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Recovery of motoneuron and locomotor function after spinal cord injury depends on constitutive activity in 5-HT2C receptors
TLDR
Blocking constitutively active 5-HT2C receptors with SB206553 or cyproheptadine in both rats and humans largely eliminates these calcium currents and muscle spasms, providing a new rationale for antispastic drug therapy. Expand
Bistability in spinal motoneurons in vivo: systematic variations in rhythmic firing patterns.
TLDR
The low thresholds of fully bistable cells mean they will be readily recruited in low force tasks like posture, where their prolonged self-sustained firing would be advantageous. Expand
Bistability in spinal motoneurons in vivo: systematic variations in persistent inward currents.
TLDR
It was found that self-sustained firing was persistent for long periods only in motoneurons with low rheobases and slow axonal conduction velocities, and IPIC accounted for the main differences in the F-I behavior seen between fully and partially bistable cells. Expand
Persistent inward currents in motoneuron dendrites: Implications for motor output
TLDR
The brainstem neuromodulatory input provides a mechanism by which the excitability of motoneurons can be varied for different motor behaviors, which is lost in spinal cord injury but PICs nonetheless recover near‐normal amplitudes in the months following the initial injury. Expand
Increased persistent Na+ current and its effect on excitability in motoneurones cultured from mutant SOD1 mice
TLDR
In spinal motoneurones cultured from presymptomatic mice expressing the glycine to alanine mutation at base pair 93 (G93A) SOD1 mutation, a marked increase in the persistent component of the Na+ current was observed, without changes in passive properties, which may explain the tendency of large mot oneurones to degenerate first in ALS. Expand
Hyperexcitable dendrites in motoneurons and their neuromodulatory control during motor behavior
TLDR
During normal motor behavior, synaptic integration might be dominated by active currents intrinsic to the dendritic tree rather than by the synaptic current entering via ionotropic channels. Expand
Motor Neuron Rescue in Spinal Muscular Atrophy Mice Demonstrates That Sensory-Motor Defects Are a Consequence, Not a Cause, of Motor Neuron Dysfunction
TLDR
It is demonstrated that the SMA phenotype autonomously originates in MNs and that sensory-motor synapse loss is a consequence, not a cause, of MN dysfunction. Expand
Altered postnatal maturation of electrical properties in spinal motoneurons in a mouse model of amyotrophic lateral sclerosis
TLDR
Most electrical properties in the SOD1 motoneurons showed an accelerated pace of maturation during this early developmental period compared with the normal mot oneurons, which could hasten the onset of normal motoneuron degeneration due to ageing and result in the development of ALS. Expand
Adjustable Amplification of Synaptic Input in the Dendrites of Spinal Motoneurons In Vivo
TLDR
The dendritic amplification with moderate or strong neuromodulatory drive was estimated to be large enough to allow the motoneurons innervating slow muscle fibers to be driven to their maximum force levels by remarkably small synaptic inputs. Expand
Motoneuron excitability: The importance of neuromodulatory inputs
TLDR
The standard tests of motoneuron excitability are strongly influenced by the level of neuromodulatory input to motoneurons, and this insight is likely to be profoundly important for clinical diagnosis and treatment. Expand
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