Palmitoylethanolamide Inhibits Glutamate Release in Rat Cerebrocortical Nerve Terminals

Lin, Tzu-Yu; Lu, Cheng Wei; Wu, Chia Chan; Huang, Shu Kuei; Wang, Su‐Jane

doi:10.3390/ijms16035555

Cited by 20 publications

(13 citation statements)

References 49 publications

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“…Accordingly, several studies suggested a key role for CB 1 receptors activation in cannabinoid neuroprotection. In agreement, CB 1 R-knockout mice have been reported to be more sensitive to inflammatory and excitotoxic insults than control animals (Pryce et al, 2003) and activation of CB 1 receptors elicits inhibitory effects by reducing glutamate release (Howlett et al, 2004;Lin et al, 2015). Interestingly, Gobira et al (2015) suggested that cannabidiol, a non-psychotomimetic constituent of Cannabis sativa, shows neuroprotection reducing glutamate release through activation of mTOR pathway.…”

Section: Cannabinoidsmentioning

confidence: 79%

“…(Tomida et al, 2004;Yazulla, 2008). Interestingly, some studies suggested that inhibition of glutamate release represents a key mechanism involved in neuroprotection mediated by the cannabinoid system (Braida et al, 2000;Sinor et al, 2000;Marsicano et al, 2003;Gobira et al, 2015;Lin et al, 2015). In 2007, our group using an animal model of acute glaucoma reported that inhibition of fatty acid amide hydrolase (FAAH) or administration of metanandamide, a stable analogue of anandamide, minimize RGC loss caused by ischemia/reperfusion and that MK801, a noncompetitive NMDA receptors antagonist, controls anandamide degradation through FAAH (Nucci et al, 2007b).…”

Section: Cannabinoidsmentioning

confidence: 99%

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New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

Nucci

Russo

Martucci

et al. 2016

European Journal of Pharmacology

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a b s t r a c tGlaucoma is a disease where retinal ganglion cells (RGC) are specifically affected though a number of evidences endorse the hypothesis that glaucoma is a neuro-degenerative disorder of the central nervous system and suggest a possible connection between glaucomatous damage and cerebrovascular alterations. The mechanisms underlying RGC loss are not yet fully known but alterations of the autophagy machinery have been recently proposed as a potential contributing factor as for Alzheimer's disease.Here we review the current literature on new strategies for neuroprotection in glaucoma, focusing on pharmacologic strategies to minimize RGC damage.

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Section: Cannabinoidsmentioning

confidence: 79%

Section: Cannabinoidsmentioning

confidence: 99%

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

Nucci

Russo

Martucci

et al. 2016

European Journal of Pharmacology

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“…Moreover, PEA is an endogenous molecule in humans and many other living organisms that can play a very important role in maintaining cellular homeostasis and in counteracting exogenous stressful events that can lead to an inflammatory reaction. Among the pharmacological strategies for sensory and affective/cognitive disorders associated with neuropathic pain, PEA showed anti-inflammatory, analgesic, immunomodulatory and neuroprotective effects as well [ 3 , 4 , 5 ] by restoring glutamatergic transmission homeostasis [ 3 , 4 , 5 , 6 , 7 , 8 , 9 ]. For example, PEA demonstrates a neuroprotective action in experimental models of neuroinflammation and neuropathic pain mediated by mast cells and in experimental models of stroke, spinal injury, traumatic brain injury and Parkinson’s disease.…”

Section: Introductionmentioning

confidence: 99%

A New Palmitoylethanolamide Form Combined with Antioxidant Molecules to Improve Its Effectivess on Neuronal Aging

