Publications by authors named "Lidia Garcia-Campmany"

Next Generation is a series of interviews with the awardees of the Travel Awards aimed at supporting early-career researchers and helping them promote their work. Sébastien R. Mouchet is a postdoctoral fellow in the Natural Photonics group led by Prof.

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Ille C. Gebeshuber is Professor of Physics at the Institute of Applied Physics at the Vienna University of Technology, Austria, where she graduated and completed her Ph.D.

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Mechanical hypersensitivity is a debilitating symptom for millions of chronic pain patients. It exists in distinct forms, including brush-evoked dynamic and filament-evoked punctate hypersensitivities. We reduced dynamic mechanical hypersensitivity induced by nerve injury or inflammation in mice by ablating a group of adult spinal neurons defined by developmental co-expression of VGLUT3 and Lbx1 (VT3 neurons): the mice lost brush-evoked nocifensive responses and conditional place aversion.

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Light mechanical stimulation of hairy skin can induce a form of itch known as mechanical itch. This itch sensation is normally suppressed by inputs from mechanoreceptors; however, in many forms of chronic itch, including alloknesis, this gating mechanism is lost. Here we demonstrate that a population of spinal inhibitory interneurons that are defined by the expression of neuropeptide Y::Cre (NPY::Cre) act to gate mechanical itch.

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Sensory circuits in the dorsal spinal cord integrate and transmit multiple cutaneous sensory modalities including the sense of light touch. Here, we identify a population of excitatory interneurons (INs) in the dorsal horn that are important for transmitting innocuous light touch sensation. These neurons express the ROR alpha (RORα) nuclear orphan receptor and are selectively innervated by cutaneous low threshold mechanoreceptors (LTMs).

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Pain information processing in the spinal cord has been postulated to rely on nociceptive transmission (T) neurons receiving inputs from nociceptors and Aβ mechanoreceptors, with Aβ inputs gated through feed-forward activation of spinal inhibitory neurons (INs). Here, we used intersectional genetic manipulations to identify these critical components of pain transduction. Marking and ablating six populations of spinal excitatory and inhibitory neurons, coupled with behavioral and electrophysiological analysis, showed that excitatory neurons expressing somatostatin (SOM) include T-type cells, whose ablation causes loss of mechanical pain.

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Inhibitory neurons in the spinal cord perform dedicated roles in processing somatosensory information and shaping motor behaviors that range from simple protective reflexes to more complex motor tasks such as locomotion, reaching and grasping. Recent efforts examining inhibition in the spinal cord have been directed toward determining how inhibitory cell types are specified and incorporated into the sensorimotor circuitry, identifying and characterizing molecularly defined cohorts of inhibitory neurons and interrogating the functional contribution these cells make to sensory processing and motor behaviors. Rapid progress is being made on all these fronts, driven in large part by molecular genetic and optogenetic approaches that are being creatively combined with neuroanatomical, electrophysiological and behavioral techniques.

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BMP activity is essential for many steps of neural development, including the initial role in neural induction and the control of progenitor identities along the dorsal-ventral axis of the neural tube. Taking advantage of chick in ovo electroporation, we show a novel role for BMP7 at the time of neurogenesis initiation in the spinal cord. Using in vivo loss-of-function experiments, we show that BMP7 activity is required for the generation of three discrete subpopulations of dorsal interneurons: dI1-dI3-dI5.

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Neural networks in the hindbrain and spinal cord generate the simple patterns of motor activity that are necessary for breathing and locomotion. These networks function autonomously, producing simple yet flexible rhythmic motor behaviours that are highly responsive to sensory inputs and central control. This review outlines recent advances in our understanding of the genetic programmes controlling the assembly and functioning of circuits in the hindbrain and spinal cord that are responsible for respiration and locomotion.

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Here we show that Smad3, a transforming growth factor beta (TGFbeta)/activin signaling effector, is expressed in discrete progenitor domains along the dorsoventral axis of the developing chick spinal cord. Restriction of Smad3 expression to the dP6-p2 and p3 domains together with exclusion from the motoneuron progenitor domain, are the result of the activity of key transcription factors responsible for patterning the neural tube. Smad3-mediated TGFbeta activity promotes cell-cycle exit and neurogenesis by inhibiting the expression of Id proteins, and activating the expression of neurogenic factors and the cyclin-dependent-kinase-inhibitor p27(kip1).

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