PKA-dependent regulation of synaptic enhancement between a buccal motor neuron and its regulatory interneuron in Lymnaea stagnalis
PKA-dependent regulation of synaptic enhancement between a buccal motor neuron and its regulatory interneuron in Lymnaea stagnalis
复制标题
DOI：
10.2108/zsj.16.387
复制
发表时间：
1999-06-01
影响因子：
0.9
通讯作者：
Ito, E
中科院分区：
文献类型：
--
作者：
Nakamura, H;Kobayashi, S;Ito, E
脑巨细胞（CGC）是一种重要的细胞因子，在调节池螺摄食反应中起重要作用。然而，从CGC到下面的颊运动神经元的信号转导机制尚不清楚。在本研究中，我们研究是否环磷酸腺苷（cAMP）依赖性蛋白激酶（PKA）有助于增强突触前CGC和突触后颊运动神经元1（B1细胞）之间的单突触连接。cAMP注入CGC或抑制磷酸二酯酶的异丁基甲基黄嘌呤在CGC增加兴奋性突触后电位（EPSP）在B1细胞的振幅，而没有变化的CGC的电特性检测。在B1细胞的突触增强被完全阻断的抑制PKA在CGC，但不需要从头蛋白质合成由于PKA磷酸化。B1细胞EPSP振幅的增加与CGC释放5-羟色胺量的增加有关。这些结果为PKA直接调节L. stagnalis，表明完全不同的机制，从充分研究的虹吸和鳃回缩反射在Aesthesia。
The cerebral giant cell (CGC) is known to play a crucial role in the regulation of feeding response in the pond snail, Lymnaea stagnalis. However, the mechanisms of signal transduction from the CGC to the following buccal motor neurons are not clear. In the present study, we examined whether cyclic AMP (cAMP)-dependent protein kinase (PKA) contributes to enhancement of a monosynaptic connection between the presynaptic CGC and the postsynaptic buccal motor neuron 1 (B1 cell). Injection of cAMP into the CGC or inhibition of phosphodiesterase by isobutylmethylxanthine in the CGC increased the amplitude of excitatory postsynaptic potential (EPSP) in the B1 cell, whereas no changes were detected in the electrical properties of the CGC. The synaptic enhancement in the B1 cell was completely blocked by inhibition of PKA in the CGC but did not require a de novo protein synthesis due to a PKA phosphorylation. The increase in the EPSP amplitude of B1 cell was associated with the increase in the amount of serotonin release from the CGC. These results hence provided the physiological evidence of the direct regulation of a synaptic enhancement by PKA in the CNS of L. stagnalis, indicating the completely different mechanism from that in the well-studied siphon- and gill-withdrawal reflex in Aplysia.