Anticonvulsive effect of swim stress in mice

被引:51
作者
Pericic, D [1 ]
Svob, D [1 ]
Jazvinscak, M [1 ]
Mirkovic, K [1 ]
机构
[1] Rudjer Boskovic Inst, Lab Mol Neuropharmacol, Zagreb 10000, Croatia
关键词
swim stress; convulsions; corticosterone; aminoglutethimide; finasteride; picrotoxin; pentylenetetrazole; kainic acid; t-[H-3]butylbicycloorthobenzoate ([H-3]TBOB) binding;
D O I
10.1016/S0091-3057(00)00267-7
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
To explore the possible involvement of glucocorticoids in the previously observed anticonvulsive effect of swim stress, mice were, prior to administration of convulsants, subjected to treatments that diminish or enhance plasma corticosterone levels. Aminoglutethimide, the inhibitor of steroid synthesis, failed to modify convulsant doses of picrotoxin, but enhanced threshold doses of pentylenetetrazole producing myoclonus and death, both in unstressed and stressed animals. The same drug prevented the effect of stress on pentylenetetrazole-induced running bouncing clonus (RB clonus) and abolished the appearance of tonic hindlimb extension (THE). Doses of kainic acid producing convulsions and death were not affected by stress, but they were enhanced by aminoglutethimide. Corticosterone administration could not imitate the effect of swim stress. Finasteride, a Soi-reductase inhibitor, did not interfere with the effect of stress on picrotoxin-induced convulsions. Swim stress failed to modify the binding of the convulsant t[H-3]-butylbicycloorthobenzoate [H-3]TBOB, to washed mouse forebrain membranes. The results confirmed an anticonvulsant effect of swim stress against convulsions produced by GABA-related convulsants, but they do not support the hypothesis suggesting the involvement of glucocorticoids or neurosteroids in this effect. (C) 2000 Elsevier Science Inc.
引用
收藏
页码:879 / 886
页数:8
相关论文
共 49 条
[1]   EFFECTS OF WATER IMMERSION STRESS ON CONVULSIONS INDUCED BY PENTYLENETETRAZOL [J].
ABEL, EL ;
BERMAN, RF .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1993, 45 (04) :823-825
[2]   Aminoglutethimide, a corticosteroid synthesis inhibitor, facilitates brain stimulation reward in food-restricted rats: an investigation of underlying mechanisms [J].
Abrahamsen, GC ;
Kandawire, MJ ;
Carr, KD .
PSYCHOPHARMACOLOGY, 1997, 133 (04) :405-412
[3]   SEX-DIFFERENCES IN THE EFFECTS OF ACUTE SWIM STRESS ON BINDING TO GABA-A RECEPTOR IN MOUSE-BRAIN [J].
AKINCI, MK ;
JOHNSTON, GAR .
JOURNAL OF NEUROCHEMISTRY, 1993, 60 (06) :2212-2216
[4]   Sex differences in the effects of gonadectomy and acute swim stress on GABA(A) receptor binding in mouse forebrain membranes [J].
Akinci, MK ;
Johnston, GAR .
NEUROCHEMISTRY INTERNATIONAL, 1997, 31 (01) :1-10
[5]   THE EFFECT OF CORTICOSTERONE IN RATS SUBMITTED TO THE ELEVATED PLUS-MAZE AND TO PENTYLENETETRAZOL-INDUCED CONVULSIONS [J].
ANDREATINI, R ;
LEITE, JR .
PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY, 1994, 18 (08) :1333-1347
[6]   EFFECT OF MICROELECTROPHORETICALLY APPLIED CORTICOSTERONE ON RAPHE NEURONS IN THE RAT [J].
AVANZINO, GI ;
ERMIRIO, R ;
RUGGERI, P ;
COGO, CE .
NEUROSCIENCE LETTERS, 1984, 50 (1-3) :307-311
[7]   Time-dependent changes in rat brain neuroactive steroid concentrations and GABA(A) receptor function after acute stress [J].
Barbaccia, ML ;
Roscetti, G ;
Trabucchi, M ;
Mostallino, MC ;
Concas, A ;
Purdy, RH ;
Biggio, G .
NEUROENDOCRINOLOGY, 1996, 63 (02) :166-172
[8]   STRESS AND BETA-CARBOLINES DECREASE THE DENSITY OF LOW AFFINITY GABA BINDING-SITES - AN EFFECT REVERSED BY DIAZEPAM [J].
BIGGIO, G ;
CONCAS, A ;
SERRA, M ;
SALIS, M ;
CORDA, MG ;
NURCHI, V ;
CRISPONI, C ;
GESSA, GL .
BRAIN RESEARCH, 1984, 305 (01) :13-18
[9]   Ovarian steroids modify the behavioral and neurochemical responses of the central benzodiazepine receptor [J].
Bitran, D ;
Dowd, JA .
PSYCHOPHARMACOLOGY, 1996, 125 (01) :65-73
[10]   ADRENALECTOMY INCREASES BICUCULLINE-INDUCED SEIZURE SENSITIVITY IN LONG-SLEEP AND SHORT-SLEEP MICE [J].
BOWERS, BJ ;
BOSY, TZ ;
WEHNER, JM .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1991, 38 (03) :593-600