Biology subjects

Piette, C.

Publications and source records attributed to Piette, C..

5 recordsLinked to original sources

bioRxiv2025

Unraveling the pathway of Copper Delivery to Cytochrome c oxidases in the Free-Living Bacterium Caulobacter vibrioides

Copper (Cu) is an essential micronutrient that serves as a cofactor for many enzymes but becomes toxic when present in excess. In most bacteria, CopA-like P1B-type ATPases mediate Cu detoxification by exporting cytoplasmic Cu to the periplasm or extracellular environment. In this study, we show that Caulobacter vibrioides lacks a canonical CopA-like ATPase but encodes a single FixI/CcoI-type Cu-transporting ATPase, previously implicated in Cu delivery to the cbb{square}-type cytochrome c oxidase (Cox) in species such as Rhodobacter capsulatus. C. vibrioides harbors two terminal cytochrome c oxidases in its cytoplasmic membrane: an aa{square}-type and a cbb{square}-type Cox. We also demonstrate that the activity of cbb{square}-Cox requires the FixI-type Cu transporter and the periplasmic Cu chaperone PccA. In contrast, aa{square}-Cox activity depends on PccA and the inner membrane-bound protein CtaG. Since the mechanism of Cu acquisition for aa{square}-Cox remains largely unknown, we conducted a genetic screen and identified a novel outer membrane TonB-dependent receptor (TccA) that is specifically required for aa{square}-Cox function. We also showed that cbb{square}-Cox is upregulated under microaerobic conditions, possibly such as those encountered on solid media where O2 diffusion is limited. Under normoxic conditions, the expression and the activity of cbb{square}-Cox decrease, and aa{square}-Cox becomes the predominant terminal oxidase. These findings demonstrate that C. vibrioides differentially utilizes its Cox enzymes in response to O2 availability and relies on a distinct Cu trafficking pathway for their maturation, including an outer membrane component that has not been previously described in bacterial Cu homeostasis.

microbiology↗

bioRxiv2024

Striatal endocannabinoid-long-term potentiation mediates one-shot learning

One-shot learning, the ability to form memories after a single, brief salient event, is essential to adapt ones behaviour in a dynamic world. However, how one-shot learning unfolds in the brain remains unknown. Challenges to elucidate its neural underpinnings stem experimentally from the scarcity of behavioral assays recapitulating one-shot learning in the laboratory, and conceptually from the limited number of neuronal plasticity mechanisms that could support learning after a small number of action potentials, as is common during a one-shot experience. Here, we overcome these challenges and identify a new mechanism for one-shot learning in dorsal striatum that relies on a non-classical form of plasticity, the endocannabinoid-mediated long-term potentiation (eCB-LTP). To do so, we develop a novel one-shot behavioral test, in which mice learn to avoid a sticky tape after a single, spontaneous and brief contact with the uncomfortable substrate, and maintain this memory for more than one month. We use the sticky tape avoidance test to demonstrate that striatal LTP emerges in vivo after one-shot learning; the observed patterns of activity in vivo suggest that eCB-LTP mediates one-shot learning, which we corroborate both ex vivo and through computational modeling. Consistent with this hypothesis, conditional knock-out mice abolishing eCB-LTP show impaired one-shot learning. These results highlight the importance of non-classical plasticity mechanisms in supporting memory formation after a single brief experience.

neuroscience↗

bioRxiv2022

Lactate supply overtakes glucose when neural computational and cognitive loads scale up

The neural computational power is determined by neuroenergetics, but how and which energy substrates are allocated to various forms of memory engram is unclear. To solve this question, we asked whether neuronal fueling by glucose or lactate scales differently upon increasing neural computation and cognitive loads. Here, using electrophysiology, two-photon imaging, cognitive tasks and mathematical modeling, we show that both glucose and lactate are involved in engram formation, with lactate supporting long-term synaptic plasticity evoked by high stimulation load activity patterns and high attentional load in cognitive tasks, and glucose being sufficient for less demanding neural computation and learning tasks. Overall, these results demonstrate that glucose and lactate metabolisms are differentially engaged in neuronal fueling depending on the complexity of the activity-dependent plasticity and behavior. One sentence summaryNeuronal fueling by lactate versus glucose scales differently according to engram level and memory load.

neuroscience↗

bioRxiv2021

Extracellular and intracellular components of theimpedance of neural tissue

Electric phenomena in brain tissue can be measured using extracellular potentials, such as the local field potential, or the electro-encephalogram. The interpretation of these signals depend on the electric structure and properties of extracellular media, but the measurements of these electric properties are still debated. Some measurements point to a model where the extracellular medium is purely resistive, and thus parameters such as electric conductivity and permittivity should be independent of frequency. Other measurements point to a pronounced frequency dependence of these parameters, with scaling laws that are consistent with capacitive or diffusive effects. However, these experiments correspond to different preparations, and it is unclear how to correctly compare them. Here, we provide for the first time, impedance measurements (in the 1-10 KHz frequency range) using the same set-up in various preparations, from primary cell cultures to acute brain slices, with a comparison with similar measurements performed in artificial cerebrospinal fluid with no biological material. The measurements show that when the current flows across a cell membrane, the frequency dependence of the macroscopic impedance between intracellular and extracellular electrodes is significant, and cannot be captured by a model with resistive media. Fitting a mean-field model to the data shows that this frequency dependence could be explained by the ionic diffusion mainly associated to Debye layers surrounding the membranes. We conclude that neuronal membranes and their ionic environment induce strong deviations to resistivity, that should be taken into account to correctly interpret extracellular potentials generated by neurons. SignificanceThe electro-encephalogram recorded at the scalp surface and local-field potentials recorded within neural tissue are generated by electric currents in neurons, and thus depend on the impedance of neural tissue. Different measured values were proposed, and it is currently unclear what is the real impedance of neural tissue. Here, we show that the impedance depends on the measurement technique. If the measurement is exclusively extracellular, the system appears as equivalent to a simple resistor. However, if the measurement includes an intracellular electrode, a more complex impedance is observed, because the current has to flow through the membrane, as happening in the brain. Thus, we provide an explanation for apparent disagreements, and indicate in which cases each impedance should be used.

neuroscience↗

bioRxiv2018

Opto-activation of cortical somatostatin interneurons alleviates parkinsonian symptoms

Deep brain stimulation of the subthalamic nucleus is a symptomatic treatment of Parkinsons disease but benefits only to a minority of patients due to stringent eligibility criteria. To investigate new targets for less invasive therapies, we aimed at elucidating key mechanisms supporting deep brain stimulation efficiency. Here, using in vivo electrophysiology, optogenetics and modeling, we found that subthalamic stimulation normalizes pathological hyperactivity of motor cortex pyramidal cells, while concurrently activating somatostatin and inhibiting parvalbumin interneurons. In vivo opto-activation of cortical somatostatin interneurons alleviates motor symptoms in a parkinsonian mouse model. A mathematical model highlights how the decrease in pyramidal neurons activity can restore information processing capabilities. Overall, these results demonstrate that activation of cortical somatostatin interneurons may constitute a less invasive alternative than subthalamic stimulation.\n\nOne-sentence SummaryDeep brain stimulation recruits cortical somatostatin interneurons, and their opto-activation is beneficial in Parkinsons.

neuroscience↗