Biology subjects

Petitjean, H.

Publications and source records attributed to Petitjean, H..

4 recordsLinked to original sources

bioRxiv2026

Sex-dependent involvement of lateral septum astrocytes in social fear: Role of oxytocin receptor signaling

Astrocytes are now widely recognized as important modulators of synaptic plasticity and socio-emotional behaviors. Recent studies highlight their involvement in anxiety- and depressive-like behaviors, particularly via oxytocin (OXT) signaling. While the specific contributions of astrocytes remain largely unexplored, the role of OXT receptor (OXTR) signaling in the lateral septum (LS) in regulating social fear expression has been well characterized. Here, we studied the differential contribution of astrocytic OXTR signaling using a social fear conditioning (SFC+) paradigm. We found the highest abundance of astrocytes, and especially of OXTR-expressing (OXTR+) astrocytes, within the caudal LC (LSc) compared to the rostral LS in both male and female mice. Interestingly, female mice displayed a significantly higher number of astrocytes and OXTR+ astrocytes in the LSc in comparison to males. However, social fear acquisition resulted in dynamic changes in LSc astrocytic morphology and calcium activity in male mice. Furthermore, we showed that pre-SFC acquisition pharmacology-induced loss of local astrocytic function facilitated the extinction of social fear in males. In support, astrocyte-specific OXTR knockdown in the LSc also facilitated social fear extinction in both males and females. Taken together, our study identifies OXTR-signaling in LSc astrocytes as a crucial component in the mechanisms underlying the regulation of social fear in a sex-dependent manner.

neuroscience↗

bioRxiv2022

Parvalbumin protein controls inhibitory tone in the spinal cord

The nervous system processes sensory information by relying on the precise coordination of neuronal networks and their specific synaptic firing patterns. In the spinal cord, disturbances to the firing pattern of the tonic firing parvalbumin (PV)-expressing inhibitory interneuron (PV neurons) disrupt the ability of the dorsal horn to integrate touch information and may result in pathological phenotypes. The parvalbumin protein (PVp) is a calcium (Ca2+)-binding protein that buffers the accumulation of Ca2+ following a train of action potential to allow for tonic firing. Here, we find that peripheral nerve injury causes a decrease in PVp expression in PV neurons and makes them transition from tonic to adaptive firing. We also show that reducing the expression of PVp causes otherwise healthy adult mice to develop mechanical allodynia and causes their PV neurons to lose their high frequency firing pattern. We show that this frequency adaptation is mediated by activation of SK channels on PV neurons. Further, we show their tonic firing can be partially restored after nerve injury by selectively inhibiting the SK2 channels of PV neurons. We also reveal that a decrease in the transcriptional coactivator, PGC-1, causes decrease PVp expression and the development of mechanical allodynia. By preventing the decrease in PVp expression before nerve injury, we were able to protect mice from developing mechanical allodynia. Our results indicate an essential role for PVp-mediated calcium buffering in PV neuron firing activity and the development of mechanical allodynia after nerve injury.

neuroscience↗

bioRxiv2020

Scaffold-scaffold interactions regulate cell polarity in a bacterium

The localization of two biochemically distinct signaling hubs at opposite cell poles provides the foundation for asymmetric cell division in Caulobacter crescentus. Here we identify an interaction between the scaffolds PodJ and PopZ that regulates the assembly of the new cell pole signaling complex. Time-course imaging of a mCherry-sfGFP-PopZ fluorescent timer throughout the cell cycle revealed that existing PopZ resides at the old cell pole while newly translated PopZ accumulates at the new cell pole. Our studies suggest that interactions between PodJ and PopZ promotes the sequestration of older PopZ and robust accumulation of newl PopZ at the new cell pole. Elimination of the PodJ-PopZ interaction impacts PopZ client proteins, leading to chromosome segregation defects in one-third of cells. Additionally, this PopZ-PodJ interaction is crucial for anchoring PodJ and preventing PodJ extracellular loss at the old cell pole through unknown mechanism. Therefore, segregation of PopZ protein at the old pole and recruitment of newly translated PopZ at the new pole via the PodJ scaffold ensures stringent inheritance and maintenance of the polarity axis within dividing C. crescentus cells.

microbiology↗

bioRxiv2018

TACAN is an essential component of the mechanosensitive ion channel responsible for pain sensing

Mechanotransduction, the conversion of mechanical stimuli into electrical signals, is a fundamental process underlying several physiological functions such as touch and pain sensing, hearing and proprioception. This process is carried out by specialized mechanosensitive ion channels whose identities have been discovered for most functions except pain sensing. Here we report the identification of TACAN (Tmem120A), an essential subunit of the mechanosensitive ion channel responsible for sensing mechanical pain. TACAN is expressed in a subset of nociceptors, and its heterologous expression increases mechanically-evoked currents in cell lines. Purification and reconstitution of TACAN in synthetic lipids generates a functional ion channel. Finally, knocking down TACAN decreases the mechanosensitivity of nociceptors and reduces behavioral responses to mechanical but not to thermal pain stimuli, without affecting the sensitivity to touch stimuli. We propose that TACAN is a pore-forming subunit of the mechanosensitive ion channel responsible for sensing mechanical pain.

neuroscience↗