http://www.cnr.it/ontology/cnr/individuo/prodotto/ID169087
Protective activation of the endocannabinoid system during ischemia in dopamine neurons. (Articolo in rivista)
- Type
- Label
- Protective activation of the endocannabinoid system during ischemia in dopamine neurons. (Articolo in rivista) (literal)
- Anno
- 2006-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.nbd.2006.04.010 (literal)
- Alternative label
Melis M., Pillolla G., Bisogno T., Minassi A., Petrosino S., Perra S., Muntoni A.L., Lutz B., Gessa G.L., Marsicano G., Di Marzo V., Pistis M. (2006)
Protective activation of the endocannabinoid system during ischemia in dopamine neurons.
in Neurobiology of disease
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Melis M., Pillolla G., Bisogno T., Minassi A., Petrosino S., Perra S., Muntoni A.L., Lutz B., Gessa G.L., Marsicano G., Di Marzo V., Pistis M. (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
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- ISI Web of Science (WOS) (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- (1) Centre of Excellence ''Neurobiology of Addiction'', University of Cagliari, Italy
(2) B.B. Brodie Department of Neuroscience, University of Cagliari, Monserrato, Italy
(3) CNR Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Pozzuoli (NA), Italy
(4) CNR Institute of Neuroscience-Cagliari, University of Cagliari, Monserrato, Italy
(5) Department of Physiological Chemistry, Johannes Gutenberg University, Mainz, Germany (literal)
- Titolo
- Protective activation of the endocannabinoid system during ischemia in dopamine neurons. (literal)
- Abstract
- Endocannabinoids act as neuroprotective molecules promptly released
in response to pathological stimuli. Hence, they may represent one
component of protection and/or repair mechanisms mobilized by
dopamine (DA) neurons under ischemia. Here, we show that the
endocannabinoid 2-arachidonoyl-glycerol (2-AG) plays a key role in
protecting DA neurons from ischemia-induced altered spontaneous
activity both in vitro and in vivo. Accordingly, neuroprotection can be
elicited through moderate cannabinoid receptor type-1 (CB1) activation.
Conversely, blockade of endocannabinoid actions through CB1
receptor antagonism worsens the outcome of transient ischemia on DA
neuronal activity. These findings indicate that 2-AG mediates neuroprotective
actions by delaying damage and/or restoring function of DA
cells through activation of presynaptic CB1 receptors. Lastly, they
point to CB1 receptors as valuable targets in protection of DA neurons
against ischemic injury and emphasize the need for a better
understanding of endocannabinoid actions in the fine control of DA
transmission. (literal)
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