Lv Jing, Feng Hao, Chen Ling, Wang Wei-Yao, Yue Xue-Ling, Jin Qing-Hua
aDepartment of Physiology and Pathophysiology, Yanbian University College of Medicine and Cellular Function Research Center, Yanbian University, Yanji, Jilin Province bAir Force Shenyang Ningshan Road Sanitarium for Retired Cadres, Shenyang, Liaoning Province, China.
Neuroreport. 2017 Oct 18;28(15):973-979. doi: 10.1097/WNR.0000000000000868.
Long-term potentiation (LTP) is widely accepted as the best studied model for neurophysiological mechanisms that could underlie learning and memory formation. Despite a number of studies indicating that β-adrenoceptors in the hippocampal dentate gyrus (DG) is involved in the modulation of learning and memory as well as LTP, few studies have used glutamate release as a visual indicator in awake animals to explore the role of β-adrenoceptors in learning-dependent LTP. Therefore, in the present study, the effects of propranolol (an antagonist of β-adrenoceptor) and isoproterenol (an agonist of β-adrenoceptor) on extracellular concentrations of glutamate and amplitudes of field excitatory postsynaptic potential were measured in the DG region during active avoidance learning in freely moving conscious rats. In the control group, the glutamate level in the DG was significantly increased during the acquisition of active avoidance behavior and returned to basal level following extinction training. In propranolol group, antagonism of β-adrenoceptors in the DG significantly reduced the change in glutamate level, and the acquisition of the active avoidance behavior was significantly inhibited. In contrast, the change in glutamate level was significantly enhanced by isoproterenol, and the acquisition of the active avoidance behavior was significantly accelerated. Furthermore, in all groups, the changes in glutamate level were accompanied by corresponding changes in field excitatory postsynaptic potential amplitude and active avoidance behavior. Our results suggest that activation of β-adrenoceptors in the hippocampal DG facilitates active avoidance learning by modulations of glutamate level and synaptic efficiency in rats.
长期增强作用（LTP）被广泛认为是对可能构成学习和记忆形成基础的神经生理机制研究得最为透彻的模型。尽管有多项研究表明海马齿状回（DG）中的β-肾上腺素能受体参与学习、记忆以及LTP的调节，但很少有研究在清醒动物中使用谷氨酸释放作为视觉指标来探究β-肾上腺素能受体在依赖学习的LTP中的作用。因此，在本研究中，在自由活动的清醒大鼠进行主动回避学习期间，测量了普萘洛尔（一种β-肾上腺素能受体拮抗剂）和异丙肾上腺素（一种β-肾上腺素能受体激动剂）对DG区域细胞外谷氨酸浓度和场兴奋性突触后电位幅度的影响。在对照组中，DG中的谷氨酸水平在主动回避行为的习得过程中显著升高，并在消退训练后恢复到基础水平。在普萘洛尔组中，DG中β-肾上腺素能受体的拮抗作用显著降低了谷氨酸水平的变化，并且主动回避行为的习得受到显著抑制。相反，异丙肾上腺素显著增强了谷氨酸水平的变化，并且主动回避行为的习得显著加速。此外，在所有组中，谷氨酸水平的变化伴随着场兴奋性突触后电位幅度和主动回避行为的相应变化。我们的结果表明，海马DG中β-肾上腺素能受体的激活通过调节大鼠的谷氨酸水平和突触效率促进主动回避学习。
