Selective lesions of the entorhinal cortex, the hippocampus, or the fimbria-fornix in rats: a comparison of effects on spontaneous and amphetamine-induced locomotion

被引:42
作者
Coutureau, E [1 ]
Galani, R [1 ]
Jarrard, LE [1 ]
Cassel, JC [1 ]
机构
[1] Univ Strasbourg, CNRS, UMR 7521, Lab Neurosci Comportementales & Cognit, F-67000 Strasbourg, France
关键词
activity; amphetamine; entorhinal cortex; fimbria-fornix; hippocampus; ibotenic acid; locomotion; NMDA;
D O I
10.1007/s002219900301
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Using adult Long-Evans male rats, this experiment compared spontaneous (assessed 15 days and 4.5 months after surgery) and amphetamine-induced (assessed from 4.5 months after surgery onwards; 1 mg/kg, i.p., ten injections, 48 h apart) locomotor activity following N-methyl-D-aspartate lesions of the entorhinal cortex, electrolytic lesions of the fimbria-fornix, or ibotenate lesions of the hippocampus. Sham-operated rats were used as controls. Hippocampal and fimbria-fornix lesions, but not entorhinal-cortex lesions induced diurnal and nocturnal hyperactivity, which was attenuated over time, but only in rats with fimbria-fornix lesions. Amphetamine-induced hyperlocomotion was assessed in a familiar environment. Lesions of the entorhinal cortex potentiated the locomotor effects of amphetamine, but not lesions of the hippocampus or interruption of the axons in the fimbria-fornix pathway. Sensitization appeared to be decreased by fimbria-fornix lesions and to be prevented by hippocampal lesions. Rats with entorhinal-cortex lesions behaved as if they had already been sensitized by the lesion. These results clearly show that lesions of the fimbria-fornix, the hippocampus, and of the entorhinal cortex have different effects on spontaneous and amphetamine-induced hyperactivity, as they also have on learning and memory tasks. (C) Springer-Verlag 2000.
引用
收藏
页码:381 / 392
页数:12
相关论文
共 58 条
[1]   SOCIAL DEPRIVATION ENHANCES THE VULNERABILITY OF MALE WISTAR RATS TO STRESSOR AND AMPHETAMINE-INDUCED BEHAVIORAL SENSITIZATION [J].
AHMED, SH ;
STINUS, L ;
LEMOAL, M ;
CADOR, M .
PSYCHOPHARMACOLOGY, 1995, 117 (01) :116-124
[2]   INFLUENCE OF NOVEL VERSUS HOME ENVIRONMENTS ON SENSITIZATION TO THE PSYCHOMOTOR STIMULANT EFFECTS OF COCAINE AND AMPHETAMINE [J].
BADIANI, A ;
BROWMAN, KE ;
ROBINSON, TE .
BRAIN RESEARCH, 1995, 674 (02) :291-298
[3]   THE DEVELOPMENT OF SENSITIZATION TO THE PSYCHOMOTOR STIMULANT EFFECTS OF AMPHETAMINE IS ENHANCED IN A NOVEL ENVIRONMENT [J].
BADIANI, A ;
ANAGNOSTARAS, SG ;
ROBINSON, TE .
PSYCHOPHARMACOLOGY, 1995, 117 (04) :443-452
[4]  
Badiani A, 1998, J NEUROSCI, V18, P10579
[5]   The potentiation of amphetamine-induced hyperlocomotion by fimbria-fornix lesions in rats is abolished by intrahippocampal grafts rich in serotonergic neurons [J].
Balse, E ;
Suhr, R ;
Haaf, A ;
Kelche, C ;
Jackisch, R ;
Cassel, JC .
NEUROSCIENCE LETTERS, 1999, 265 (02) :79-82
[6]   The effects of kainic acid lesions on dopaminergic responses to haloperidol and clozapine [J].
Bardgett, ME ;
Salaris, SL ;
Jackson, JL ;
Harding, J ;
Csernansky, JG .
PSYCHOPHARMACOLOGY, 1997, 133 (02) :142-151
[7]   THE PATTERNS OF AFFERENT INNERVATION OF THE CORE AND SHELL IN THE ACCUMBENS PART OF THE RAT VENTRAL STRIATUM - IMMUNOHISTOCHEMICAL DETECTION OF RETROGRADELY TRANSPORTED FLUOROGOLD [J].
BROG, JS ;
SALYAPONGSE, A ;
DEUTCH, AY ;
ZAHM, DS .
JOURNAL OF COMPARATIVE NEUROLOGY, 1993, 338 (02) :255-278
[8]   Fimbria-fornix lesions do not block sensitization to the psychomotor activating effects of amphetamine [J].
Browman, KE ;
Badiani, A ;
Robinson, TE .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1996, 53 (04) :899-902
[9]   EVIDENCE OF A COMPLETE INDEPENDENCE OF THE NEUROBIOLOGICAL SUBSTRATES FOR THE INDUCTION AND EXPRESSION OF BEHAVIORAL SENSITIZATION TO AMPHETAMINE [J].
CADOR, M ;
BJIJOU, Y ;
STINUS, L .
NEUROSCIENCE, 1995, 65 (02) :385-395
[10]   The fimbria-fornix cingular bundle pathways: A review of neurochemical and behavioural approaches using lesions and transplantation techniques [J].
Cassel, JC ;
Duconseille, E ;
Jeltsch, H ;
Will, B .
PROGRESS IN NEUROBIOLOGY, 1997, 51 (06) :663-716