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Literature highlights that serotonergic descending pathways [14] are implicated in somatosensory functions in the spinal cord and that serotonin (5-HT) in the dorsal horn might play a role in motor function through proprioceptive feedback [3, 8, 9, 13]. We hypothesized that 5-HT release in dorsal horn might represent an important factor in the completion of locomotion by facilitation of the spinocerebellar tract [8] and/or by modulation of spinal reflex pathways [9]. The present study demonstrates that during locomotor activity, 5-HT is released in layers II, III, IV, V of Rexed laminae. Microdialysis in combination with HPLC was used to measure concentrations of neurotransmitters in the lumbar dorsal horn before, during, and after a treadmill running exercise. Our results show a significant 41% increase of 5-HT release within the dorsal horn during a running exercise. 5-HT release is temporally related to exercise. The present study demonstrates that dorsal horn 5-HT release might modulate locomotion.

Effective quadrupedal locomotor behaviors require the coordination of many muscles in the limbs, back, neck, and tail. Because of the spinal motoneuronal somatotopic organization, motor coordination implies interactions among distant spinal networks. Here, we investigated some of the interactions between the lumbar locomotor networks that control limb movements and the thoracic networks that control the axial muscles involved in trunk movement. For this purpose, we used anin vitroisolated newborn rat spinal cord (from T2 to sacrococcygeal) preparation. Using extracellular ventral root recordings, we showed that, while the thoracic cord possesses an intrinsic rhythmogenic capacity, the lumbar circuits, if they are rhythmically active, will entrain the rhythmicity of the thoracic circuitry. However, if the lumbar circuits are rhythmically active, these latter circuits will entrain the rhythmicity of the thoracic circuitry. Blocking the synaptic transmission in some thoracic areas revealed that the lumbar locomotor network could trigger locomotor bursting in distant thoracic segments through short and long propriospinal pathways. Patch-clamp recordings revealed that 72% of the thoracic motoneurons (locomotor-driven motoneurons) expressed membrane potential oscillations and spiking activity coordinated with the locomotor activity expressed by the lumbar cord. A biphasic excitatory (glutamatergic)/inhibitory (glycinergic) synaptic drive was recorded in thoracic locomotor-driven motoneurons. Finally, we found evidence that part of this locomotor drive involved a monosynaptic component coming directly from the lumbar locomotor network. We conclude that the lumbar locomotor network plays a central role in the generation of locomotor outputs in the thoracic cord by acting at both the premotoneuronal and motoneuronal levels.

OBJECT Spinopelvic alignment is crucial in assessing an energy-efficient posture in both normal and disease states, such as high-displacement developmental spondylolisthesis (HDDS). The overall effect in patients with HDDS who have undergone local surgical correction of lumbosacral imbalance for the global correction of spinal balance remains unclear. This paper reports the progressive spontaneous improvement of global sagittal balance following surgical correction of lumbosacral imbalance in patients with HDDS. METHODS The records of 15 patients with HDDS who underwent surgery between 2005 and 2010 were reviewed. The treatment consisted of L4–sacrum reduction and fusion via a posterior approach, resulting in complete correction of lumbosacral kyphosis. Preoperative, 6-month postoperative, and final follow-up postoperative angular measurements were taken from full-spine lateral radiographs obtained with the patient in a standard standing position. Radiographic measurements included pelvic incidence, sacral slope, lumbar lordosis, and thoracic kyphosis. The degree of lumbosacral kyphosis was evaluated by the lumbosacral angle. Because of the small number of patients, nonparametric tests were considered for data analysis. RESULTS Preoperative lumbosacral kyphosis and L-5 anterior slip were corrected by instrumentation. Transient neurological complications were noted in 5 patients. Statistical analysis showed a significant increase of thoracic kyphosis on 6-month postoperative and final follow-up radiographs (p < 0.001). A statistically significant decrease of lumbar lordosis was noted between preoperative and 6-month control radiographs (p < 0.001) and between preoperative and final follow-up radiographs (p < 0.001). CONCLUSIONS Based on the authors' observations, this technique resulted in an effective reduction of L-5 anterior slip and significant reduction of lumbosacral kyphosis (from 69.8° to 105.13°). Due to complete reduction of lumbosacral kyphosis and anterior trunk displacement associated with L-5 anterior slipping, lumbar lordosis progressively decreased and thoracic kyphosis progressively increased postoperatively. Adjusting the sagittal trunk balance produced not only pelvic anteversion, but also reciprocal adjustment of lumbar lordosis and thoracic kyphosis, creating a satisfactory level of compensated global sagittal balance.

