Autaptic Strength Research Articles

Inhibitory autapses enhance coherence resonance of a neuronal network

The counterintuitive phenomenon that inhibitory autapses enhance coherence resonance (CR) is investigated in a Hodgkin–Huxley neuronal network, which can be well interpreted by post-inhibitory rebound (PIR) spikes. Noise can induce CR in the network with excitatory coupling. After introducing inhibitory autapses, multiple CRs induced by noise appear at multiple time delays of inhibitory autapses. The degree of CRs can be enhanced by inhibitory autapses with time delays approximating to 10 ms or the sum of 10 ms and multiples of the firing period. For these time delays, each delayed inhibitory current pulse can induce a PIR spike, which is a signature of the stable focus near the Hopf bifurcation. The degree of CRs can be reduced by inhibitory autapses for time delays nearly equaling multiples of the firing period, because the inhibitory autaptic current pulses take effect near the spikes, resulting in the reduced irregularity of the spikes. More detailed dynamics of CR is investigated in planes composed of every two parameters out of the noise intensity, the autaptic strength, and the time delay. The counterintuitive phenomenon that inhibitory autapses can enhance the CR degree is in contrast to the conventional notion that inhibitory effects suppress the neuronal activities, which not only enriches the content of nonlinear dynamics, but also provides an approach to modulate CR or the firing regularity of neuronal networks.

Nonlinear mechanism of excitatory autapse-induced reduction or enhancement of firing frequency of neuronal bursting

Excitatory and inhibitory effect always induces the enhancement and inhibitory effect of neural electronic activities, which is the common viewpoint of the modulations to the neural firing and plays important roles in the information processing of the nervous system. In the present paper, the Homoclinic/Homoclinic bursting pattern with alternation behavior between burst containing multiple spikes and subthreshold oscillations and the tough value of the burst lower than that of the subthreshold oscillations is chosen as representative, and the excitatory effect on the complex nonlinear dynamics of the representative bursting pattern is studied. For the excitatory autapse with suitable autaptic time delay and strength, the autaptic current pulse applied to the trough of the burst can induce the number of spikes within a burst to decrease and then the average firing frequency to decline, which presents a novel example different from the common viewpoint of the excitatory effect. The excitatory autapse induces the average firing frequency to increase in the remained parameter region of two-parameter plane of the autaptic time delay and strength. With bifurcations acquired by the fast/slow variable dissection method and phase trajectory, the subthreshold oscillations of the bursting correspond to a subthreshold limit cycle of the fast subsystem and the spike within burst corresponds to a suprathreshold limit cycle, and excitatory autaptic current can induce the transition from suprathreshold limit cycle to subthreshold limit cycle, which leads the spike to terminate in advance and is the cause for reducing the average firing frequency. The results is the present paper are compared with the phenomenon and bifurcation mechanism that the excitatory autapse can induce the spike number to decrease within a burst but the average firing frequency to increase as indicated in a recent study on the Fold/Homoclinic bursting. These results enrich the uncommon phenomenon of the neuronal electrical activities, reveal the underlying nonlinear mechanism, provide a new way to regulate the bursting pattern, and disclose the potential functions of the excitatory autapse.

Strong preference for autaptic self-connectivity of neocortical PV interneurons facilitates their tuning to γ-oscillations.

Parvalbumin (PV)-positive interneurons modulate cortical activity through highly specialized connectivity patterns onto excitatory pyramidal neurons (PNs) and other inhibitory cells. PV cells are autoconnected through powerful autapses, but the contribution of this form of fast disinhibition to cortical function is unknown. We found that autaptic transmission represents the most powerful inhibitory input of PV cells in neocortical layer V. Autaptic strength was greater than synaptic strength onto PNs as a result of a larger quantal size, whereas autaptic and heterosynaptic PV-PV synapses differed in the number of release sites. Overall, single-axon autaptic transmission contributed to approximately 40% of the global inhibition (mostly perisomatic) that PV interneurons received. The strength of autaptic transmission modulated the coupling of PV-cell firing with optogenetically induced γ-oscillations, preventing high-frequency bursts of spikes. Autaptic self-inhibition represents an exceptionally large and fast disinhibitory mechanism, favoring synchronization of PV-cell firing during cognitive-relevant cortical network activity.

