Effects of lnterleukin-2 on Various Models of Experimental Epilepsy in DBA/2 Mice
作者:
Giovambattista De Sarro,
Domenicantonio Rotiroti,
Maria Giulia Audino,
Santo Gratteri,
Giuseppe Nisticó,
期刊:
Neuroimmunomodulation
(Karger Available online 1994)
卷期:
Volume 1,
issue 6
页码: 361-369
ISSN:1021-7401
年代: 1994
DOI:10.1159/000097189
出版商: S. Karger AG
关键词: Epilepsy;Interleukin-2;Convulsants;Audiogenic seizures;Bicuculline;Kainate;Cephazolin
数据来源: Karger
摘要:
The effects of interleukin-2 (IL-2) on various models of experimental epilepsy were studied after intracerebroventricular administration in DBA/2 mice, a strain genetically susceptible to sound-induced seizures. Convulsions were induced by physical stimulus (sound of 109 dB, 12-16 kHz) or by chemical compounds (bicuculline, cephazolin or kainate). The present study demonstrated that human recombinant IL-2 (hr-IL-2) and mouse recombinant IL-2 (mr-IL-2) not only did not antagonize audiogenic seizures in DBA/2 mice but increased the incidence of seizures after the highest doses studied. In addition, hr-IL-2 and mr-IL-2 dose dependency facilitated sound-induced seizures at subthreshold sound exposure (8 3 dB). Pretreatment with monoclonal rat-anti-mouse IL-2 antibodies significantly affected the changes of occurrence of audiogenic seizures in DBA/2 mice induced by mr-IL-2. In addition, pretreatment with anti-IL-2 receptor monoclonal antibodies (anti-Tac) was able to completely antagonize or reduce the effects of IL-2 on audiogenic seizures. The effects of mr-IL-2 were also studied in two different models of epilepsy: the bicuculline and cephazolin models, due to impairment of GABAergic transmission, and the kainate model, due to an increase in excitatory amino acid transmission. In all models, mr-ILr2 demonstrated to facilitate the seizures induced by these chemoconvulsants. Since the proconvulsant properties of IL-2 were antagonized by specific monoclonal antibodies, we suggest that some epileptic phenomena may be linked to stimulation of IL-2 receptors. Further experiments will be necessary in order to ascertain whether IL-2 acts via the potentialization of the effects of excitatory amino acids or via inhibition of GABA activity, or both in the brain.
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