Effects of the nitric oxide donor molsidomine on different memory components as assessed in the object-recognition task in the rat

被引:38
作者
Pitsikas, N [1 ]
Rigamonti, AE [1 ]
Cella, SG [1 ]
Muller, EE [1 ]
机构
[1] Univ Milan, Dept Med Pharmacol, I-20129 Milan, Italy
关键词
nitric oxide; molsidomine; object recognition; acquisition; storage; retrieval; memory; rat;
D O I
10.1007/s00213-002-1090-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Rationale: Nitric oxide (NO) is sought to be a novel intracellular messenger in the central nervous system. Recently, NO involvement in learning and memory processes has been proposed. Compounds that inhibit NO synthase, the key synthesizing enzyme, may block cognition, while NO donors may facilitate it. Objectives: The present study was designed to further investigate in the rat the effects on distinct memory processes exerted by the NO donor molsidomine. For this aim, the object-recognition task was chosen. This test is based on the differential exploration of a new and familiar object. Methods: Object recognition was evaluated in a two-trial nonrewarded paradigm. In a first study, the influence of the retention time (the delay between the two trials) on the performance of 3-month-old male rats was assessed. Subsequently, the effects of molsidomine (2 mg/kg and 4 mg/kg), injected i.p., on acquisition, storage, and retrieval of information were evaluated. For the latter experiments, the delay condition at which recognition memory was extinguished in the normal rat was used (24 h). Results: Under our experimental conditions, object recognition was extinguished in the rat when an intertrial interval (ITI) of 24 h was utilized. Using this ITI, molsidomine at 4 mg/kg but not at 2 mg/kg improved the animal's performance in the object-recognition task, suggesting that molsidomine affected acquisition, storage, and retrieval of information. Conclusions: These results indicate that the NO donor molsidomine may modulate different aspects of memory.
引用
收藏
页码:239 / 245
页数:7
相关论文
共 51 条
[1]  
[Anonymous], [No title captured]
[2]  
[Anonymous], 1988, HDB PSYCHOPHARMACOLO
[3]   Nitric oxide acts directly in the presynaptic neuron to produce long-term potentiation in cultured hippocampal neurons [J].
Arancio, O ;
Kiebler, M ;
Lee, CJ ;
LevRam, V ;
Tsien, RY ;
Kandel, ER ;
Hawkins, RD .
CELL, 1996, 87 (06) :1025-1035
[4]   Aniracetam restores object recognition impaired by age, scopolamine, and nucleus basalis lesions [J].
Bartolini, L ;
Casamenti, F ;
Pepeu, G .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1996, 53 (02) :277-283
[5]   ROLE OF HIPPOCAMPAL NO IN THE ACQUISITION AND CONSOLIDATION OF INHIBITORY AVOIDANCE-LEARNING [J].
BERNABEU, R ;
DESTEIN, ML ;
FIN, C ;
IZQUIERDO, I ;
MEDINA, JH .
NEUROREPORT, 1995, 6 (11) :1498-1500
[6]   State-dependent impairment in object recognition after hippocampal NOS inhibition [J].
Blokland, A ;
Prickaerts, J ;
Honig, W ;
de Vente, J .
NEUROREPORT, 1998, 9 (18) :4205-4208
[7]   Local inhibition of hippocampal nitric oxide synthase does not impair place learning in the Morris water escape task in rats [J].
Blokland, A ;
de Vente, J ;
Prickaerts, J ;
Honig, W ;
Markerink-van Ittersum, M ;
Steinbusch, H .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1999, 11 (01) :223-232
[8]   LONG-TERM ADMINISTRATION OF L-ARGININE, L-NAME, AND THE EXOGENOUS NO DONOR MOLSIDOMINE MODULATES URINARY NITRATE AND CGMP EXCRETION IN RATS [J].
BOGER, RH ;
BODEBOGER, SM ;
GERECKE, U ;
FROLICH, JC .
CARDIOVASCULAR RESEARCH, 1994, 28 (04) :494-499
[9]   ALTERED SYNAPTIC PLASTICITY AND MEMORY FORMATION IN NITRIC-OXIDE SYNTHASE INHIBITOR-TREATED RATS [J].
BOHME, GA ;
BON, C ;
LEMAIRE, M ;
REIBAUD, M ;
PIOT, O ;
STUTZMANN, JM ;
DOBLE, A ;
BLANCHARD, JC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (19) :9191-9194
[10]   SPATIAL BUT NOT OBJECT RECOGNITION IS IMPAIRED BY AGING IN RATS [J].
CAVOY, A ;
DELACOUR, J .
PHYSIOLOGY & BEHAVIOR, 1993, 53 (03) :527-530