The behavioral learning of animal could be blocked with the stimulation of 1hz while the stimulation of 5 hz did not show any effect on it . it indicated that the ne afferent to hippocampus participated in the reversal of ld - ltp and even the mechanisms of the memory loss ( " forgetting " ) . it also suggested that not only the ihz - dp or the 5hz - dp has different relation with the presynaptic mechanisms but also has different effects on the behavioral learning 上述实验结果表明: ihz和shz刺激dneb对mf . c八3习得性ltp均可产生完全的dp ，但就对行为习得的影响而言， 1比比shz有效，提示海马的ne输入参与了习得性ltp的dp乃至遗忘的机制，该过程可能还与突触前机制有关;结果还提示ihz诱导的dp与shz诱导的dp不仅在与突触前机制的关系上还是各自产生的行为效应上均存在不同。
Since many of the kinases studied are involved in the plasticity of hippocampal cells as well as learning and memory in hippocampus , and jnk and p38 are involved in the process of cell death or apoptosis in hippocampal cells , it is suggested that the mapks activation by gc " s nongenomic action maybe in some extent in relevance to neuronal plasticity and / or apoptosis in hippocampus in view of the fact that gc activated mapks translocated into the cell nucleus , and maintained in a sustained high level for a long duration , we propose that a genomic consequence could be evoked by this gc activation of mapks B ? bsa引起的核转位与b类似，而且在b ? bsa的15分钟的作用后1小时，仍能看到p38的核转位现象在研究海马的学习和记忆功能时发现神经元的可塑性与许多激酶(包括mapks )有关，而jnk和p38往往又和海马神经元的凋亡有关，这提示我们考虑gc通过快速的非基因组作用激活的mapks是否与海马细胞的可塑性以及凋亡有关。鉴于gc可以激活mapks ，其中持续的高水平激活p38和jnk又有转位入核的现象，我们认为gc快速的激活mapks后，可以引导出基因组活动。
Other neuroscientists also confirmed the existence of the mrd in the neostriatum with immunohistochemical or physiological method [ 14 , 15 ] " . heimer and his colleagues described the mrd as one part of the ventral striatal areas . in order to investigate the electrophysiology property of the nmdar , we observe the single channel properties of nmda receptors in the acutely dissociated neurons of the marginal division in the rat striatum , and to compare them to those of nmdar in the hippocampus , cortox and cerebellum 在中枢神经发育的过程中， nmda受体通过不同亚型的选择性表达，改变自身的结构和功能，进而影响nmda受体介导的ca2 +内流，调节神经元内ca2 +依赖的第二信使系统，并引起海马的长时程增强( long - term - potentiation , ltp )和小脑长时程抑制( long - term - depression , ltd )的产生，人们普遍认为这是学习记忆的神经生物学和电生理学基础。
