Elazar Z, Peleg N, Paz M, Ring G
Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, Ramat Aviv, Israel.
Naunyn Schmiedebergs Arch Pharmacol. 1995 Aug;352(2):187-93. doi: 10.1007/BF00176773.
We have found previously that microinjections of carbachol into the pontine reticular formation (PRF) of rats induce an intense cataleptic state which is similar behaviorally with the catalepsy induced by systemic administration of neuroleptic drugs. In the experiments described in the present article we studied the possibility that the pontine carbachol catalepsy is generated via the intermediary of the dopaminergic cataleptogenic mechanism in the striatum. To this purpose we produced kainic acid lesions in the striatum and in the output stations of the striatal cataleptogenic mechanism-substantia nigra reticulata and the VM thalamic nucleus. Catalepsy was tested after systemic haloperidol (2 mg/kg) and pontine microinjections of carbachol (5 micrograms/1 microliter) before and after the kainic lesions. The cataleptogenic effect of carbachol injected in the pons was not attenuated by any of the three types of lesions. On the contrary, the cataleptogenic effect of haloperidol was greatly attenuated by the same lesions. These results suggest that the pontine catalepsy produced by microinjections of carbachol in PRF is generated independently of the dopaminergic cataleptogenic mechanism in basal ganglia.
我们之前发现,向大鼠脑桥网状结构(PRF)微量注射卡巴胆碱会诱发强烈的僵住状态,这种行为状态与全身给予抗精神病药物所诱发的僵住症相似。在本文所述的实验中,我们研究了脑桥卡巴胆碱诱发的僵住症是否通过纹状体中多巴胺能诱发僵住症机制介导产生的可能性。为此,我们在纹状体以及纹状体诱发僵住症机制的输出部位——黑质网状部和丘脑腹内侧核制造了海人酸损伤。在进行海人酸损伤前后,分别对全身注射氟哌啶醇(2毫克/千克)以及脑桥微量注射卡巴胆碱(5微克/1微升)后的僵住症进行了测试。向脑桥注射卡巴胆碱的致僵住效应并未因上述三种损伤中的任何一种而减弱。相反,相同的损伤却极大地减弱了氟哌啶醇的致僵住效应。这些结果表明,在PRF中微量注射卡巴胆碱所产生的脑桥僵住症是独立于基底神经节中多巴胺能诱发僵住症机制而产生的。