Snijders R, Kramarcy N R, Hurd R W, Nemeroff C B, Dunn A J
Neuropharmacology. 1982 May;21(5):465-8. doi: 10.1016/0028-3908(82)90032-6.
Intracerebroventricular (i.c.v.) injection of neurotensin (NT) induced catalepsy in mice at doses greater than or equal to 0.02 microgram. The cataleptic effect progressively increased, reaching a maximum at approx. 2 hr after injection. In contrast, the hypothermic effect of neurotensin reached a maximum 1 hr after the injection, and was declining at 2 hr. Not all mice that showed hypothermia also showed catalepsy, and some mice showed catalepsy without hypothermia. Catalepsy induced by intracerebroventricular injection of neurotensin was not significantly correlated with the hypothermia. Furthermore, oxotremorine induced hypothermia without catalepsy. Thus, several lines of evidence indicate that the catalepsy induced by neurotensin is not the consequence of the neurotensin induced hypothermia. Thyrotropin releasing hormone (TRH), injected either intracerebroventricularly with neurotensin, or intraperitoneally before neurotensin abolished the hypothermia but only diminished the catalepsy scores. The cataleptic effect of neurotensin is consistent with its other neuroleptic-like activities.
脑室内（i.c.v.）注射神经降压素（NT），剂量大于或等于0.02微克时会在小鼠中诱发僵住症。僵住症效应逐渐增强，在注射后约2小时达到最大值。相比之下，神经降压素的降温效应在注射后1小时达到最大值，并在2小时时下降。并非所有出现体温过低的小鼠都表现出僵住症，有些小鼠表现出僵住症但没有体温过低。脑室内注射神经降压素诱发的僵住症与体温过低没有显著相关性。此外，氧化震颤素诱发体温过低但不诱发僵住症。因此，多项证据表明，神经降压素诱发的僵住症不是神经降压素诱发体温过低的结果。促甲状腺激素释放激素（TRH），与神经降压素一起脑室内注射，或在神经降压素之前腹腔注射，可消除体温过低，但仅降低僵住症评分。神经降压素的僵住症效应与其其他类抗精神病活性一致。
