Feedback and Feedforward Inhibition May Resonate Distinctly in the Ripple Symphony

Abstract

Review of Donoso et al. Hippocampal sharp waves are transient deflections of local field potentials (LFPs) recorded in the stratum radiatum of CA1 during immobility and slow-wave sleep. Ripple oscillations are superimposed on sharp waves, but they emerge from the stratum pyramidale. These sharp-wave ripple complexes are considered a biomarker for episodic memory (Buzsáki, 2015). Data from normal (Sullivan et al., 2011) and epileptic hippocampus (Valero et al., 2017) suggest that the complex spectral structure of ripples cannot be explained by simple mechanisms. Nonetheless, a recent computational study published in The Journal of Neuroscience shed light on a microcircuit mechanism that can explain part of the spectral phenomenology of ripples (Donoso et al., 2018). Ripples associated with sharp waves were initially identified at the high-frequency band (150-200 Hz), but subsequent data revealed a contribution at the fast gamma band (90-150 Hz) (Sullivan et al., 2011; Buzsaki, 2015). High-fre

Regulating synchronous oscillations of cerebellar granule cells by different types of inhibition

“…Feedback inhibition has been suggested as a general mechanism in generating oscillation of neural networks [ 51 , 52 ]. In the granular layer of the cerebellar cortex, previous studies have indicated that neural oscillations relate to the feedback loop between GoCs and GCs [ 19 , 30 , 35 , 53 ].…”

Clinical Neurophysiology of Epileptogenic Networks

“…This maximizes the amplitude of the oscillation and recruits a massive number of unit oscillators into excessive and hypersynchronous oscillatory activity. In both physiological and pathological high-frequency activities modelled, there was always a massive inhibitory response to the initial overexcitation wave front, something that is of note as it suggests that for any organized large-scale oscillatory activity to develop a critical level of synchronization of unit oscillators is required through recurrent cycles of excitation and inhibition [79]. This is achieved with the early excessive feedback wave of inhibition that follows the initial huge wave of excitation, resulting in an excessive hyperpolarization of the excitatory neurons.…”

“…When a small oscillating or periodic depolarization force is applied near a resonant frequency of a dynamic system, the system will oscillate at a higher amplitude than when the same force is applied at other, nonresonant frequencies [35]. Obviously, the resonant frequencies of local neocortex or allocortex are defined by the critical combination of local structural and functional connectivity, periodic thalamic or septal input, synaptic weights, interaction of excitatory (recurrent excitatory synapses) and inhibitory (loss of inhibition or disinhibition) components and intrinsic neuronal excitability (endogenous bursting) [78,79].…”

“…Schaffer collateral axons from the CA3 pyramidal neurons (main afferent input) activate the CA1 principal neurons (hippocampal pyramidal cells). At the same time collateral feedforward projections to GABAergic inhibitory interneurons activate their somata, before or during activation of the apical dendrites of the CA1 pyramidal neurons [66,[79][80][81][82]100,128].…”

“…These ultimately determine the intrinsic excitability and oscillatory dynamics of the individual neuron and its interactions with other structurally/functionally interconnected neurons. The membrane excitability characteristics and shortening of time integration constant (via a "push-and-pull" mechanism) of synchronized, coincidental or critically interacting excitatory (EPSP) and inhibitory (IPSP) postsynaptic potentials can increase or decrease the excitability of the entire network (Figure 26) [79,[85][86][87][88][89][90][91][92][93][94][95][96][97].…”