Endocannabinoids and beta-amyloid-induced neurotoxicity in
vivo: effect of pharmacological elevation of endocannabinoid
levels

J 2006

Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels

STELT, Van der; M MAZZOLA; G ESPOSITO; I MATIAS; S PETROSINO et al.

Základní údaje

Originální název

Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels

Autoři

STELT, Van der; M MAZZOLA; G ESPOSITO; I MATIAS; S PETROSINO; D DE FILIPPIS; Vincenzo MICALE; L STEARDO; Filippo DRAGO; T IUVONE a V DI MARZO

Vydání

Cellular and molecular life sciences, BASEL, BIRKHAUSER VERLAG AG, 2006, 1420-682X

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30000 3. Medical and Health Sciences

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 4.655

Označené pro přenos do RIV

DOI

https://doi.org/10.1007/s00018-006-6037-3

UT WoS

000238531600006

Klíčová slova anglicky

anandamide; 2-arachidonoyl glycerol; cannabinoid; memory; receptor; neuroprotection; apoptosis

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 9. 8. 2012 08:13, Olga Křížová

Anotace

V originále

We investigated the involvement of endocannabinoids in the control of neuronal damage and memory retention loss in rodents treated with the beta-amyloid peptide (1-42) (BAP). Twelve days after stereotaxic injection of BAP into the rat cortex, and concomitant with the appearance in the hippocampus of markers of neuronal damage, 2-arachidonoyl glycerol, but not anandamide, levels were enhanced in the hippocampus. VDM-11 (5 mg/kg, i.p.), an inhibitor of endocannabinoid cellular reuptake, significantly enhanced rat hippocampal and mouse brain endocannabinoid levels when administered sub-chronically starting either 3 or 7 days after BAP injection and until the 12-14th day. VDM-11 concomitantly reversed hippocampal damage in rats, and loss of memory retention in the passive avoidance test in mice, but only when administered from the 3rd day after BAP injection. We suggest that early, as opposed to late, pharmacological enhancement of brain endocannabinoid levels might protect against beta-amyloid neurotoxicity and its consequences.

Citovat

STELT, Van der; M MAZZOLA; G ESPOSITO; I MATIAS; S PETROSINO; D DE FILIPPIS; Vincenzo MICALE; L STEARDO; Filippo DRAGO; T IUVONE a V DI MARZO. Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels. Cellular and molecular life sciences. BASEL: BIRKHAUSER VERLAG AG, 2006, roč. 63, č. 12, s. 1410-1424. ISSN 1420-682X. Dostupné z: https://doi.org/10.1007/s00018-006-6037-3.

@article{988773,
   author = {Stelt, Van der and Mazzola, M and Esposito, G and Matias, I and Petrosino, S and De Filippis, D and Micale, Vincenzo and Steardo, L and Drago, Filippo and Iuvone, T and Di Marzo, V},
   article_location = {BASEL},
   article_number = {12},
   doi = {https://doi.org/10.1007/s00018-006-6037-3},
   keywords = {anandamide; 2-arachidonoyl glycerol; cannabinoid; memory; receptor; neuroprotection; apoptosis},
   language = {eng},
   issn = {1420-682X},
   journal = {Cellular and molecular life sciences},
   title = {Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels},
   volume = {63},
   year = {2006}
}

TY  - JOUR
ID  - 988773
AU  - Stelt, Van der - Mazzola, M - Esposito, G - Matias, I - Petrosino, S - De Filippis, D - Micale, Vincenzo - Steardo, L - Drago, Filippo - Iuvone, T - Di Marzo, V
PY  - 2006
TI  - Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels
JF  - Cellular and molecular life sciences
VL  - 63
IS  - 12
SP  - 1410-1424
EP  - 1410-1424
PB  - BIRKHAUSER VERLAG AG
SN  - 1420682X
KW  - anandamide
KW  - 2-arachidonoyl glycerol
KW  - cannabinoid
KW  - memory
KW  - receptor
KW  - neuroprotection
KW  - apoptosis
N2  - We investigated the involvement of endocannabinoids in the control of neuronal damage and memory retention loss in rodents treated with the beta-amyloid peptide (1-42) (BAP). Twelve days after stereotaxic injection of BAP into the rat cortex, and concomitant with the appearance in the hippocampus of markers of neuronal damage, 2-arachidonoyl glycerol, but not anandamide, levels were enhanced in the hippocampus. VDM-11 (5 mg/kg, i.p.), an inhibitor of endocannabinoid cellular reuptake, significantly enhanced rat hippocampal and mouse brain endocannabinoid levels when administered sub-chronically starting either 3 or 7 days after BAP injection and until the 12-14th day. VDM-11 concomitantly reversed hippocampal damage in rats, and loss of memory retention in the passive avoidance test in mice, but only when administered from the 3rd day after BAP injection. We suggest that early, as opposed to late, pharmacological enhancement of brain endocannabinoid levels might protect against beta-amyloid neurotoxicity and its consequences.
ER  -

STELT, Van der; M MAZZOLA; G ESPOSITO; I MATIAS; S PETROSINO; D DE FILIPPIS; Vincenzo MICALE; L STEARDO; Filippo DRAGO; T IUVONE a V DI MARZO. Endocannabinoids and beta-amyloid-induced neurotoxicity in vivo: effect of pharmacological elevation of endocannabinoid levels. \textit{Cellular and molecular life sciences}. BASEL: BIRKHAUSER VERLAG AG, 2006, roč.~63, č.~12, s.~1410-1424. ISSN~1420-682X. Dostupné z: https://doi.org/10.1007/s00018-006-6037-3.

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