Biology subjects

Kolta, A.

Publications and source records attributed to Kolta, A..

4 recordsLinked to original sources

bioRxiv2025

The astroglial protein S100β regulates axon initial segment plasticity

One key regulator of neuronal excitability is the axon initial segment (AIS), a highly specialized axonal region, enriched in ion channels, where action potentials are initiated. The AIS can undergo significant morphological changes to fine-tune neuronal excitability in response to external perturbations. Long considered solely a homeostatic mechanism operating over long timescales (hours to days) to adjust excitability, we show here that this phenomenon can also occur rapidly, within minutes, following a brief period of high activity in layer 5 pyramidal neurons of the visual cortex. Because astrocytes have been known to regulate neuronal excitability, we explored the effects of gliotransmitters on this process and identified the calcium-binding protein S100{beta} from astrocytes to be required for the rapid reorganization of the AIS. O_FIG O_LINKSMALLFIG WIDTH=169 HEIGHT=200 SRC="FIGDIR/small/667937v3_ufig1.gif" ALT="Figure 1"> View larger version (30K): org.highwire.dtl.DTLVardef@1765348org.highwire.dtl.DTLVardef@155bf98org.highwire.dtl.DTLVardef@95c300org.highwire.dtl.DTLVardef@356376_HPS_FORMAT_FIGEXP M_FIG Graphical abstract C_FIG

neuroscience↗

bioRxiv2025

Integration of sensory and cortical information in the brainstem during mastication in mice

Mastication is a vital function that relies on precise synchronization among multiple brainstem regions, known as being part of a central pattern generator (CPG). Movements can be triggered either by stimulating a sensory-motor region called the cortical masticatory area (CMA), well-documented in various species but not yet formally identified in mice, or by stimulating the oro-facial sensory primary afferents which fibers form the trigeminal tract (Vtr). However, its unclear whether these different inputs activate distinct components of the CPG or converge on the same. This study aims at mapping brainstem areas activated by cortical and sensory inputs using immunohistochemistry against the cellular activity marker, c-Fos and Ca2+-imaging, respectively. Optogenetic stimulation of the cortical masticatory area (CMA) in awake, head-fixed mice reliably induced rhythmic jaw movements (RJMs) and increased c-Fos expression in multiple brainstem regions, with strongest activation in the peritrigeminal area (PeriV) and parvocellular reticular formation (PCRt) ventral to the trigeminal motor nucleus (NVmt). In contrast, in vitro electrical stimulation of trigeminal sensory afferents (Vtr) predominantly activated neurons and astrocytes in the main sensory nucleus (NVsnpr), the dorsal area of PeriV, adjacent to it, and PCRt. The areas containing the highest numbers of activated cells differed clearly according to the type of inputs and overlapped only in the PCRt, ventral and slightly medial to the trigeminal motor nucleus and the most dorso-medial part of PeriV. These findings demonstrate that cortical and sensory inputs take part in distinct components of the brainstem masticatory circuitry, with PCRt emerging as a point of convergence and provide new insights into the components of the CPG of mastication.

neuroscience↗

bioRxiv2025

The gliotransmitter S100β regulates synaptic plasticity in the visual cortex

Synaptic plasticity is a fundamental mechanism of memory storage in the brain. Among the various rules governing changes in synaptic strength, Spike Timing-Dependent Plasticity (STDP) stands out for its strong physiological relevance in vivo. Ubiquitous across brain regions and neuronal types, STDP is a complex and multifactorial process influenced by factors such as neuromodulation, extracellular calcium levels, and activity patterns. However, one relatively understudied factor is the role of astrocytes, despite their well-established involvement in regulating synaptic transmission and neuronal excitability through gliotransmitter release. While some factors have garnered significant attention, others, like S100{beta}, have remained relatively underexplored despite their potential importance in regulating synaptic plasticity. S100{beta} is a calcium-binding protein, allowing it to influence extracellular Ca{superscript 2} concentration and potentially all Ca2+-dependent plasticity processes. Building on our previous research in the visual cortex, where we examined the regulation of neuronal excitability by S100{beta}, we chose to further investigate the role of astrocytes and S100{beta} in synaptic plasticity at layer 2/3-layer 5 synapses in the visual cortex. We demonstrated that S100{beta} is an important gliotransmitter to consider, capable of regulating long-term potentiation.

neuroscience↗

bioRxiv2024

Astrocyte-induced firing in primary afferent axons

The mesencephalic trigeminal nucleus is unique in that it contains the cell bodies of large-caliber primary afferents that are usually located in the periphery in the dorsal root ganglia or trigeminal ganglia. The activity of these afferents is typically associated with proprioception of the jaw-closing muscles or mechanoreception on the teeth and periodontal ligament. However, like other large-caliber afferents from the body which display ectopic firing in neuropathic pain models, these afferents exhibit increased excitability and ectopic discharges even in a relatively mild muscle pain model. These discharges normally emerge from subthreshold membrane oscillations (SMOs) supported by a persistent sodium current (INaP) which is exquisitely sensitive to extracellular Ca2+-decreases. We have shown in the trigeminal main sensory nucleus that the release of a Ca2+-binding astrocytic protein, S100{beta}, is sufficient to modulate this sodium current. Here, we explore if this astrocyte-dependent mechanism contributes to emergence of this hyperexcitability and aim to localize the cellular site where ectopic discharge may arise using whole-cell patch-clamp recordings, confocal imaging, and immunohistochemistry methods on mice brain slices. We found that astrocytes, by lowering [Ca2+]e at focal points along the axons of NVmes neurons through S100{beta}, enhance the amplitude of the NaV1.6-dependent SMOs leading to ectopic firing. These findings suggest a crucial role for astrocytes in excitability regulation and raise questions about this neuron-astrocyte interaction as a key contributor to hyperexcitability in several pathologies.

neuroscience↗