Consolo S, Wang J X, Forloni G L, Mocchetti I, Racagni G, Ladinsky H
Life Sci. 1985 Aug 5;37(5):449-60. doi: 10.1016/0024-3205(85)90407-2.
Neurotoxin-induced lesion of the serotonergic raphe-hippocampal pathway produced about a 50% increase in the density of a nM affinity alpha-adrenergic binding site for (3H)WB-4101 in rat hippocampus 18 days postlesion without altering the specific binding of (3H)5-HT to serotonergic receptors. The chronic i.c.v. infusion of serotonin by minipump started at the appropriate time averted or reverted the effect. The dynamics of noradrenergic neurotransmission in the hippocampus was not impaired by lesion of the median raphe nucleus as determined by the uptake and turnover of noradrenaline as well as its release - as reflected by the normetanephrine concentration. In addition, neurotoxin-induced lesion of the dorsal noradrenergic bundle failed to alter either the Bmax or the Kd of (3H)WB-4101 binding to the nM site. Kainic acid-induced destruction of perikarya depressed the nM (3H)WB-4101 binding sites by 60% and completely prevented the up regulation caused by lesion of the median raphe nucleus. Thus, the supersensitivity-like response of the adrenoceptors to the lack of serotonin appears to be localized on kainate-sensitive cells within the hippocampus.
神经毒素诱导的中缝-海马5-羟色胺能通路损伤，在损伤后18天，大鼠海马中对(3H)WB-4101具有纳摩尔亲和力的α-肾上腺素能结合位点密度增加了约50%，而(3H)5-羟色胺对5-羟色胺能受体的特异性结合未发生改变。在适当时间开始通过微型泵进行慢性脑室内5-羟色胺输注可避免或逆转这种效应。通过去甲肾上腺素的摄取、周转及其释放（以去甲变肾上腺素浓度反映）来确定，中缝核损伤并未损害海马中去甲肾上腺素能神经传递的动力学。此外，神经毒素诱导的背侧去甲肾上腺素能束损伤未能改变(3H)WB-4101与纳摩尔位点结合的Bmax或Kd。海人酸诱导的神经元胞体破坏使纳摩尔(3H)WB-4101结合位点减少60%，并完全阻止了中缝核损伤所引起的上调。因此，肾上腺素能受体对5-羟色胺缺乏的超敏样反应似乎定位于海马内对海人酸敏感的细胞上。
