Asynchronous Glutamate Release at Autapses Regulates Spike Reliability and Precision in Mouse Neocortical Pyramidal Cells. (7th December 2020)

• Record Type: Journal Article
• Authors: Li, Junlong; Deng, Suixin; He, Quansheng; Ke, Wei; Shu, Yousheng
• Is Part Of: Cerebral cortex. Volume 31:Number 4(2021)
• Page Start: 2278
• Page End: 2290
• Publication Date: 2020-12-07
• Subjects: action potential -- asynchronous release -- autapse -- prefrontal cortex -- pyramidal cell; Cerebral cortex -- Periodicals; Brain -- Periodicals; 612.825
• DOI: 10.1093/cercor/bhaa361
• Languages: English
• ISSNs: 1047-3211

Abstract

Abstract: Autapses are self-synapses of a neuron. Inhibitory autapses in the neocortex release GABA in 2 modes, synchronous release and asynchronous release (AR), providing precise and prolonged self-inhibition, respectively. A subpopulation of neocortical pyramidal cells (PCs) also forms functional autapses, activation of which promotes burst firing by strong unitary autaptic response that reflects synchronous glutamate release. However, it remains unclear whether AR occurs at PC autapses and plays a role in neuronal signaling. We performed whole-cell recordings from layer-5 PCs in slices of mouse prefrontal cortex (PFC). In response to action potential (AP) burst, 63% of PCs showed robust long-lasting autaptic AR, much stronger than synaptic AR between neighboring PCs. The autaptic AR is mediated predominantly by P/Q-type Ca 2+ channels, and its strength depends on the intensity of PC activity and the level of residual Ca 2+ . Further experiments revealed that autaptic AR enhances spiking activities but reduces the temporal precision of post-burst APs. Together, the results show the occurrence of AR at PC autapses, the delayed and persistent glutamate AR causes self-excitation in individual PCs but may desynchronize the autaptic PC population. Thus, glutamatergic autapses should be essential elements in PFC and contribute to cortical information processing.