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Functional Self-Excitatory Autapses (Auto-Synapses) on Neocortical Pyramidal Cells

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Functional Self-Excitatory Autapses (Auto-Synapses) on Neocortical Pyramidal Cells Neurosci. Bull. December, 2019, 35(6):1106–1109 www.neurosci.cn https://doi.org/10.1007/s12264-019-00391-8 www.springer.com/12264 INSIGHT Functional Self-Excitatory Autapses (Auto-synapses) on Neocortical Pyramidal Cells 1 1 1 Wei Ke • Quansheng He • Yousheng Shu Received: 27 February 2019 / Accepted: 9 March 2019 / Published online: 16 May 2019 Ó Shanghai Institutes for Biological Sciences, CAS 2019 Synapses are essential structures in the nervous system and potentials (APs) [7, 9–12]. The temporal separation of APs normally form between two cells. However, some occur in a and autaptic responses is due to the narrow AP waveforms single neuron between the axon and its own dendrites and in these neurons. However, because PCs generate much soma. These special synapses are known as autapses (or auto- broader APs than GABAergic cells, autaptic responses synapses or self-synapses) [1]. Previous studies have shown might be masked by the AP waveforms [13]. Our recent that autapses were much more abundant in cultured neurons study tackled this waveform-overlapping problem and [2–4] than in the intact brain, so there was suspicion that provided the first piece of physiological evidence showing autapses in vivo may be wiring errors or redundant structures that neocortical PCs form functional autapses [8]. [5]. However, accumulating evidence indicates that autapses Just like paired recordings from pre- and postsynaptic are actually abundant in certain types of neurons [6]. They cells to examine unitary synaptic transmission, we per- selectively form on fast-spiking GABAergic interneurons but formed simultaneous recordings from the soma (postsy- not on low-threshold spiking interneurons [6, 7]. Recently, we naptic) and the axon (presynaptic) of a single layer V PC in showed that autapses selectively occur on subcortically- prefrontal cortical (PFC) slices [14] and isolated the two projecting layer V pyramidal cells (PCs); they produced giant compartments by 2-photon laser axotomy. Therefore, the AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic evoked axonal action potentials (APs) would not reach the acid)-only postsynaptic responses and promoted burst firing soma by back-propagation and mask autaptic responses. and coincidence detection [8]. Therefore, PC autapses are The short onset latency of these responses (\ 2 ms) agrees important circuit elements in the intact brain, and their role in well with monosynaptic transmission. Since they were regulating cortical information-processing needs to be con- completely blocked by the AMPA/kainic acid receptor sidered seriously. antagonist CNQX, they were actually autaptic excitatory postsynaptic currents (aEPSCs) mediated by ionotropic glutamate receptors. Furthermore, our experiments using Neocortical PCs Form Autapses: Physiological Sr2?-containing bath solution also revealed the occurrence Evidence of autapses in PCs. Since Sr2? delays and prolongs neurotransmitter release, aEPSCs that normally overlap Electrophysiological recordings in GABAergic neurons with APs were unmasked and readily detectable. Indeed, have revealed the occurrence of autapse-mediated inhibi- we recorded desynchronized autaptic events, which only tory postsynaptic currents (IPSCs) immediately after action occurred in the stimulated PC, and not in unstimulated neighboring PC. These results suggest that the desynchro- nized events are due to monosynaptic release at autapses, & Yousheng Shu not through polysynaptic transmission. If transmission was [email protected] polysynaptic, the neighboring PCs in some of the paired 1 recordings would also receive delayed synaptic inputs. State Key Laboratory of Cognitive Neuroscience and 2? Learning, IDG/McGovern Institute for Brain Research, Further experiments in a Sr bath containing tetrodotoxin Beijing Normal University, Beijing 100875, China (TTX) that blocks AP generation and thus abolishing 123 W. Ke et al.: Autapses of pyramidal cells 1107 polysynaptic transmission showed desynchronized autaptic (\ 1) was lower than that of EPSCs ([ 1), indicating a events, confirming monosynaptic transmission. In these higher release probability at PC autapses. Close examina- experiments, Cs?