Wang D, Maler L
Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):7133-8. doi: 10.1073/pnas.95.12.7133.
The electrosensory lateral line lobe (ELL) of the electric fish Apteronotus leptorhynchus is a layered medullary region receiving electroreceptor input that terminates on basal dendrites of interneurons and projection (pyramidal) cells. The molecular layer of the ELL contains two distinct glutamatergic feedback pathways that terminate on the proximal (ventral molecular layer, VML) and distal (dorsal molecular layer) apical dendrites of pyramidal cells. Western blot analysis with an antibody directed against mammalian Ca2+/calmodulin-dependent kinase 2, alpha subunit (CaMK2alpha) recognized a protein of identical size in the brain of A. leptorhynchus. Immunohistochemistry demonstrated that CaMK2 alpha expression in the ELL was restricted to fibers and terminals in the VML. Posttetanic potentiation (PTP) could be readily elicited in pyramidal cells by stimulation of either VML or DML in brain slices of the ELL. PTP in the VML was blocked by extracellular application of a CaMK2 antagonist (KN62) while intracellular application of KN62 or a CaMK2 inhibitory peptide had no effect, consistent with the presynaptic localization of CaMK2 alpha in VML. PTP in the dorsal molecular layer was not affected by extracellular application of KN62. Anti-Hebbian plasticity has also been demonstrated in the VML, but was not affected by KN62. These results demonstrate that, while PTP can occur independent of CaMK2, it is, in some synapses, dependent on this kinase.
线纹电鳗(Apteronotus leptorhynchus)的电感受侧线叶(ELL)是一个分层的延髓区域,接收电感受器输入,该输入终止于中间神经元和投射(锥体)细胞的基底树突上。ELL的分子层包含两条不同的谷氨酸能反馈通路,它们终止于锥体细胞的近端(腹侧分子层,VML)和远端(背侧分子层)顶端树突上。用针对哺乳动物Ca2+/钙调蛋白依赖性激酶2α亚基(CaMK2α)的抗体进行的蛋白质免疫印迹分析,在线纹电鳗的脑中识别出一种大小相同的蛋白质。免疫组织化学表明,ELL中CaMK2α的表达仅限于VML中的纤维和终末。通过刺激ELL脑片的VML或DML,可轻易在锥体细胞中诱发强直后增强(PTP)。VML中的PTP可被细胞外应用CaMK2拮抗剂(KN62)阻断,而细胞内应用KN62或CaMK2抑制性肽则无影响,这与CaMK2α在VML中的突触前定位一致。背侧分子层中的PTP不受细胞外应用KN62的影响。在VML中也证明了反赫布可塑性,但不受KN62影响。这些结果表明,虽然PTP可以独立于CaMK2发生,但在某些突触中,它依赖于这种激酶。