Topic: Dorsal root ganglion neurons

Research has shown that individuals with Down syndrome experience altered pain sensitivity, with varying results depending on the type of nociceptive stimulus. GRIK1, a gene coding for the GluK1 subunit of kainate receptors is triplicated in Down syndrome. This subunit is heavily expressed in Dorsal Root Ganglion neurons and has been implicated in modulating pain perception. To investigate this further, we have conducted experiments in the Ts2Cje mouse model of Down syndrome, comparing them to mice lacking Grik1. The results suggest that altered pain perception in Down syndrome is dependent on

Spinal cord injury is associated with axonal damage and degeneration, leading to the dysfunction of neuronal networks and hence, severe impairment of neurological function. Injured neurons response depends both on extracellular cues (mainly non-permissive, such as myelin debris, extracellular matrix protein such as CSPG, glial and fibrotic scar, inflammatory cues, …) and their intrinsic capacity. How microtubule-associated protein (MAP) contribute to this response is the objective of the present work. MAP6 is the first neuronal microtubule (MT) inner protein discovered and preliminary results

Restoring the regenerative capacity of adult neurons after spinal cord injury has been an important challenge of the past decades. Unlike the peripheral branch of the nervous system, CNS axons fail to regenerate following injury. This inability has a two-fold origin, a neuron-extrinsic and -intrinsic one. The former has been well described in literature and is related to the inhibitory effect of the CNS environment on outgrowth of adult neurites. The latter has been attributed to the cellular makeup of adult neurons which is primed toward synaptic maturity and functionality, as opposed to rege