-containing pipette solution blocks K? tion of the reconstructed PCs revealed more putative channels and the recorded cell is electrically more com- autaptic contacts than PC-PC synaptic contacts. Thus, the pact, so somatic depolarization would reach the autapses higher release probability and more autaptic contacts may and trigger neurotransmitter release. contribute to the generation of giant aEPSCs. Anatomical observation also revealed a preference for autapse forma- tion at the basal dendrites, relatively close to the soma Selective Formation of Autapses in A Subpopula- (\ 100 lm from the soma). tion of Neocortical PCs Previous studies have demonstrated that recurrent PC- PC synapses contain both N-methyl-D-aspartate (NMDA) Using Golgi preparations of the rabbit occipital cortex, Van and non-NMDA receptors. To determine whether autapses der Loos and Glasers found self-innervating synapses in express NMDA receptors, we performed experiments with half of the PCs examined [1]. Later anatomical studies in aCs?-based pipette solution and a modified bath solution: electrophysiologically-recorded PCs reported inconsistent replacing Ca2? with Sr2? to desynchronize glutamate results. Most of the recorded layer V PCs (80%) in release; omitting Mg2? but adding glycine or D-serine to somatosensory cortical slices of juvenile rats possess enhance NMDA receptor activity at negative membrane autaptic contacts [13], whereas only 10% of the PCs in potentials; adding picrotoxin to block fast inhibitory the superficial layers (layers II–IV) in adult cat visual postsynaptic potentials; and adding TTX to block APs cortex have autapses [6]. Typical synaptic structure of and epileptiform activity. The Cs? pipette solution made autapses was revealed by electron microscopy in both the cell more electrically compact. Voltage pulses at the studies. Since GABAergic autapses only occur in fast- soma caused long-lasting desynchronized aEPSC events. spiking interneurons but not low-threshold spiking These events were completely blocked by NBQX, a interneurons [6, 7], it is of interest to know whether the selective AMPA/kainic acid receptor antagonist, indicating abundance of autaptic PCs is cell-type-specific. the absence of NMDA components. Consistently, the In our experiments, we used two approaches to investigate NMDA receptor antagonist APV had no effect on the the abundance of PC autapses in cortical slices. In the paired decay time constant of mini-aEPSCs. However, it reduced soma-axon recording experiments together with 2-photon the decay time constant of mini-EPSCs (presumably from axotomy, we found that * 55% of the layer V PCs showed other PCs). Therefore, autapses tend not to express NMDA autaptic responses. Adding Sr2? to the bath provided an receptors. efficient way to assess the abundance of autapses on PCs. In Apparently, the physiological properties of autapses thepresenceofSr2?, the percentage of layer V PCs with differ from those of PC-PC synapses. Future electron autapses was similar to that in the axotomy experiments. In microscopic studies are required for the examination of sharp contrast, considerably fewer layer II/III PCs (* 12%) autaptic contacts and the expression of NMDA receptors in exhibited autaptic responses. Among the layer V PCs, different synapses. It remains unknown whether individual subcortically-projecting cells tended to have autapses (up to autaptic contacts have larger numbers of release sites. 85%), whereas those projecting to the contralateral PFC tended not to form autapses (only 3%). These results indicate a selective formation of autapses in layer V PCs projecting to Physiological Function of PC Autapses subcortical regions, such as the pontine nuclei and the habenula. The inconsistent anatomical observations noted Autapses in GABAergic interneurons produce IPSCs above might be attributable to differences among the cortical immediately after individual APs [7, 9–12]. This self- layers. However, whether the abundance of autaptic PCs inhibition suppresses AP generation [7] and increases depends on species, brain region, and age needs to be further spiking precision in neocortical fast-spiking interneurons examined. [9]. In addition, neurotransmission at GABAergic autapses can also be asynchronous under physiological conditions [10, 11](i.e. vesicle release is not tightly coupled to PC Autapses Produce Giant AMPA-Only Autaptic individual APs, similar to the Sr2?-induced desynchronized Responses release); delayed and prolonged asynchronous GABA release at autapses induced by high-frequency firing Compared with the EPSCs between two layer V PCs, the reduces the reliability of subsequent APs in fast-spiking aEPSCs were much larger, * 5-fold greater in amplitude interneurons [11]. These studies reveal an important role of than PC-PC EPSCs. The paired-pulse ratio of aEPSCs GABAergic autapses in regulating neuronal signaling. For 123 1108 Neurosci. Bull. December, 2019, 35(6):1106–1109 Fig. 1 Glutamatergic autapses selectively form in layer V PCs reliably cause postsynaptic responses and spiking activity (due to projecting to subcortical regions. PC autapses produce giant AMPA- supralinear summation) in the target regions, thus enhancing func- only autaptic postsynaptic responses, which promote burst firing and tional connectivity between remote brain regions. Note that the axon the coincidence-detection
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