et al. 2020

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Palmitoylethanolamide is a nutraceutical compound naturally produced in many plants and animal source foods, but the natural form is poorly water-soluble. It has demonstrated an anti-inflammatory role as a neuroprotective mediator, acting on several molecular targets of the central nervous system involved on brain aging process. In healthy adults, palmitoylethanolamide is an endogenous PPAR-α (peroxisome proliferator-activated receptor α) agonist through which it performs anti-inflammatory activity and provides its effects by activating the cannabinoid receptor. The different formulations of palmitoylethanolamide (micronized palmitoylethanolamide, FM-LipoMatrix® palmitoylethanolamide and FM-LipoMatrix® palmitoylethanolamide plus lipoic acid and vitamin D3) were analyzed starting from intestinal barrier, to verify their bioavailability, to in primary astrocytes in which cell viability, reactive oxygen species (ROS) and nitric oxide (NO) production, NFKB activity, MAPK, p53 and PPARα activities were investigated. Additionally, cannabinoid and estrogen receptors were analyzed using the western blot technique. The combination of palmitoylethanolamide in FM-LipoMatrix®, lipoic acid and vitamin D3 shows better absorption predicting an improvement on plasma concentration; this formulation also shows a reduction in ROS and NO production and the data show the interaction of palmitoylethanolamide with cannabinoids and estrogen receptors inhibiting neuroinflammatory markers. All these data support the hypothesis of a new potential strategy to restore brain function and slow down brain aging in humans.

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“…26 Moreover, PEA has been reported to inhibit glutamate release in rat cerebrocortical nerve terminals. 27 Previously, we compared alterations of circulating levels of eCBs and NAEs 28,29 and glutamate 30 in subjects with chronic widespread pain and healthy controls (HC); however, no clear biological roles of this alteration were determined. Here, we investigate the effect of a 30-min dynamic load arm cycling intervention with respect to circulating levels of eCBs, NAEs and glutamate in subjects with chronic neck and shoulder pain (CNSP) and in HC.…”

Section: Introductionmentioning

confidence: 99%

Altered relationship between anandamide and glutamate in circulation after 30 min of arm cycling: A comparison of chronic pain subject with healthy controls

Stensson

Grimby-Ekman²

2019

Mol Pain

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The insufficient knowledge of biochemical mechanisms behind the emergence and maintenance of chronic musculoskeletal pain conditions constrains the development of diagnostic and therapeutic tools for clinical use. However, physical activity and exercise may improve pain severity and physical function during chronic pain conditions. Nevertheless, the biochemical consequences of physical activity and exercise in chronic pain need to be elucidated to increase the precision of this therapeutic tool in chronic pain treatment. The endocannabinoid system has been suggested to play an important role in exercise-induced reward and pain inhibition. Moreover, glutamatergic signalling has been suggested as an important factor for sensation and transmission of pain. In addition, a link has been established between the endocannabinoid system and glutamatergic pathways. This study examines the effect of dynamic load arm cycling (30 min) on levels of lipid mediators related to the endocannabinoid system and glutamate in plasma of chronic pain subjects and pain-free controls. Pain assessments and plasma levels of arachidonoylethanolamide (anandamide), 2-aracidonoylglycerol, oleoylethanolamide, palmitoylethanolamide, stearoylethanolamide and glutamate from 21 subjects with chronic neck pain (chronic pain group) and 11 healthy controls were analysed pre and post intervention of dynamic load arm cycling. Pain intensity was significantly different between groups pre and post exercise. Post exercise, anandamide levels were significantly decreased in health controls but not in the chronic pain group. A strong positive correlation existed between anandamide and glutamate in the control group post exercise but not in the chronic pain group. Moreover, the glutamate/anandamide ratio increased significantly in the control group and differed significantly with the chronic pain group post exercise. The altered relationship between anandamide and glutamate after the intervention in the chronic pain group might reflect alterations in the endocannabinoid-glutamate mechanistic links in the chronic pain group compared to the painfree control group.

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Palmitoylethanolamide Inhibits Glutamate Release in Rat Cerebrocortical Nerve Terminals

Cited by 20 publications

References 49 publications

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

New strategies for neuroprotection in glaucoma, a disease that affects the central nervous system

A New Palmitoylethanolamide Form Combined with Antioxidant Molecules to Improve Its Effectivess on Neuronal Aging

Altered relationship between anandamide and glutamate in circulation after 30 min of arm cycling: A comparison of chronic pain subject with healthy controls

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