De Luca L A, Barbosa S P, Menani J V
Departamento Fisiologia e Patologia, Faculdade de Odontologia, Universidade Estadual Paulista, Rua Humaitá 1680, 14801-903 Araraquara, São Paulo, Brazil.
Neuroscience. 2003;121(4):1055-61. doi: 10.1016/s0306-4522(03)00316-6.
Serotonin antagonism in the lateral parabrachial nucleus (LPBN) enhances sodium appetite induced by hypovolaemia and angiotensin-mineralocorticoid activation, but produces no sodium intake in euhydrated animals. In the present work, male adult rats (n=21) that received bilateral injections of the serotonergic antagonist methysergide (4 microg/0.2 microl) into the LPBN combined to intragastric load of 2 M NaCl (2 ml/rat), ingested hypertonic NaCl (ingestion of 4.3 +/- 1.6 ml/2 h of 0.3 M NaCl versus vehicle into LPBN: 0.2 +/- 0.2 ml/2 h, P<0.05). Methysergide- and vehicle-treated animals also ingested water (9.5 +/- 0.7 and 7.2+/-0.5 ml/2 h, respectively, P>0.05) as expected from the state of cell dehydration produced by the load. Ingestion of water (11.0 +/- 1.2 ml/2 h), and of 0.3 M NaCl (1.1 +/- 0.7 ml/2 h) were not altered by methysergide in NaCl loaded rats with misplaced LPBN injections (n=15).The ingestion of hypertonic NaCl by rats with serotonergic blockade in the LPBN suggests that the circuits subserving sodium appetite are activated, but at the same time strongly inhibited through the LPBN, during cell dehydration.
外侧臂旁核(LPBN)中的5-羟色胺拮抗作用可增强由血容量减少和血管紧张素-盐皮质激素激活诱导的钠食欲,但在水合正常的动物中不会引起钠摄入。在本研究中,向LPBN双侧注射5-羟色胺能拮抗剂甲基麦角新碱(4微克/0.2微升)并结合2M NaCl胃内负荷(2毫升/只大鼠)的成年雄性大鼠(n = 21)摄入了高渗NaCl(0.3M NaCl摄入4.3±1.6毫升/2小时,而向LPBN注射溶剂的大鼠为0.2±0.2毫升/2小时,P<0.05)。甲基麦角新碱处理组和溶剂处理组的动物也摄入了水(分别为9.5±0.7和7.2±0.5毫升/2小时,P>0.05),这与负荷产生的细胞脱水状态预期一致。在LPBN注射位置错误的NaCl负荷大鼠中(n = 15),甲基麦角新碱未改变水(11.0±1.2毫升/2小时)和0.3M NaCl(1.1±0.7毫升/2小时)的摄入。LPBN中存在5-羟色胺能阻断的大鼠对高渗NaCl的摄入表明,在细胞脱水期间,维持钠食欲的神经回路被激活,但同时通过LPBN受到强烈抑制。