Blitz Dawn M, Beenhakker Mark P, Nusbaum Michael P
Department of Neuroscience, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-6074, USA.
J Neurosci. 2004 Dec 15;24(50):11381-90. doi: 10.1523/JNEUROSCI.3219-04.2004.
Considerable research has focused on issues pertaining to sensorimotor integration, but in most systems precise information remains unavailable regarding the specific pathways by which different sensory systems regulate any single central pattern-generating circuit. We address this issue by determining how two muscle stretch-sensitive neurons, the gastropyloric receptor neurons (GPRs), influence identified projection neurons that regulate the gastric mill circuit in the stomatogastric nervous system of the crab and then comparing these actions with those of the ventral cardiac neuron (VCN) mechanosensory system. Here, we show that the GPR neurons activate the gastric mill rhythm in the stomatogastric ganglion (STG) via their excitation of two identified projection neurons, modulatory commissural neuron 1 (MCN1) and commissural projection neuron 2 (CPN2), in the commissural ganglion. Support for this conclusion comes from the ability of the modulatory proctolin neuron (MPN), a projection neuron that suppresses the gastric mill rhythm via its inhibitory actions on MCN1 and CPN2, to inhibit the GPR-elicited gastric mill rhythm. Selective elimination of MCN1 and CPN2 access to the STG also prevents GPR activation of this rhythm. The VCN neurons also elicit the gastric mill rhythm by coactivating MCN1 and CPN2, but the GPR-elicited gastric mill rhythm is distinct. These distinct rhythms are likely to result partly from different MCN1 activity levels under these two conditions and partly from the presence of additional GPR actions in the STG. These results support the hypothesis that different sensory systems differentially regulate neuronal circuit activity despite their convergent actions on a single subpopulation of projection neurons.
大量研究聚焦于与感觉运动整合相关的问题,但在大多数系统中,关于不同感觉系统调节任何单个中枢模式发生器回路的具体途径,仍缺乏精确信息。我们通过确定两种肌肉拉伸敏感神经元,即胃幽门受体神经元(GPRs),如何影响蟹口胃神经系统中调节胃磨回路的已确定投射神经元,然后将这些作用与腹侧心神经元(VCN)机械感觉系统的作用进行比较,来解决这个问题。在这里,我们表明GPR神经元通过兴奋联合神经节中的两种已确定投射神经元,即调制联合神经元1(MCN1)和联合投射神经元2(CPN2),激活口胃神经节(STG)中的胃磨节律。这一结论的依据是,调制普罗托林神经元(MPN),一种通过对MCN1和CPN2的抑制作用来抑制胃磨节律的投射神经元,能够抑制GPR引发的胃磨节律。选择性消除MCN1和CPN2进入STG的通路也会阻止GPR对这种节律的激活。VCN神经元也通过共同激活MCN1和CPN2引发胃磨节律,但GPR引发的胃磨节律是不同的。这些不同的节律可能部分源于这两种情况下不同的MCN1活动水平,部分源于STG中存在额外的GPR作用。这些结果支持了这样一种假设,即尽管不同感觉系统对单个投射神经元亚群有趋同作用,但它们对神经元回路活动的调节是有差异的。