Paulin Renata Fabris, Menani José V, Colombari Eduardo, De Paula Patrícia Maria, Colombari Débora Simões Almeida
Department of Physiology and Pathology, School of Dentistry, São Paulo State University, Rua Humaitá 1680, Araraquara, SP, Brazil.
Brain Res. 2009 Nov 17;1298:145-52. doi: 10.1016/j.brainres.2009.08.067. Epub 2009 Aug 31.
Peripheral injection of pilocarpine, a cholinergic muscarinic agonist, induces salivation, water intake and hypertension. The medial septal area (MSA) is involved in cardiovascular control and fluid-electrolyte balance. Therefore, the effects of lesions or muscarinic cholinergic blockade in the MSA on the salivation, water intake and pressor responses induced by peripheral pilocarpine (4 micromol/kg of body weight) were investigated. Male Holtzman rats with stainless steel cannulas implanted in the MSA or submitted to electrolytic lesion of MSA were used. MSA lesion (1 day) reduced the salivation (262+/-45 vs. sham: 501+/-30 mg/7 min) and water intake (2.6+/-0.4 vs. sham: 4+/-0.4 ml/1 h) induced by intraperitoneal pilocarpine, whereas 15-day MSA lesion reduced only the pilocarpine-induced water intake (2.3+/-0.5 ml/1 h). Pre-treatment with the muscarinic cholinergic antagonist atropine methyl bromide (4 nmol/0.5 microl) into MSA also reduced the pilocarpine-induced salivation (420+/-33 mg/7 min) and water intake (1.4+/-0.4 ml/1 h). Conversely, MSA lesions or the blockade of muscarinic receptors in the MSA did not change the pressor response induced by intravenous pilocarpine. The results show that MSA and its muscarinic receptors are part of the forebrain circuitry activated by peripheral pilocarpine that induce salivary secretion and water intake. Moreover, they suggest that different central mechanisms are involved in the salivatory, dipsogenic and cardiovascular effects of peripheral pilocarpine in rats.
外周注射毛果芸香碱(一种胆碱能毒蕈碱激动剂)可引起唾液分泌、饮水和血压升高。内侧隔区(MSA)参与心血管控制和体液电解质平衡。因此,研究了内侧隔区损伤或毒蕈碱胆碱能阻断对由外周毛果芸香碱(4微摩尔/千克体重)诱导的唾液分泌、饮水和升压反应的影响。使用了在MSA植入不锈钢套管或接受MSA电解损伤的雄性霍尔兹曼大鼠。MSA损伤(1天)可减少腹腔注射毛果芸香碱引起的唾液分泌(262±45对假手术组:501±30毫克/7分钟)和饮水(2.6±0.4对假手术组:4±0.4毫升/1小时),而15天的MSA损伤仅减少毛果芸香碱诱导的饮水(2.3±0.5毫升/1小时)。向MSA预先注射毒蕈碱胆碱能拮抗剂甲基溴化阿托品(4纳摩尔/0.5微升)也可减少毛果芸香碱诱导的唾液分泌(420±33毫克/7分钟)和饮水(1.4±0.4毫升/1小时)。相反,MSA损伤或MSA中毒蕈碱受体的阻断并未改变静脉注射毛果芸香碱引起的升压反应。结果表明,MSA及其毒蕈碱受体是由外周毛果芸香碱激活的前脑回路的一部分,该回路可诱导唾液分泌和饮水。此外,它们表明不同的中枢机制参与了外周毛果芸香碱对大鼠的唾液分泌、致渴和心血管作用。