Biology subjects

Huan, M.

Publications and source records attributed to Huan, M..

4 recordsLinked to original sources

bioRxiv2026

Decoding the oxytocinergic and behavioral signatures of milk ejection

Oxytocin-mediated milk ejection (ME) is pivotal to effective breastfeeding and productive health, yet behaviorally decoding and revealing neural mechanisms of ME remains challenging. Here, we combined in vivo calcium imaging and intramammary pressure recording to uncover the temporal connections between episodic activity of oxytocin neurons and ME in conscious lactating rats. Leveraging the association and behavioral responses in dam and pup, we developed a supervised machine learning framework (ME Decoder) to enable automated analyses of ME. Inspired by its interpretable features, we defined the activity-coupled dam-pup interactions (ADPI), manifested by high kyphosis of the dam followed by pup treading and stretch, as the behavioral signatures of ME. By ME Decoder and ADPI analyses, we detected reduced ME but unaffected activity of oxytocinergic neurons after systemic blockade of oxytocin receptor. Our study uncovers the oxytocinergic and behavioral signatures of ME and provides a generalizable approach for further investigation.

neuroscience↗

bioRxiv2025

Off-target effects of PLX5622 revealed: mixing microglial function in anesthesia and addiction withdrawal

Microglia have gained increasing attention as important regulators in the brain. Acute microglial depletion using the colony-stimulating factor 1 receptor (CSF1R) inhibitor, PLX5622, has become a popular approach to uncover microglial function. PLX5622 treatment has been recently shown to significantly promote anesthetic emergence. In characterizing underlying mechanisms, we found that PLX5622 treatment did not change the global neuronal activity during anesthesia, but robustly enhanced anesthetic metabolism. Moreover, PLX5622 dramatically induced the expression of hepatic enzymes that extensively modify xenobiotic and endobiotic metabolism. Blocking increased enzymatic activity significantly reduced the arousal-promoting effects of PLX5622 in anesthesia, irrespective of microglial elimination. In addition, we demonstrate that enhanced drug metabolism also contributed to PLX5622-induced attenuation in nicotine-withdrawal anxiety. By revealing previously unrecognized effects of PLX5622, our findings raise caution in interpreting data generated from PLX5622 treatment and bring forward the need for designing more specific CSF1R inhibitors.

neuroscience↗

bioRxiv2023

Temporal physiological, transcriptomic and metabolomic analyses revealed molecular mechanism of Canna indica's response to Cr stress

Chromium (Cr) can interfere with plant gene expression, change the content of metabolites and affect plant growth. However, the molecular response mechanism of wetland plants at different time sequences under Cr stress has yet to be fully understood.The results showed that Cr stress increased the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX) and peroxidase (POD), the contents of glutathione (GSH), malondialdehyde (MDA), and oxygen free radical (ROS), and inhibited the biosynthesis of photosynthetic pigments, thus leading to changes in plant growth and biomass. that Cr stress mainly affected 12 metabolic pathways, involving 38 differentially expressed metabolites, including amino acids, phenylpropane, and flavonoids. A total of 16247 differentially expressed genes were identified, among which, at the early stage of stress, C. indica responds to Cr toxicity mainly through galactose, starch and sucrose metabolism. With the extension of stress time, plant hormone signal transduction and MAPK signaling pathway in C. indica in the treatment group were significantly affected. Finally, in the late stage of stress, C. indica co-defuses Cr toxicity by activating its Glutathione metabolism and Phenylpropanoid biosynthesis. In conclusion, this study revealed the molecular response mechanism of C. indica to Cr stress at different times through multi-omics methods. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=118 SRC="FIGDIR/small/524062v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@c2fec6org.highwire.dtl.DTLVardef@1e47da8org.highwire.dtl.DTLVardef@1f5be49org.highwire.dtl.DTLVardef@9fcf87_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

bioRxiv2021

mTOR-neuropeptide Y signaling sensitizes nociceptors to drive neuropathic pain

Neuropathic pain is a refractory condition that involves de novo protein synthesis in the nociceptive pathway. The mechanistic target of rapamycin (mTOR) is a master regulator of protein translation; however, mechanisms underlying its role in neuropathic pain remain elusive. Using spared nerve injury-induced neuropathic pain model, we found that mTOR is preferentially activated in large-diameter dorsal root ganglion (DRG) neurons and spinal microglia. However, selective ablation of mTOR in DRG neurons, rather than microglia, alleviated neuropathic pain. We show that injury- induced mTOR activation promoted transcriptional induction of NPY likely via signal transducer and activator of transcription 3 (STAT3) phosphorylation. NPY further acted primarily on Y2 receptors (Y2R) to enhance nociceptor excitability. Peripheral replenishment of NPY reversed pain alleviation upon mTOR removal, whereas Y2R antagonists prevented pain restoration. Our findings reveal an unexpected link between mTOR and NPY in promoting nociceptor sensitization and neuropathic pain, through NPY/Y2R signaling-mediated intra-ganglionic transmission.

neuroscience↗