Department of Physiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90112, Thailand; Research Unit for EEG Biomarkers of Neuronal diseases, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90112, Thailand.
Department of Physiology, Faculty of Science, Prince of Songkla University, Hat Yai, Songkhla, 90112, Thailand.
Neurosci Lett. 2019 Sep 14;709:134398. doi: 10.1016/j.neulet.2019.134398. Epub 2019 Jul 22.
Food deprivation is known to trigger hunger sensation and motivation to eat for energy replenishing. However, brain mechanisms associated with hunger and neural circuitries that mediate hunger driven responses remained to be investigated. To understand neural signaling of hunger, local field potentials (LFPs) in the lateral hypothalamus (LHa), nucleus accumbens (NAc), dorsal hippocampus (HP) and olfactory bulb (OB) and their interconnectivities were studied in freely moving adult male Albino mice during 18-20 h food deprivation and fed periods. Raw LFP signals were recorded and analyzed for mean values of spectral frequency power and coherence values. One-way repeated measures ANOVA revealed significant increases in spectral powers of beta and gamma frequency ranges induced by food deprivation in the LHa, HP, NAc but not OB. No change of spectral power in these brain regions was induced by food feeding. The analyses of coherent activity between brain regions also deliniated some distributed neural network activities correlated with hunger. In particular, coherent function indicated the increased beta and gamma phase synchrony between the pairs of LHa-HP and NAc-OB regions, and decreased gamma synchrony between the pairs of LHa-NAc and NAc-HP induced by food deprivation. It was found that plasma glucose level, locomotor count, travelled distance and time spent on moving were not altered by food deprivation. These results suggest that changes in LFP hallmarks in these brain regions were associated with hunger driven by negative energy balance.
食物剥夺已知会引发饥饿感和进食以补充能量的动机。然而，与饥饿相关的大脑机制和介导饥饿驱动反应的神经回路仍有待研究。为了了解饥饿的神经信号，在自由活动的成年雄性白化小鼠中研究了外侧下丘脑（LHa）、伏隔核（NAc）、背侧海马（HP）和嗅球（OB）中的局部场电位（LFPs）及其相互连接，在 18-20 小时的禁食和喂食期间。记录并分析原始 LFPs 信号的频谱频率功率和相干值的平均值。单向重复测量方差分析显示，食物剥夺诱导 LHa、HP 和 NAc 中的β和γ频带的频谱功率显著增加，但 OB 中没有。这些大脑区域的光谱功率没有因进食而改变。对大脑区域之间相干活动的分析也描绘了一些与饥饿相关的分布式神经网络活动。特别是，相干功能表明，食物剥夺诱导了 LHa-HP 和 NAc-OB 区域之间的β和γ相位同步增加，以及 LHa-NAc 和 NAc-HP 区域之间的γ同步减少。发现血浆葡萄糖水平、运动计数、运动距离和运动时间不受食物剥夺的影响。这些结果表明，这些大脑区域中 LFPs 特征的变化与负能平衡驱动的饥饿有关。
