杏仁中央核损毁对缺钠大鼠钠欲行为启动和表达的影响
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摘要
目的:探讨杏仁中央核(CeA)损毁对缺钠大鼠钠欲行为启动和表达的影响。方法:将18只成年雄性SD大鼠随机分为3组(n=6):双侧Ce A损毁组、假损毁组和不损毁组,手术恢复后给予大鼠14 d低钠饲料摄食以建立缺钠大鼠模型,运用单笼双瓶选择测试方法观察缺钠大鼠在24 h内5个不同时间段对0.3 mol/L NaCl和自由饮水的摄入情况。应用免疫荧光化学染色方法观察杏仁中央核损毁与否对缺钠或正常大鼠孤束核内醛固酮敏感神经元活动的影响。结果:低钠饮食14 d后,大鼠对0.3 mol/L NaCl 24 h内饮用量和偏爱率比低钠饮食前明显增加(P<0.01);杏仁中央核损毁后缺钠大鼠对0.3 mol/L Na Cl溶液的摄入量和偏爱率显著下降(P<0.01)。杏仁中央核损毁对低钠饮食诱发的大鼠孤束核内醛固酮敏感神经元活动增加没有影响。结论:低钠饮食诱导大鼠钠欲行为表达增加;杏仁中央核损毁压抑缺钠大鼠钠欲行为的表达,而对缺钠大鼠的钠欲行为的启动没有影响。
Objective: To investigate the effects of central nucleus of amygdala( Ce A) lesion on the initiation and expression of sodium appetite in sodium-deficient rats. Methods: Three groups of SD rats( n = 6 in each group) were treated with bilateral Ce A lesion,sham lesion or no lesion. After the recovery,the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L Na Cl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii( NTS) was used to investigate the effect of Ce A lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency. Results: After fed with low-sodium diet for14 days,the volume and preference rate of 0.3 mol/L Na Cl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet( P<0.01). The intake volume and the preference rate of 0.3 mol/L Na Cl in Ce A lesion rats were significantly decreased than those in Ce A sham lesion rats and normal rats in the sodium-deficient condition( P<0.01). The Ce A lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet.Conclusion: Low-sodium diet induces an increase in the expression of sodium appetite in rats. Ce A lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.
Objective: To investigate the effects of central nucleus of amygdala( Ce A) lesion on the initiation and expression of sodium appetite in sodium-deficient rats. Methods: Three groups of SD rats( n = 6 in each group) were treated with bilateral Ce A lesion,sham lesion or no lesion. After the recovery,the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L Na Cl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii( NTS) was used to investigate the effect of Ce A lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency. Results: After fed with low-sodium diet for14 days,the volume and preference rate of 0.3 mol/L Na Cl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet( P<0.01). The intake volume and the preference rate of 0.3 mol/L Na Cl in Ce A lesion rats were significantly decreased than those in Ce A sham lesion rats and normal rats in the sodium-deficient condition( P<0.01). The Ce A lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet.Conclusion: Low-sodium diet induces an increase in the expression of sodium appetite in rats. Ce A lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.
引文
[1]Geerling JC,Loewy AD.Central regulation of sodium appetite[J].Exp Physiol,2008,93(2):177-209.
[2]康怡,闫剑群,黄涛.损毁大鼠杏仁中央核对不同味觉溶液摄入的影响[J].中国应用生理学杂志,2004,20(3):69-72.
[3]Andrade-Franze GM,Andrade CA,De Luca LA Jr,et al.Lesions in the central amygdala impair sodium intake induced by the blockade of the lateral parabrachial nucleus[J].Brain Res,2010,1332:57-64.
[4]Sakai RR,Ma LY,Zhang DM,et al.Intracerebral administration of mineralocorticoid receptor antisense oligonucleotides attenuate adrenal steroid-induced salt appetite in rats[J].Neuroendocrinology,1996,64(6):425-429.
[5]Geerling JC,Loewy AD.Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst[J].Am J Physiol Regul Integr Comp Physiol,2007,292(3):R1338-1348.
[6]Jacobs KM,Mark GP,Scott TR.Taste responses in the nucleus tractus solitarius of sodium-deprived rats[J].JPhysiol,1988,406:393-410.
[7]Nakamura K,Norgren R.Sodium-deficient diet reduces gustatory activity in the nucleus of the solitary tract of behaving rats[J].Am J Physiol,1995,269(3 Pt 2):R647-661.
[8]McCaughey SA,Scott TR.Rapid induction of sodium appetite modifies taste-evoked activity in the rat nucleus of the solitary tract[J].Am J Physiol Regul Integr Comp Physiol,2000,279(3):R1121-1131.
[9]Dietz DM,Curtis KS,Contreras RJ.Taste,salience,and increased Na Cl ingestion after repeated sodium depletions[J].Chem Senses,2006,31(1):33-41.
