Amnesia induced by beta-amyloid fragments is counteracted by
cannabinoid CB1 receptor blockade

J 2003

Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade

MAZZOLA, Carmen; Vincenzo MICALE a Filippo DRAGO

Základní údaje

Originální název

Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade

Autoři

MAZZOLA, Carmen; Vincenzo MICALE a Filippo DRAGO

Vydání

European Journal of Pharmacology, AMSTERDAM, Elsevier, 2003, 0014-2999

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30000 3. Medical and Health Sciences

Stát vydavatele

Nizozemské království

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 2.352

Označené pro přenos do RIV

DOI

https://doi.org/10.1016/j.ejphar.2003.08.026

UT WoS

000185806400004

Klíčová slova anglicky

amnesia; beta-amyloid fragment; cannabinoid CB1 receptor; cannabinoid; avoidance retention

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 9. 8. 2012 07:38, Olga Křížová

Anotace

V originále

Administration of drugs activating cannabinoid CB1 receptors in the brain induces memory deficit in rodents, and blockade of these receptors may restore memory capacity in these animals. Central administration of beta-amyloid or beta-amyloid fragments may also lead to memory disturbances. This study was undertaken to study the involvement of cannabinoid CB1 receptors in amnesia induced by beta-amyloid fragments in mice tested in a step-through passive avoidance paradigm. Pre-training intracerebroventricular (i.c.v.) injection of beta-amyloid fragments, beta-amyloid peptide-(25-35) (4, 8 or 16 nmol/mouse) or beta-amyloid peptide-(1-42) (200, 400, 800 pmol/mouse) 7 days prior to the learning trial reduced in a dose-dependent manner the retention of passive avoidance response. This effect was observed in two retention tests, 1 and 7 days after the learning trial. The two beta-amyloid fragments showed similar potency in reducing retention of passive avoidance behavior. This effect was counteracted by a single intraperitoneal (i.p.) injection of the cannabinoid CB1 receptor antagonist, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A, 1 mg/kg), made 30 min prior to the second retention test. The injection of SR141716A per se did not affect memory capacity of mice. The i.c.v. administration of beta-amyloid peptide-(25-35) (8 mol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) made 30 min prior to the learning trial failed to affect the retention capacity of mice as measured 1 and 7 days later. Also, the i.p. injection of SR 141716A (1 mg/kg) made 30 min prior to the learning trial did not influence the behavioral response of mice injected with beta-amyloid peptide-(25-35) (8 nmol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) 7 days prior to the learning trial. These results show that beta-amyloid fragments induce a dose-dependent memory deficit. Their effect on memory retention depends upon the time of administration and seems to involve cannabinoid CB1 receptors in the brain. (C) 2003 Elsevier B.V. All rights reserved.

Citovat

MAZZOLA, Carmen; Vincenzo MICALE a Filippo DRAGO. Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade. European Journal of Pharmacology. AMSTERDAM: Elsevier, 2003, roč. 477, č. 3, s. 219-225. ISSN 0014-2999. Dostupné z: https://doi.org/10.1016/j.ejphar.2003.08.026.

@article{988765,
   author = {Mazzola, Carmen and Micale, Vincenzo and Drago, Filippo},
   article_location = {AMSTERDAM},
   article_number = {3},
   doi = {https://doi.org/10.1016/j.ejphar.2003.08.026},
   keywords = {amnesia; beta-amyloid fragment; cannabinoid CB1 receptor; cannabinoid; avoidance retention},
   language = {eng},
   issn = {0014-2999},
   journal = {European Journal of Pharmacology},
   title = {Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade},
   volume = {477},
   year = {2003}
}

TY  - JOUR
ID  - 988765
AU  - Mazzola, Carmen - Micale, Vincenzo - Drago, Filippo
PY  - 2003
TI  - Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade
JF  - European Journal of Pharmacology
VL  - 477
IS  - 3
SP  - 219-225
EP  - 219-225
PB  - Elsevier
SN  - 00142999
KW  - amnesia
KW  - beta-amyloid fragment
KW  - cannabinoid CB1 receptor
KW  - cannabinoid
KW  - avoidance retention
N2  - Administration of drugs activating cannabinoid CB1 receptors in the brain induces memory deficit in rodents, and blockade of these receptors may restore memory capacity in these animals. Central administration of beta-amyloid or beta-amyloid fragments may also lead to memory disturbances. This study was undertaken to study the involvement of cannabinoid CB1 receptors in amnesia induced by beta-amyloid fragments in mice tested in a step-through passive avoidance paradigm. Pre-training intracerebroventricular (i.c.v.) injection of beta-amyloid fragments, beta-amyloid peptide-(25-35) (4, 8 or 16 nmol/mouse) or beta-amyloid peptide-(1-42) (200, 400, 800 pmol/mouse) 7 days prior to the learning trial reduced in a dose-dependent manner the retention of passive avoidance response. This effect was observed in two retention tests, 1 and 7 days after the learning trial. The two beta-amyloid fragments showed similar potency in reducing retention of passive avoidance behavior. This effect was counteracted by a single intraperitoneal (i.p.) injection of the cannabinoid CB1 receptor antagonist, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride (SR141716A, 1 mg/kg), made 30 min prior to the second retention test. The injection of SR141716A per se did not affect memory capacity of mice. The i.c.v. administration of beta-amyloid peptide-(25-35) (8 mol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) made 30 min prior to the learning trial failed to affect the retention capacity of mice as measured 1 and 7 days later. Also, the i.p. injection of SR 141716A (1 mg/kg) made 30 min prior to the learning trial did not influence the behavioral response of mice injected with beta-amyloid peptide-(25-35) (8 nmol/mouse) or of beta-amyloid peptide-(1-42) (400 pmol/mouse) 7 days prior to the learning trial. These results show that beta-amyloid fragments induce a dose-dependent memory deficit. Their effect on memory retention depends upon the time of administration and seems to involve cannabinoid CB1 receptors in the brain. (C) 2003 Elsevier B.V. All rights reserved.
ER  -

MAZZOLA, Carmen; Vincenzo MICALE a Filippo DRAGO. Amnesia induced by beta-amyloid fragments is counteracted by cannabinoid CB1 receptor blockade. \textit{European Journal of Pharmacology}. AMSTERDAM: Elsevier, 2003, roč.~477, č.~3, s.~219-225. ISSN~0014-2999. Dostupné z: https://doi.org/10.1016/j.ejphar.2003.08.026.

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