Voorhies Ann C, Bernstein Ilene L
Department of Psychology, Guthrie Hall, University of Washington, P.O. Box 351525, Seattle, WA 98195, USA.
Behav Brain Res. 2006 Sep 15;172(1):90-6. doi: 10.1016/j.bbr.2006.04.020. Epub 2006 May 18.
Sodium depletion is a strong natural motivator that creates a pronounced sodium appetite and has been shown to activate neural regions associated with fluid and sodium balance. However, it is not known whether sodium appetite affects the mesolimbic circuitry associated with reward motivation. The present studies examined expression of the immediate early gene Fos in the nucleus accumbens (NAc) as a marker of neuronal activation following the induction and expression of furosemide-induced sodium appetite. During sodium appetite expression, sham-drinking and normal drinking were used to dissociate effects of NaCl taste stimulation from the repletion that follows absorption of sodium. These studies revealed that the combination of NaCl taste stimulation and persistent sodium depletion experienced by sham-drinking animals dramatically activates the NAc, while neither induction nor expression of sodium appetite alone is sufficient to increase Fos expression in this region. Results are discussed in terms of current theories of reward motivation.
钠缺乏是一种强烈的自然驱动力,会引发明显的钠食欲,并已被证明能激活与体液和钠平衡相关的神经区域。然而,尚不清楚钠食欲是否会影响与奖励动机相关的中脑边缘回路。本研究检测了即刻早期基因Fos在伏隔核(NAc)中的表达,以此作为速尿诱导的钠食欲诱导和表达后神经元激活的标志物。在钠食欲表达期间,假饮水和正常饮水被用于区分氯化钠味觉刺激的作用与钠吸收后的补充作用。这些研究表明,假饮水动物所经历的氯化钠味觉刺激和持续钠缺乏的结合会显著激活伏隔核,而单独的钠食欲诱导或表达都不足以增加该区域的Fos表达。研究结果将根据当前的奖励动机理论进行讨论。