Goldstein R
Neuropeptides. 1985 Jul;6(4):303-10. doi: 10.1016/0143-4179(85)90003-4.
The cisternal cerebrospinal fluid (CSF) samples, taken at 30, 60, 120 and 180 minutes after multiple electrolitic lesions of lateral habenular (LHB) lesions or of thalamus, performed in urethane anesthetized cats, were assayed for their antidiuretic and hydroosmotic activities before and after trypsine or thioglycollate incubation. LHB but not thalamic lesions, specifically induced the appearance of antidiuretic and hydroosmotic activities at 60 and 120 minutes. The activities decreased under the bioassays sensibilities at 180 minutes. The biological activities of the CSF samples, their ratio as well as their susceptibility to tryptic digestion and thioglycollate incubation suggest that LHB lesions induce the release of a basic peptide with a disulfide bound, indistinguishable from arginine vasotocin (AVT). Since it was previously argued that there is a pineal-habenula circuit with AVT as neuromudulator, it is advanced the hypothesis that LHB lesions interfere with an inhibitory feed-back loop between habenula and the pineal gland.
在氨基甲酸乙酯麻醉的猫身上，对侧脑室脑脊液（CSF）样本进行检测，这些样本是在外侧缰核（LHB）或丘脑多次电解损伤后30、60、120和180分钟采集的，检测其在胰蛋白酶或巯基乙酸盐孵育前后的抗利尿和水渗透活性。LHB损伤而非丘脑损伤，在60和120分钟时特异性地诱导了抗利尿和水渗透活性的出现。在180分钟时，这些活性在生物测定敏感性下降低。CSF样本的生物活性、它们的比例以及它们对胰蛋白酶消化和巯基乙酸盐孵育的敏感性表明，LHB损伤诱导释放一种与精氨酸血管催产素（AVT）难以区分的具有二硫键结合的碱性肽。由于之前有人认为存在一个以AVT作为神经调节剂的松果体-缰核回路，因此提出了一个假设，即LHB损伤干扰了缰核与松果体之间的抑制性反馈回路。
