pathways may contribute to cannabinoid neuroprotective action. These pro-survival signals occur, at least in part, by the cross-talk between CB1 receptors and growth factor tyrosine kinase receptors. Besides promoting neuroprotection, a role for the endocannabinoid system in the control of neurogenesis from neural progenitors has been put forward. In addition, activation of CB2 cannabinoid receptors on glial cells may also participate in neuroprotection by limiting the extent of neuroinflammation. Altogether, these findings support that endocannabinoids constitute a new family of lipid mediators that act as instructive signals in the control of neuron survival.
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Cite this article as:
Galve-Roperh Ismael, Aguado Tania, Palazuelos Javier and Guzman Manuel, Mechanisms of Control of Neuron Survival by the Endocannabinoid System, Current Pharmaceutical Design 2008; 14 (23) . https://dx.doi.org/10.2174/138161208785740117
DOI https://dx.doi.org/10.2174/138161208785740117 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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