On Dec 1st, 2010, a research article from the Laboratory of Dendrite Development and Neural Circuit Formation entitled "Postsynaptic spiking homeostatically induces cell-autonomous regulation of inhibitory inputs via retrograde signaling" was published as a cover article in the Journal of Neuroscience. This work was carried out by graduate students Yi-Rong Peng and Si-Yu Zeng under the supervision of Dr. Xiang Yu.

Developing neural circuits face the dual challenge of growing in an activity-induced fashion and maintaining stability through homeostatic mechanisms. Compared to our understanding of homeostatic regulation of excitatory synapses, relatively little is known about the mechanism mediating homeostatic plasticity of inhibitory synapses, especially that following activity elevation. Yi-Rong Peng and Si-Yu Zeng found that elevating neuronal activity in cultured hippocampal neurons for 4 hours significantly induced homeostatic up-regulation of inhibitory synaptic transmission, before detectable change at excitatory synapses. Consistently, increases in the density of GABAergic synapses were observed. This rapid, activity-induced regulation of inhibitory synaptic transmission occurred cell-autonomously, requiring change in the firing activity of individual postsynaptic neurons and retrograde signaling to inputting presynaptic inhibitory terminals by brain-derived neurotrophic factor (BDNF). Importantly, elevating activity in vivo by kainate injection increased inhibitory synaptic transmission in CA1 pyramidal neurons. Thus, spiking-induced, cell-autonomous upregulation of GABAergic synaptic inputs, through retrograde BDNF signaling, represents an early adaptive response of neural circuits to elevated network activity.

This work was supported by the grants from the Chinese Academy of Sciences, the Ministry of Science and Technology and the National Natural Science Foundation of China.