Bifurcations of enhanced neuronal bursting activities induced by the negative current mediated by inhibitory autapse

In contrast to the traditional viewpoint that inhibitory effect can often induce the reduction of neural firing activities, negative self-feedback current mediated by inhibitory autapse is identified to enhance neuronal bursting activities in the Chay model composed of fast and slow subsystems. With increasing autaptic strength of the autapse, bursting patterns exhibit period-adding bifurcations, which leads to the increase in the mean firing frequency. Such a phenomenon can be well interpreted with fast–slow variable dissection and bifurcation analysis to the bursting patterns. The initial and termination phases of the burst correspond to a saddle-node bifurcation and a saddle-homoclinic (SH) bifurcation of the fast subsystem, respectively. With increasing the autaptic strength, the termination phase of the burst delays and the initial phase remains nearly unchanged. Therefore, the width of the burst becomes wider to contain more spikes, which leads to the period-adding bifurcations and the increases of mean firing frequency. The detailed relationship between the delay of termination phase (SH point) and the characteristic of the inhibitory autaptic current is identified. Moreover, the distinction between the present paper and the previous investigations of the enhancement of bursting activities induced by inhibitory current with time delay is discussed. Based on the results that inhibitory autapse without time delay can enhance bursting activities via bifurcation mechanism, a novel case of nonlinear dynamics in contrast to the traditional viewpoint of the inhibitory effect, a possible function of the autapse, a novel potential measure to modulate bursting activities are present.

Coherence resonance in a modified FHN neuron with autapse and phase noise

The influences of phase noise together with autapse on the resonance dynamics in a modified FitzHugh–Nagumo (FHN) neuron are investigated by numerical simulation, where the neuronal model is in the environment of electromagnetic induction. First, it is found that phase noise can induce double coherence resonances, which is further confirmed to be robust to the feedback gain of induction current. Surprisingly, by individually changing the period of phase noise and the feedback gain, a resonance-like behavior also appears. Subsequently, the significant phenomenon of autapse-induced multiple coherence resonances is discovered. Moreover, the phenomenon of multiple coherence resonances can emerge at a broad parameter range of autaptic strength and autaptic delay.

Multiple Actions of Rotenone, an Inhibitor of Mitochondrial Respiratory Chain, on Ionic Currents and Miniature End-Plate Potential in Mouse Hippocampal (mHippoE-14) Neurons

Background/Aims: Rotenone (Rot) is known to suppress the activity of complex I in the mitochondrial chain reaction; however, whether this compound has effects on ion currents in neurons remains largely unexplored. Methods: With the aid of patch-clamp technology and simulation modeling, the effects of Rot on membrane ion currents present in mHippoE-14 cells were investigated. Results: Addition of Rot produced an inhibitory action on the peak amplitude of I_Na with an IC₅₀ value of 39.3 µM; however, neither activation nor inactivation kinetics of I_Na was changed during cell exposure to this compound. Addition of Rot produced little or no modifications in the steady-state inactivation curve of I_Na. Rot increased the amplitude of Ca²⁺-activated Cl^- current in response to membrane depolarization with an EC₅₀ value of 35.4 µM; further addition of niflumic acid reversed Rot-mediated stimulation of this current. Moreover, when these cells were exposed to 10 µM Rot, a specific population of ATP-sensitive K⁺ channels with a single-channel conductance of 18.1 pS was measured, despite its inability to alter single-channel conductance. Under current clamp condition, the frequency of miniature end-plate potentials in mHippoE-14 cells was significantly raised in the presence of Rot (10 µM) with no changes in their amplitude and time course of rise and decay. In simulated model of hippocampal neurons incorporated with chemical autaptic connection, increased autaptic strength to mimic the action of Rot was noted to change the bursting pattern with emergence of subthreshold potentials. Conclusions: The Rot effects presented herein might exert a significant action on functional activities of hippocampal neurons occurring in vivo.

Influences of autapse and channel blockage on multiple coherence resonance in a single neuron

We study how the spiking regularity of a single stochastic Hodgkin–Huxley neuron is effected in the presence of ion channel blocking and autaptic connection. In this study, we consider a chemical autapse expressed by its coupling strength and delay time. It is found that the neuron exhibits multiple coherence resonance (MCR) behavior induced by autaptic time delay at an appropriate level of ion channel blocking and autaptic coupling strength. This MCR behavior increases with the decrement of working potassium ion channels, whereas it decreases or completely disappears with the increment of a fraction of sodium ion channels blocking, regardless of autaptic coupling strength. Furthermore, this behavior is more explicit at intermediate autaptic coupling strength regardless of the ion channel blocking type. We briefly discuss the obtained results with the underlying reasons in terms of ion channel blocking type and autapse parameters. We also showed that ion channel noise, thus membrane patch size, should be at an optimal level to obtain MCR behavior otherwise, this behavior would be destroyed. The obtained results also showed that autaptic time delay is more operative on regularity than its coupling strength regardless of ion channel blocking. Considering the importance of spiking regularity on neuronal information processing, our results may help to understand the intersection of ion channel blocking and autaptic connections of a single neuron.

Autapse-induced multiple stochastic resonances in a modular neuronal network.

