Biology subjects

Fidelin, K.

Publications and source records attributed to Fidelin, K..

3 recordsLinked to original sources

bioRxiv2026

Whole brain mapping of spinal-projecting neurons in larval zebrafish

To elicit voluntary movements and integrative reflexes underlying behavior, the brain sends command signals to the spinal cord via specialized long-range descending neurons, known as spinal-projecting neurons (SPNs). The vast and widespread distribution of SPNs, combined with their complex long-distance connectivity, poses a significant challenge for mapping their anatomical organization and associating specific populations with distinct functions. Here we took advantage of the transparency and genetic accessibility of larval zebrafish to uncover the fundamental principles of SPN anatomical organization in a Teleost. Using an optical backfilling method relying on photoactivable GFP, we generate a whole-brain map of all neurons sending axons towards the spinal cord. This approach reveals far more SPNs than previously described through conventional strategies, offering an unparalleled opportunity to revisit distinct spinal-projecting nuclei distributed across hindbrain, midbrain, and diencephalic structures. Combining information on cell location, morphology, and projection patterns, we propose tentative homological designations for zebrafish of SPN nuclei based on established descriptions in mammals and other vertebrates.

neuroscience↗

bioRxiv2026

Noradrenaline prolongs the state of motor arrest via cerebrospinal fluid signaling

Neuromodulators can mediate whole-body physiological changes, however how signaling from relatively small populations of neurons produces widespread and sustained effects remains incompletely understood. Here, we demonstrate that sustained noradrenergic activation induces prolonged motor arrest accompanied by postural collapse, bradycardia, and emetic responses. Motor suppression arises from inhibition of brainstem commands to the spinal cord rather than motoneuron silencing. Noradrenaline induces a glial calcium wave that propagates throughout the central nervous system. This wave most prominently persists at the brainstem-spinal cord boundary and ventricular midline. At this location, ependymal radial glia express Adra1a receptors on cilia contacting cerebrospinal fluid (CSF). Ventricular noradrenaline injections recapitulated the glial wave and motor arrest, while CSF administration of an Adra1 antagonist shortened motor arrest. Altogether, noradrenaline sustains motor arrest by signaling through the CSF via ciliary Adra1a receptors on ependymal radial glia showing that cerebrospinal fluid as a critical transmission route for persistence of behavioral states. HighlightsO_LINoradrenergic surges coordinate a whole-body response with motor arrest, postural disruptions, bradycardia, and emesis-like reflexes C_LIO_LIMotor arrest results from silencing of brainstem motor commands to the spinal cord C_LIO_LINoradrenaline-induced glial calcium waves last longest at the obex/ventricular midline where cilia of CSF-contacting glial cells bear Adra1 receptors C_LIO_LINoradrenergic signaling in the CSF is necessary and sufficient for motor arrest to persist C_LI

neuroscience↗

bioRxiv2021

Spinal sensory neurons project onto hindbrain to stabilize posture and enhance locomotor speed

In the spinal cord, cerebrospinal fluid-contacting neurons (CSF-cNs) are GABAergic interoceptive sensory neurons that detect spinal curvature via a functional coupling with the Reissner fiber. This mechanosensory system has recently been found involved in spine morphogenesis and postural control but the underlying mechanisms are not fully understood. In zebrafish, CSF-cNs project an ascending and ipsilateral axon reaching two to six segments away. Rostralmost CSF-cNs send their axons ipsilaterally into the hindbrain, a brain region containing motor nuclei and reticulospinal neurons (RSNs), which send descending motor commands to spinal circuits. Until now, the synaptic connectivity of CSF-cNs has only been investigated in the spinal cord where they synapse onto motor neurons and premotor excitatory interneurons. The identity of CSF-cN targets in the hindbrain and the behavioral relevance of these sensory projections from spinal cord to hindbrain are unknown. Here, we provide anatomical and molecular evidence that rostralmost CSF-cNs synapse onto the axons of large RSNs including the Mauthner cells and early born chx10+ neurons. Functional anatomy and optogenetic-assisted mapping reveal that rostral CSF-cNs also synapse onto the soma and dendrites of cranial motor neurons innervating hypobranchial muscles. During acousto-vestibular evoked escape responses, ablation of rostralmost CSF-cNs results in a weaker escape response with a decreased C-bend amplitude, lower speed and a deficient postural control. Our study demonstrates that spinal sensory feedback enhances speed and stabilizes posture, and reveals a novel spinal gating mechanism acting on the output of descending commands sent from the hindbrain to the spinal cord. eTOCCerebrospinal fluid-contacting neurons are mechanosensory cells that detect spinal curvature. Wu et al. show here that rostralmost CSF-cNs synapse in the hindbrain onto cranial motor neurons and the descending axons of reticulospinal neurons, and enhance speed and power as well as postural control during active locomotion. HighlightsO_LICerebrospinal fluid-contacting neurons (CSF-cNs) in rostral spinal cord form inhibitory synapses onto cranial motor neurons C_LIO_LIRostral CSF-cNs synapse onto descending axons of reticulospinal neurons C_LIO_LICSF-cN sensory feedback in the rostral spinal cord enhance speed and power of locomotion C_LIO_LIRostral CSF-cNs projecting to the hindbrain contribute to postural control C_LI

neuroscience↗