Barofsky A L, Taylor J, Tizabi Y, Kumar R, Jones-Quartey K
Endocrinology. 1983 Nov;113(5):1884-93. doi: 10.1210/endo-113-5-1884.
Impairments in lactation after electrolytic lesions of the median raphe (MR) nucleus have been corrected by treatment with PRL. Specific serotonin neurotoxin lesions were used in the present study to determine whether decrements in litter growth after electrolytic lesions could be attributed to serotonergic neuron damage at the MR locus, and whether MR lesions (MRL) disrupted suckling-induced PRL release. Intracerebral microinjection of 5,7-dihydroxytryptamine (5,7-DHT) into the MR nucleus produced dose-related decrements in litter growth after either 4 micrograms (sham, 1.35 +/- 0.05; MRL, 1.04 +/- 0.05 g/pup X day; P less than 0.001) or 8 micrograms 5,7-DHT (sham, 1.35 +/- 0.06; MRL, 0.87 +/- 0.11 g/pup X day; P less than 0.001). Despite hypothalamic serotonin depletions of 15% and 55%, respectively, for the two doses of 5,7-DHT, there was no difference between sham and MRL animals in either basal or suckling-induced PRL release. When lesions were placed on day 1 of lactation (L) so that killing on day 7-L corresponded to the early maximal neurotoxin effect, MRL mothers still showed litter growth decrements (0.37 +/- 0.07; sham, 0.98 +/- 0.08 g/pup X day; P less than 0.001) and normal PRL values. When maternal behavior was examined, MRL animals exhibited a higher incidence of abnormal behaviors (failure to retrieve pups, cannibalism, and failure to initiate suckling during a 1-h test period; Fisher's exact P, Sham vs. MRL, less than 0.01, less than 0.05, and 0.15, respectively) than sham animals or animals with 5,7-DHT lesions in the dorsal raphe nucleus or superior colliculus. In addition, suckling behavior scores, determined from daily suckling behavior observations, were lowest in the MRL group and correlated with litter growth only in this group (r = 0.789; P less than 0.01). These data suggest that serotonergic elements in the MR nucleus play an obligatory role in maintaining normal maternal behavior during lactation, but they are not involved in suckling induced PRL release.
中缝正中核(MR)电解损伤后泌乳功能受损,可通过催乳素(PRL)治疗得到纠正。本研究采用特异性5-羟色胺神经毒素损伤,以确定电解损伤后窝仔生长减少是否可归因于MR位点的5-羟色胺能神经元损伤,以及MR损伤(MRL)是否会破坏哺乳诱导的PRL释放。向MR核内脑室内微量注射5,7-二羟色胺(5,7-DHT),在注射4微克(假手术组,1.35±0.05;MRL组,1.04±0.05克/幼崽×天;P<0.001)或8微克5,7-DHT后(假手术组,1.35±0.06;MRL组,0.87±0.11克/幼崽×天;P<0.001),窝仔生长出现剂量相关的减少。尽管两种剂量的5,7-DHT分别使下丘脑5-羟色胺减少了15%和55%,但假手术组和MRL组动物在基础或哺乳诱导的PRL释放方面均无差异。当在泌乳第1天(L)进行损伤,使得在第7-L天处死对应于早期最大神经毒素效应时,MRL组母鼠仍表现出窝仔生长减少(0.37±0.07;假手术组,0.98±0.08克/幼崽×天;P<0.001)且PRL值正常。当检查母性行为时,MRL组动物出现异常行为的发生率更高(在1小时测试期内未能找回幼崽、同类相食以及未能开始哺乳;Fisher精确检验P值,假手术组与MRL组相比,分别为<0.01、<0.05和0.15),高于假手术组或在中缝背核或上丘有5,7-DHT损伤的动物。此外,根据每日哺乳行为观察确定的哺乳行为评分,在MRL组中最低,且仅在该组与窝仔生长相关(r = 0.789;P<0.01)。这些数据表明,MR核中的5-羟色胺能成分在维持泌乳期正常母性行为中起重要作用,但它们不参与哺乳诱导的PRL释放。