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Interplay of different synchronization modes and synaptic plasticity in a system of class I neurons.

ABSTRACT: We analyze the effect of spike-timing-dependent plasticity (STDP) on a system of pulse-coupled class I neurons. Our research begins with a system of two mutually connected quadratic integrate-and-fire (QIF) neurons, which are canonical representatives of class I neurons. Along with various asymptotic modes previously observed in other neuronal models with plastic synapses, we found a stable synchronous mode characterized by unidirectional link from a slower neuron to a faster neuron. In this frequency-locked mode, the faster neuron emits multiple spikes per cycle of the slower neuron. We analytically obtain the Arnold tongues for this mode without STDP and with STDP. We also consider larger plastic networks of QIF neurons and show that the detected mode can manifest itself in such a way that slow neurons become pacemakers. As a result, slow and fast neurons can form large synchronous clusters that generate low-frequency oscillations. We demonstrate the generality of the results obtained with two connected QIF neurons using Wang-Buzsáki and Morris-Lecar biophysically plausible class I neuron models.

SUBMITTER: Ratas I

PROVIDER: S-EPMC9668974 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature

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Interplay of different synchronization modes and synaptic plasticity in a system of class I neurons.

Ratas Irmantas I Pyragas Kestutis K

Scientific reports 20221116 1

We analyze the effect of spike-timing-dependent plasticity (STDP) on a system of pulse-coupled class I neurons. Our research begins with a system of two mutually connected quadratic integrate-and-fire (QIF) neurons, which are canonical representatives of class I neurons. Along with various asymptotic modes previously observed in other neuronal models with plastic synapses, we found a stable synchronous mode characterized by unidirectional link from a slower neuron to a faster neuron. In this fre ...[more]

PMID: 36385488

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Project description:The descending auditory system modulates the ascending system at every level. The final descending, or efferent, stage comprises lateral olivocochlear and medial olivocochlear (MOC) neurons. MOC somata in the ventral brainstem project axons to the cochlea to synapse onto outer hair cells (OHC), inhibiting OHC-mediated cochlear amplification. MOC suppression of OHC function is implicated in cochlear gain control with changing sound intensity, detection of salient stimuli, attention and protection against acoustic trauma. Thus, sound excites MOC neurons to provide negative feedback of the cochlea. Sound also inhibits MOC neurons via medial nucleus of the trapezoid body (MNTB) neurons. However, MNTB-MOC synapses exhibit short-term depression, suggesting reduced MNTB-MOC inhibition during sustained stimuli. Further, due to high rates of both baseline and sound-evoked activity in MNTB neurons in vivo, MNTB-MOC synapses may be tonically depressed. To probe this, we characterized short-term plasticity of MNTB-MOC synapses in mouse brain slices. We mimicked in vivo-like temperature and extracellular calcium conditions, and in vivo-like activity patterns of fast synaptic activation rates, sustained activation and prior tonic activity. Synaptic depression was sensitive to extracellular calcium concentration and temperature. During rapid MNTB axon stimulation, postsynaptic currents in MOC neurons summated but with concurrent depression, resulting in smaller, sustained currents, suggesting tonic inhibition of MOC neurons during rapid circuit activity. Low levels of baseline MNTB activity did not significantly reduce responses to subsequent rapid activity that mimics sound stimulation, indicating that, in vivo, MNTB inhibition of MOC neurons persists despite tonic synaptic depression. KEY POINTS: Inhibitory synapses from the medial nucleus of the trapezoid body (MNTB) onto medial olivocochlear (MOC) neurons exhibit short-term plasticity that is sensitive to calcium and temperature, with enhanced synaptic depression occurring at higher calcium concentrations and at room temperature. High rates of background synaptic activity that mimic the upper limits of spontaneous MNTB activity cause tonic synaptic depression of MNTB-MOC synapses that limits further synaptic inhibition. High rates of activity at MNTB-MOC synapses cause synaptic summation with concurrent depression to yield a response with an initial large amplitude that decays to a tonic inhibition.

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Interplay of different synchronization modes and synaptic plasticity in a system of class I neurons.

Publications

Interplay of different synchronization modes and synaptic plasticity in a system of class I neurons.

Similar Datasets

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