[10]Flynn FW,Grill HJ,Schulkin J,et al.Central gustatory lesions:II.Effects on sodium appetite,taste aversion learning,and feeding behaviors[J].Behav Neurosci,1991,105(6):944-954.
[11]沈毅弘,王为民,虞燕琴,等.杏仁中央核在躯体传入冲动抑制中枢性升压反应中的作用[J].中国应用生理学杂志,2007,23(3):309-313.
[12]Geerling JC,Loewy AD.Aldosterone-sensitive NTS neurons are inhibited by saline ingestion during chronic mineralocorticoid treatment[J].Brain Res,2006,1115(1):54-64.
[13]Formenti S,Bassi M,Nakamura NB,et al.Hindbrain mineralocorticoid mechanisms on sodium appetite[J].Am J Physiol Regul Integr Comp Physiol,2013,304(3):R252-259.
[14]Geerling JC,Loewy AD.Aldosterone-sensitive neurons in the nucleus of the solitary tract:bidirectional connections with the central nucleus of the amygdala[J].J Comp Neurol,2006,497(4):646-657.
[15]Jiang E,Chapp AD,Fan Y,et al.Expression of proinflammatory cytokines is upregulated in the hypothalamic paraventricular nucleus of Dahl salt-sensitive hypertensive rats[J].Front Physiol,2018,9:104.
[16]高晓磊,尹桂东,邴艳华,等.下丘脑室旁核内GABA在中枢高渗刺激诱发的心血管反应中的作用[J].中国应用生理学杂志,2009,25(4):462-466.
[2]康怡,闫剑群,黄涛.损毁大鼠杏仁中央核对不同味觉溶液摄入的影响[J].中国应用生理学杂志,2004,20(3):69-72.
[3]Andrade-Franze GM,Andrade CA,De Luca LA Jr,et al.Lesions in the central amygdala impair sodium intake induced by the blockade of the lateral parabrachial nucleus[J].Brain Res,2010,1332:57-64.
[4]Sakai RR,Ma LY,Zhang DM,et al.Intracerebral administration of mineralocorticoid receptor antisense oligonucleotides attenuate adrenal steroid-induced salt appetite in rats[J].Neuroendocrinology,1996,64(6):425-429.
[5]Geerling JC,Loewy AD.Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst[J].Am J Physiol Regul Integr Comp Physiol,2007,292(3):R1338-1348.
[6]Jacobs KM,Mark GP,Scott TR.Taste responses in the nucleus tractus solitarius of sodium-deprived rats[J].JPhysiol,1988,406:393-410.
[7]Nakamura K,Norgren R.Sodium-deficient diet reduces gustatory activity in the nucleus of the solitary tract of behaving rats[J].Am J Physiol,1995,269(3 Pt 2):R647-661.
[8]McCaughey SA,Scott TR.Rapid induction of sodium appetite modifies taste-evoked activity in the rat nucleus of the solitary tract[J].Am J Physiol Regul Integr Comp Physiol,2000,279(3):R1121-1131.
[9]Dietz DM,Curtis KS,Contreras RJ.Taste,salience,and increased Na Cl ingestion after repeated sodium depletions[J].Chem Senses,2006,31(1):33-41.
[10]Flynn FW,Grill HJ,Schulkin J,et al.Central gustatory lesions:II.Effects on sodium appetite,taste aversion learning,and feeding behaviors[J].Behav Neurosci,1991,105(6):944-954.
[11]沈毅弘,王为民,虞燕琴,等.杏仁中央核在躯体传入冲动抑制中枢性升压反应中的作用[J].中国应用生理学杂志,2007,23(3):309-313.
[12]Geerling JC,Loewy AD.Aldosterone-sensitive NTS neurons are inhibited by saline ingestion during chronic mineralocorticoid treatment[J].Brain Res,2006,1115(1):54-64.
[13]Formenti S,Bassi M,Nakamura NB,et al.Hindbrain mineralocorticoid mechanisms on sodium appetite[J].Am J Physiol Regul Integr Comp Physiol,2013,304(3):R252-259.
[14]Geerling JC,Loewy AD.Aldosterone-sensitive neurons in the nucleus of the solitary tract:bidirectional connections with the central nucleus of the amygdala[J].J Comp Neurol,2006,497(4):646-657.
[15]Jiang E,Chapp AD,Fan Y,et al.Expression of proinflammatory cytokines is upregulated in the hypothalamic paraventricular nucleus of Dahl salt-sensitive hypertensive rats[J].Front Physiol,2018,9:104.
[16]高晓磊,尹桂东,邴艳华,等.下丘脑室旁核内GABA在中枢高渗刺激诱发的心血管反应中的作用[J].中国应用生理学杂志,2009,25(4):462-466.
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