This study investigates the nontrivial effects of autapse on stochastic resonance in a modular neuronal network subjected to bounded noise. The resonance effect of autapse is detected by imposing a self-feedback loop with autaptic strength and autaptic time delay to each constituent neuron. Numerical simulations have demonstrated that bounded noise with the proper level of amplitude can induce stochastic resonance; moreover, the noise induced resonance dynamics can be significantly shaped by the autapse. In detail, for a specific range of autaptic strength, multiple stochastic resonances can be induced when the autaptic time delays are appropriately adjusted. These appropriately adjusted delays are detected to nearly approach integer multiples of the period of the external weak signal when the autaptic strength is very near zero; otherwise, they do not match the period of the external weak signal when the autaptic strength is slightly greater than zero. Surprisingly, in both cases, the differences between arbitrary two adjacent adjusted autaptic delays are always approximately equal to the period of the weak signal. The phenomenon of autaptic delay induced multiple stochastic resonances is further confirmed to be robust against the period of the external weak signal and the intramodule probability of subnetwork. These findings could have important implications for weak signal detection and information propagation in realistic neural systems.

Autaptic effects on synchrony of neurons coupled by electrical synapses

In this paper, we numerically study the effects of a special synapse known as autapse on synchronization of population of Morris-Lecar (ML) neurons coupled by electrical synapses. Several configurations of the ML neuronal populations such as a pair or a ring or a globally coupled network with and without autapses are examined. While most of the papers on the autaptic effects on synchronization have used networks of neurons of same spiking rate, we use the network of neurons of different spiking rates. We find that the optimal autaptic coupling strength and the autaptic time delay enhance synchronization in our neural networks. We use the phase response curve analysis to explain the enhanced synchronization by autapses. Our findings reveal the important relationship between the intraneuronal feedback loop and the interneuronal coupling.

Effect of Autaptic Activity on Intrinsic Coherence Resonance in Newman–Watts Networks of Stochastic Hodgkin–Huxley Neurons

In this paper, we study the effect of autaptic activity on intrinsic coherence resonance (CR) induced by channel noise in Newman–Watts (NW) networks of stochastic Hodgkin–Huxley (HH) neurons. It is found that autaptic strength and autaptic delay have a big effect on the intrinsic CR. As autaptic strength increases, there is optimal autaptic strength by which the intrinsic CR is most highly enhanced. Autaptic delay can enhance, reduce, or destroy the intrinsic CR, depending on the delay length. Moreover, there are optimal coupling strength and network randomness by which autaptic activity can most highly enhance the intrinsic CR. These results show that autaptic activity has different effects on the intrinsic CR in the neuronal networks, and it can most highly enhance the intrinsic CR at optimal coupling strength and network randomness. These findings could find potential implications of channel noise and autaptic activity for the information processing and transmission in neural systems.

Mutual and intermittent enhancements of synchronization transitions by autaptic and synaptic delay in scale-free neuron networks

In neural networks, there exist both synaptic delays among different neurons and autaptic self-feedback delays in a neuron itself. In this paper, we study synchronization transitions induced by synaptic and autaptic delays in scale-free neuron networks, mainly exploring how these two time delays affect synchronization transitions induced by each other. It is found that the synchronization transitions induced by synaptic (autaptic) delay are intermittently enhanced when autaptic (synaptic) delay is varied. There are optimal autaptic strength and synaptic coupling strength by which the synchronization transitions induced by autaptic and synaptic delays become strongest. The underlying mechanisms are briefly discussed in terms of the relationships of autaptic delay, synaptic delay, and inter-burst interval. These results show that synaptic and autaptic delays could contribute to each other and enhance synchronization transitions in the neuronal networks. This implies that autaptic and synaptic delays could play a vital role for the information transmission in neural systems.

Enhancement of pacemaker induced stochastic resonance by an autapse in a scale-free neuronal network

An autapse is an unusual synapse that occurs between the axon and the soma of the same neuron. Mathematically, it can be described as a self-delayed feedback loop that is defined by a specific time-delay and the so-called autaptic coupling strength. Recently, the role and function of autapses within the nervous system has been studied extensively. Here, we extend the scope of theoretical research by investigating the effects of an autapse on the transmission of a weak localized pacemaker activity in a scale-free neuronal network. Our results reveal that by mediating the spiking activity of the pacemaker neuron, an autapse increases the propagation of its rhythm across the whole network, if only the autaptic time delay and the autaptic coupling strength are properly adjusted. We show that the autapse-induced enhancement of the transmission of pacemaker activity occurs only when the autaptic time delay is close to an integer multiple of the intrinsic oscillation time of the neurons that form the network. In particular, we demonstrate the emergence of multiple resonances involving the weak signal, the intrinsic oscillations, and the time scale that is dictated by the autapse. Interestingly, we also show that the enhancement of the pacemaker rhythm across the network is the strongest if the degree of the pacemaker neuron is lowest. This is because the dissipation of the localized rhythm is contained to the few directly linked neurons, and only afterwards, through the secondary neurons, it propagates further. If the pacemaker neuron has a high degree, then its rhythm is simply too weak to excite all the neighboring neurons, and propagation therefore fails.

