PMID- 29802570
OWN - NLM
STAT- MEDLINE
DCOM- 20190711
LR  - 20210109
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 56
IP  - 2
DP  - 2019 Feb
TI  - The Pharmacological Inhibition of Fatty Acid Amide Hydrolase Prevents Excitotoxic 
      Damage in the Rat Striatum: Possible Involvement of CB1 Receptors Regulation.
PG  - 844-856
LID - 10.1007/s12035-018-1129-2 [doi]
AB  - The endocannabinoid system (ECS) actively participates in several physiological 
      processes within the central nervous system. Among such, its involvement in the 
      downregulation of the N-methyl-D-aspartate receptor (NMDAr) through a modulatory 
      input at the cannabinoid receptors (CBr) has been established. After its 
      production via the kynurenine pathway (KP), quinolinic acid (QUIN) can act as an 
      excitotoxin through the selective overactivation of NMDAr, thus participating in 
      the onset and development of neurological disorders. In this work, we evaluated 
      whether the pharmacological inhibition of fatty acid amide hydrolase (FAAH) by 
      URB597, and the consequent increase in the endogenous levels of anandamide, can 
      prevent the excitotoxic damage induced by QUIN. URB597 (0.3 mg/kg/day x 7 days, 
      administered before, during and after the striatal lesion) exerted protective 
      effects on the QUIN-induced motor (asymmetric behavior) and biochemical (lipid 
      peroxidation and protein carbonylation) alterations in rats. URB597 also 
      preserved the structural integrity of the striatum and prevented the neuronal 
      loss (assessed as microtubule-associated protein-2 and glutamate decarboxylase 
      localization) induced by QUIN (1 muL intrastriatal, 240 nmol/muL), while modified 
      the early localization patterns of CBr1 (CB1) and NMDAr subunit 1 (NR1). 
      Altogether, these findings support the concept that the pharmacological 
      manipulation of the endocannabinoid system plays a neuroprotective role against 
      excitotoxic insults in the central nervous system.
FAU - Aguilera-Portillo, Gabriela
AU  - Aguilera-Portillo G
AD  - Laboratorio de Aminoacidos Excitadores, Instituto Nacional de Neurologia y 
      Neurocirugia Manuel Velasco Suarez, Insurgentes Sur 3877, 14269, Mexico, Mexico.
AD  - Posgrado en Biologia Experimental, DCBS, Universidad Autonoma 
      Metropolitana-Iztapalapa, 09310, Mexico, Mexico.
FAU - Rangel-Lopez, Edgar
AU  - Rangel-Lopez E
AD  - Laboratorio de Aminoacidos Excitadores, Instituto Nacional de Neurologia y 
      Neurocirugia Manuel Velasco Suarez, Insurgentes Sur 3877, 14269, Mexico, Mexico.
FAU - Villeda-Hernandez, Juana
AU  - Villeda-Hernandez J
AD  - Laboratorio de Patologia Experimental, Instituto Nacional de Neurologia y 
      Neurocirugia, 14269, Mexico, Mexico.
FAU - Chavarria, Anahi
AU  - Chavarria A
AD  - Unidad de Investigacion en Medicina Experimental, Facultad de Medicina, 
      Universidad Nacional Autonoma de Mexico, 04510, Mexico, Mexico.
FAU - Castellanos, Pilar
AU  - Castellanos P
AD  - Departamento de Ingenieria Electrica, Division de Ciencias Biologicas y de la 
      Salud, Universidad Autonoma Metropolitana-Iztapalapa, 09310, Mexico, Mexico.
FAU - Elmazoglu, Zubeyir
AU  - Elmazoglu Z
AD  - Cellular Stress Response and Signal Transduction Research Laboratory, Faculty of 
      Medicine, Department of Medical Pharmacology, Gazi University, Besevler, 06500, 
      Ankara, Turkey.
FAU - Karasu, Cimen
AU  - Karasu C
AD  - Cellular Stress Response and Signal Transduction Research Laboratory, Faculty of 
      Medicine, Department of Medical Pharmacology, Gazi University, Besevler, 06500, 
      Ankara, Turkey.
FAU - Tunez, Isaac
AU  - Tunez I
AD  - Instituto Maimonides de Investigacion Biomedica de Cordoba (IMIBIC) & Departmento 
      de Bioquimica y Biologia Molecular, Facultad de Medicina y Enfermeria, 
      Universidad de Cordoba, Cordoba, Spain.
FAU - Pedraza, Gibran
AU  - Pedraza G
AD  - Departamento de Ciencias de la Salud, Division de Ciencias Biologicas y de la 
      Salud, Universidad Autonoma Metropolitana-Iztapalapa, 09310, Mexico, Mexico.
FAU - Konigsberg, Mina
AU  - Konigsberg M
AD  - Departamento de Ciencias de la Salud, Division de Ciencias Biologicas y de la 
      Salud, Universidad Autonoma Metropolitana-Iztapalapa, 09310, Mexico, Mexico.
FAU - Santamaria, Abel
AU  - Santamaria A
AUID- ORCID: 0000-0002-9874-7182
AD  - Laboratorio de Aminoacidos Excitadores, Instituto Nacional de Neurologia y 
      Neurocirugia Manuel Velasco Suarez, Insurgentes Sur 3877, 14269, Mexico, Mexico. 
      absada@yahoo.com.
LA  - eng
GR  - 265991/CONACYT-TUBITAK/
GR  - CVU486539/CONACYT/
PT  - Journal Article
DEP - 20180525
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Arachidonic Acids)
RN  - 0 (Endocannabinoids)
RN  - 0 (Polyunsaturated Alkamides)
RN  - 0 (Receptor, Cannabinoid, CB1)
RN  - EC 3.5.- (Amidohydrolases)
RN  - EC 3.5.1.- (fatty-acid amide hydrolase)
RN  - F6F0HK1URN (Quinolinic Acid)
RN  - UR5G69TJKH (anandamide)
SB  - IM
MH  - Amidohydrolases/*drug effects
MH  - Animals
MH  - Arachidonic Acids/pharmacology
MH  - Corpus Striatum/*drug effects/injuries
MH  - Endocannabinoids/pharmacology
MH  - Lipid Peroxidation/drug effects
MH  - Male
MH  - Neostriatum/drug effects/metabolism
MH  - Polyunsaturated Alkamides/pharmacology
MH  - Quinolinic Acid/*pharmacology
MH  - Rats, Wistar
MH  - Receptor, Cannabinoid, CB1/*drug effects/metabolism
OTO - NOTNLM
OT  - Cannabinoid receptor agonists
OT  - Endocannabinoid system
OT  - Excitotoxicity
OT  - Fatty acid amide hydrolase
OT  - Neuroprotection
OT  - Oxidative stress
EDAT- 2018/05/29 06:00
MHDA- 2019/07/12 06:00
CRDT- 2018/05/27 06:00
PHST- 2018/03/06 00:00 [received]
PHST- 2018/05/14 00:00 [accepted]
PHST- 2018/05/29 06:00 [pubmed]
PHST- 2019/07/12 06:00 [medline]
PHST- 2018/05/27 06:00 [entrez]
AID - 10.1007/s12035-018-1129-2 [pii]
AID - 10.1007/s12035-018-1129-2 [doi]
PST - ppublish
SO  - Mol Neurobiol. 2019 Feb;56(2):844-856. doi: 10.1007/s12035-018-1129-2. Epub 2018 
      May 25.