Lett Kawasi M, Garcia Veronica J, Temporal Simone, Bucher Dirk, Schulz David J
Division of Biological Sciences, University of Missouri-Columbia, Columbia, Missouri.
Whitney Laboratory for Marine Bioscience, University of Florida, St. Augustine, Florida; and.
J Neurophysiol. 2017 Sep 1;118(3):1749-1761. doi: 10.1152/jn.00383.2017. Epub 2017 Jun 28.
We studied the changes in sensitivity to a peptide modulator, crustacean cardioactive peptide (CCAP), as a response to loss of endogenous modulation in the stomatogastric ganglion (STG) of the crab Our data demonstrate that removal of endogenous modulation for 24 h increases the response of the lateral pyloric (LP) neuron of the STG to exogenously applied CCAP. Increased responsiveness is accompanied by increases in CCAP receptor (CCAPr) mRNA levels in LP neurons, requires de novo protein synthesis, and can be prevented by coincubation for the 24-h period with exogenous CCAP. These results suggest that there is a direct feedback from loss of CCAP signaling to the production of CCAPr that increases subsequent response to the ligand. However, we also demonstrate that the modulator-evoked membrane current () activated by CCAP is greater in magnitude after combined loss of endogenous modulation and activity compared with removal of just hormonal modulation. These results suggest that both receptor expression and an increase in the target conductance of the CCAP G protein-coupled receptor are involved in the increased response to exogenous hormone exposure following experimental loss of modulation in the STG. The nervous system shows a tremendous amount of plasticity. More recently there has been an appreciation for compensatory actions that stabilize output in the face of perturbations to normal activity. In this study we demonstrate that neurons of the crustacean stomatogastric ganglion generate apparent compensatory responses to loss of peptide neuromodulation, adding to the repertoire of mechanisms by which the stomatogastric nervous system can regulate and stabilize its own output.
我们研究了蟹类口胃神经节（STG）中对肽调节剂——甲壳类心脏活性肽（CCAP）的敏感性变化，以此作为对内源性调节缺失的一种反应。我们的数据表明，去除内源性调节24小时会增加STG的外侧幽门（LP）神经元对外源性施加的CCAP的反应。反应性增加伴随着LP神经元中CCAP受体（CCAPr）mRNA水平的升高，需要从头合成蛋白质，并且可以通过在24小时内与外源性CCAP共同孵育来预防。这些结果表明，从CCAP信号缺失到CCAPr产生存在直接反馈，这会增加随后对配体的反应。然而，我们还证明，与仅去除激素调节相比，在内源性调节和活动联合缺失后，由CCAP激活的调节剂诱发的膜电流（）幅度更大。这些结果表明，受体表达和CCAP G蛋白偶联受体的靶电导增加都参与了STG实验性调节缺失后对外源性激素暴露反应的增加。神经系统表现出极大的可塑性。最近，人们认识到了在面对正常活动受到干扰时稳定输出的补偿作用。在本研究中，我们证明了甲壳类口胃神经节的神经元对肽神经调节的缺失产生明显的补偿反应，这增加了口胃神经系统调节和稳定自身输出的机制。