Autaptic pacemaker mediated propagation of weak rhythmic activity across small-world neuronal networks

We study the effects of an autapse, which is mathematically described as a self-feedback loop, on the propagation of weak, localized pacemaker activity across a Newman–Watts small-world network consisting of stochastic Hodgkin–Huxley neurons. We consider that only the pacemaker neuron, which is stimulated by a subthreshold periodic signal, has an electrical autapse that is characterized by a coupling strength and a delay time. We focus on the impact of the coupling strength, the network structure, the properties of the weak periodic stimulus, and the properties of the autapse on the transmission of localized pacemaker activity. Obtained results indicate the existence of optimal channel noise intensity for the propagation of the localized rhythm. Under optimal conditions, the autapse can significantly improve the propagation of pacemaker activity, but only for a specific range of the autaptic coupling strength. Moreover, the autaptic delay time has to be equal to the intrinsic oscillation period of the Hodgkin–Huxley neuron or its integer multiples. We analyze the inter-spike interval histogram and show that the autapse enhances or suppresses the propagation of the localized rhythm by increasing or decreasing the phase locking between the spiking of the pacemaker neuron and the weak periodic signal. In particular, when the autaptic delay time is equal to the intrinsic period of oscillations an optimal phase locking takes place, resulting in a dominant time scale of the spiking activity. We also investigate the effects of the network structure and the coupling strength on the propagation of pacemaker activity. We find that there exist an optimal coupling strength and an optimal network structure that together warrant an optimal propagation of the localized rhythm.

Autaptic self-feedback-induced synchronization transitions in Newman-Watts neuronal network with time delays

Autapse is a special synapse that connects a neuron to itself. In this work, we numerically study the effect of chemical autapse on the synchronization of Newman-Watts Hodgkin-Huxley neuron network with time delays. It is found that the neurons exhibit synchronization transitions as autaptic self-feedback delay is varied, and the phenomenon enhances when autaptic self-feedback strength increases. Moreover, this phenomenon becomes strongest when network time delay or coupling strength is optimal. It is also found that the synchronization transitions by network time delay can be enhanced by autaptic activity and become strongest when autaptic delay is optimal. These results show that autaptic delayed self-feedback activity can intermittently enhance and reduce the synchronization of the neuronal network and hence plays an important role in regulating the synchronization of the neurons. These findings could find potential implications for the information processing and transmission in neural systems.

Autaptic activity-induced synchronization transitions in Newman-Watts network of Hodgkin-Huxley neurons.

In this paper, we numerically study the effect of autapse on the synchronization of Newman-Watts small-world Hodgkin-Huxley neuron network. It is found that the neurons exhibit synchronization transitions as autaptic self-feedback delay is varied, and the phenomenon becomes strongest when autaptic self-feedback strength is optimal. This phenomenon also changes with the change of coupling strength and network randomness and become strongest when they are optimal. There are similar synchronization transitions for electrical and chemical autapse, but the synchronization transitions for chemical autapse occur more frequently and are stronger than those for electrical synapse. The underlying mechanisms are briefly discussed in quality. These results show that autaptic activity plays a subtle role in the synchronization of the neuronal network. These findings may find potential implications of autapse for the information processing and transmission in neural systems.

Control of bursting behavior in neurons by autaptic modulation

Firing properties of biological neurons have long been recognized to be determined by extrinsic synaptic afferents that neurons receive and intrinsic ionic mechanisms that neurons possess, however, previous researches have also demonstrated that firing behavior of single neurons can be modulated by the neurons themselves, realized by the autapses. Thus in this investigation, we argued that how autaptic modulations shape the bursting behavior of biological neurons. We considered the issue from the following two aspects: autaptic-excitation and -inhibition. Our results suggested that for autaptic-excitation, under the condition of relatively weak stimulus, regular bursting was more incline to occur when the autaptic strength was weak, while regular spiking was more likely to appear when the autaptic strength was strong. However, larger stimulus would diminish the portion of bursting, but increase the portion of spiking. For autaptic-inhibition, under relatively weak stimulus, a wide range of regular bursting emerges when the autaptic strength was small, but when stronger stimulus were applied, the range of regular bursting shrinked into a small region. Meanwhile, we observed that synaptic delays have no obvious effects in the case of autaptic-excitation, while a subtle effect of synaptic delays was observed in the case of autaptic-inhibition. These results showed that bursting behavior of neurons could be controlled and modulated by the autaptic mechanisms that biological neurons intrinsically possess, and the final results may further promote the understanding in the generation of various neuronal firing patterns.