Homeostasis established by coordination of subcellular compartment plasticity improves spike encoding

Abstract

Homeostasis in cells maintains their survival and functions. The plasticity at neurons and synapses may destabilize their signal encoding. The rapid recovery of cellular homeostasis is needed to secure the precise and reliable encoding of neural signals necessary for well-organized behaviors. We report a homeostatic process that is rapidly established through Ca2+-induced coordination of functional plasticity among subcellular compartments. An elevation of cytoplasmic Ca2+ levels raises the threshold potentials and refractory periods of somatic spikes, and strengthens the signal transmission at glutamatergic and GABAergic synapses, in which synaptic potentiation shortens refractory periods and lowers threshold potentials. Ca2+ signals also induce an inverse change of membrane excitability at the soma versus the axon. The integrative effect of Ca2+-induced plasticity among the subcellular compartments is homeostatic in nature, because it stabilizes neuronal activities and improves spike timing precision. Our study of neuronal homeostasis that is fulfilled by rapidly coordinating subcellular compartments to improve neuronal encoding sheds light on exploring homeostatic mechanisms in other cell types.

Voltage-independent sodium channels emerge for an expression of activity-induced spontaneous spikes in GABAergic neurons

“…A mutual substitution in the functions of VGSCs and voltage-independent sodium channels is a basis that AISS’s onset compensates the weakness of evoked spikes (Figure 2D ~ E). These facts grant a notion that the neural homeostasis is maintained among subcellular compartments and network neurons [16]. …”

“…For instance, GABAergic synapses express activity-dependent potentiation [12-15]. Excitatory synapses on GABAergic neurons are potentiated by Ca 2+ signals [16-18]. The intrinsic properties of GABAergic neurons are changed in behavioral plasticity [19-21].…”

Input-dependent subcellular localization of spike initiation between soma and axon at cortical pyramidal neurons

“…Different from this slow onset plasticity, the input-dependent plasticity of spike initiation location in our study develops quickly, shifts between the soma and axon (Figures 1, 2 and 3) and depends on local VGSC kinetics (Figures 4, 5 and 6). This subcellular relocation of spike initiation is a novel type of neuronal plasticity, compared to long-term plasticity in neuronal excitability [47-54], neuronal homeostasis [55] and VGSC redistribution [29,30]. …”

“…Spike thresholds were measured by depolarization pulses with the inverse changes in their intensities and durations. Spike refractory periods were measured by injecting two pulses (5% above threshold) with various durations into the neurons after each spike, in which inter-pulse intervals were adjusted [32,33,55,68,72]. In the measurement of spike refractory periods versus pulse durations, the increment of depolarization duration was inversely associated with the reduction of its intensities, which were 5% above thresholds.…”

Acidosis and alkalosis impair brain functions through weakening spike encoding at cortical GABAergic neurons

“…With these pipettes for wholecell recording, intracellular pH will be balanced with the pipettes within a few minutes. Under this condition, the recording in the beginning of a few minutes can be used as the control, an approach similar to infusing other reagents [6,9,27,34,35].…”