An endogenous cannabinoid (2-AG) is neuroprotective after brain injury

By D. Panikashvili, C. Simeonidou, S. Ben-Shabat, L. Hanuš, A. Breuer, R. Mechoulam, E. Shohami. Nature, 2001

747 citations recorded by the source corpus.

Subfields: Pathology and Forensic Medicine, Pharmacology, Toxicology

View Paper: https://www.semanticscholar.org/paper/f05eb7b03dca6b73bd6a1730649b3c2c6548009d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Pathology and Forensic Medicine

1. V. Di Marzo

In Pharmacology

1. V. Di Marzo
2. K. Mackie
3. George Kunos
4. P. Pacher
5. S. Batkai
6. T. Klein
7. Tamás F. Freund
8. M. Guzmán

In Toxicology

1. Tamás F. Freund
2. I. Katona
3. George Kunos
4. V. Di Marzo

Citations in the corpus

• Nonpsychotropic Cannabinoid Receptors Regulate Microglial Cell Migration (2003, background): “In summary, 2-AG production is dramatically increased by three pathological stimuli that affect neurons, microglial cells, or astrocytes, a finding that corroborates the observed increase in this particular endocannabinoid during neuroinflammation induced in vivo (Baker et al., 2001; Panikashvili et”
• The endocannabinoid system and its therapeutic exploitation (2004, positive): “and that 2-AG is protective in a model of head traum”
• Cloning of the first sn1-DAG lipases points to the spatial and temporal regulation of endocannabinoid signaling in the brain (2003, background): “…context, there is a growing interest in 2-AG/CB1 signaling in terms of therapies for a range of conditions including neurodegenerative diseases (Di Marzo et al., 2000; Panikashvili et al., 2001), obesity (Di Marzo et al., 2001), and the extinction of aversive memories (Marsicano et al., 2002).”
• The endocannabinoid system controls key epileptogenic circuits in the hippocampus. (2006, neutral): “Given the central neuroprotective function of the endocannabinoid system in several models of neuronal insults (Panikashvili et al., 2001; van der Stelt et al., 2002; Lutz, 2004) and the proposed therapeutic exploitation of this system for the treatment of several diseases (Di Marzo et al., 2004;…”
• Endocannabinoid signaling as a synaptic circuit breaker in neurological disease (2008, background): “A large body of literature shows that various forms of neuronal insults (for example, closed-head injury or convulsants) induce the release of endocannabinoids, including 2-A”
• Prevention of Alzheimer's Disease Pathology by Cannabinoids: Neuroprotection Mediated by Blockade of Microglial Activation (2005, background): “, 1999), acute brain trauma (Panikashvili et al., 2001), and ouabain-induced excitotoxicity (van der Stelt et al.”
• The Endocannabinoid System as an Emerging Target of Pharmacotherapy (2006, background): “Finally, brain levels of endocannabinoids are increased during ischemic (Schmid et al., 1995; Schabitz et al., 2002; Berger et al., 2004; Muthian et al., 2004) and other types of brain injury (Sugiura et al., 2000; Hansen et al., 2001a,b; Panikashvili et al., 2001).”
• Cannabis and the brain. (2003, background): “The endocannabinoid 2-AG protected against damage elicited by closed head injury in mouse brain, and the protective effects were blocked by rimonabant (Panikashvili et al., 2001).”
• Cannabinoid-based drugs as anti-inflammatory therapeutics (2005, background): “For example, levels of endogenous 2-AG were found to be markedly increased in mice with closed head injury, and administration of 2-AG following injury reduced brain oedema (a consequence of inflammation) and led to a better clinical outcom”