Topic: corticospinal tract

Voluntary movement in animal is regulated be the sensorimotor cortex. The cortex generates the motor command as well as signals to increase the weight of relevant sensory information (sensory gating) that are both essential for the realization of adapted and coordinated movements. The corticospinal tract (CST) is the most direct pathway conveying these signals. Our previous work on anesthetized mice has shown that the lumbar projecting CST induces mainly the modulation of sensory information rather than the direct control of muscle contraction. The aim of our study is to identify the implicati

The corticospinal tract is a complex system of paramount importance for the control of voluntary movements. It originates in the cerebral cortex from upper motor neurons which directly contact the lower motor neurons located in the ventral horns of the spinal cord. Lower motor neurons, in turn, form synapses with skeletal muscle cells delivering the signal generated in the brain. Insults to this system, such as spinal cord injuries or amyotrophic lateral sclerosis, cause dysfunction and degeneration of motor neurons leading to severe and untreatable pathological conditions. We aim to explore t

The corticospinal tract (CST) facilitates skilled, precise movements, which necessitates that corticospinal neurons (CSN) establish segmentally specific connectivity with spinal circuitry. Recent work has identified CSN-intrinsic molecular determinants that regulate CSN axonal projections to specific segmental levels of the neuraxis and that these are expressed by CSN subpopulations that project to distinct levels of the neuraxis. In the present study, we establish the use of a newly generated Klhl14-T2A-Cre knock-in reporter mouse line to investigate axonal projections of a specific CSN subpo

Pain expectation is known to influence pain perception, but the underlying neuronal mechanisms remain unclear. While the motor role of the corticospinal tract is well characterized, only recently was it established that the corticospinal neurons originating from the primary somatosensory cortex (S1-CSNs) specifically contact the sensory region of the spinal cord, providing top-down regulation of sensations including pain. S1-CSNs neurons are therefore ideally positioned to modulate spinal nociception based on sensory representations and expectations. To test whether S1-CSNs activity is modulat

After spinal cord injury (SCI), astrocytes become reactive in a process called astrogliosis. These reactive astrocytes surround the lesion and form an astrocyte scar border. Our lab recently previously discovered that LZK (or MAP3K13) regulates reactive astrogliosis and scar formation after a dorsal spinal cord crush injury. The effect of LZK-mediated astrogliosis on neural repair and regeneration is still not clear. We aim to investigate this question utilizing genetically modified mice and RNA sequencing. We are testing the effect of astrocytic LZK overexpression or deletion on behavioral re