Amyotrophic lateral sclerosis is a lethal, adult-onset disease characterized by progressive degeneration of motoneurons. Recent data have suggested that the disease could be linked to abnormal development of the motor nervous system. Therefore, we investigated the electrical properties of lumbar motoneurons in an in-vitro neonatal spinal cord preparation isolated from SOD1(G85R) mice, which is a transgenic model of amyotrophic lateral sclerosis. The study was performed on young animals at the beginning of their second week, between postnatal days 6 and 10. Measurements of resting membrane potential and action potential characteristics of motoneurons were similar in wild-type and SOD1(G85R) mice. However, the input resistance of motoneurons from transgenic mice was significantly lower than that of wild-type animals, whereas their membrane capacitance was increased, strongly suggesting larger SOD1(G85R) motoneurons. Furthermore, the slope of the frequency-intensity curve was steeper in motoneurons from wild-type pups. Interestingly, the input resistance as well as the slope of the frequency-intensity curves of other spinal neurons did not show such differences. Finally, the amplitude of dorsal root-evoked potentials following high-intensity stimulation was significantly smaller in SOD1(G85R) motoneurons. The superoxide dismutase 1 mutation thus induces specific alterations of the functional properties of motoneurons early in development.

Background The appearance of Aβ42 peptide deposits is admitted to be a key event in the pathogenesis of Alzheimer's disease, although amyloid deposits also occur in aged non-demented subjects. Aβ42 is a degradation product of the amyloid protein precursor (APP). It can be catabolized by several enzymes, reabsorbed by capillaries or cleared into cerebrospinal fluid (CSF). The possible involvement of a decrease in CSF turnover in A4β2 deposit formation is up to now poorly known. We therefore investigated a possible relationship between a reduced CSF turnover and the CSF levels of the A4β2 peptide. To this aim, CSF of 31 patients with decreased CSF turnover were studied. These patients presented chronic hydrocephalus communicating or obstructive, which required surgery (ventriculostomy or ventriculo-peritoneal shunt). Nine subjects had idiopathic normal pressure hydrocephalus (iNPH), and the other 22 chronic hydrocephalus from other origins (oCH). The Aβ42 peptide concentration was measured by an ELISA test in 31 ventricular CSF samples and in 5 lumbar CSF samples from patients with communicating hydrocephalus. Results The 5 patients with lumbar CSF analysis had similar levels of lumbar and ventricular Aβ42. A significant reduction in Aβ42 ventricular levels was observed in 24 / 31 patients with hydrocephalus. The values were lower than 300 pg/ml in 5 out of 9 subjects with iNPH, and in 15 out of 22 subjects with oCH. Conclusion The decrease of CSF Aβ42 seems to occur independently of the surgical hydrocephalus aetiology. This suggests that a CSF reduced turnover may play an important role in the decrease of CSF Aβ42 concentration.

International audience; In halothane-anesthetized, paralyzed, and artificially ventilated rats, the putative 5-hydroxytryptamine1A receptor agonist 8-OHDPAT (13.1 micrograms/kg iv) produced hypotension (-14.6 +/- 1.3 mmHg, n = 35), reduced lumbar sympathetic nerve discharge (SND, -17.8%, n = 35), and slowed the discharge rate of sympathoexcitatory neurons recorded in the rostroventrolateral medulla (RVLM, -17.6%, n = 20). The gain of the baroreflex was unaffected by the drug, but SND and RVLM unit discharges were silenced at significantly reduced levels of mean arterial pressure (MAP; 153 vs. 171 mmHg for SND, 155 vs. 172 mmHg for RVLM cells). Subsequent intravenous administration of the alpha 2-adrenergic receptor agonist clonidine (5.3 micrograms/kg) produced an additional decrease in MAP (-21.2 +/- 1.9 mmHg, n = 24) and SND (-24%, n = 24), Bilateral microinjections of 8-OHDPAT into the RVLM (1 nmol/side, n = 9) or into the raphe pallidus-obscurus (2 injections of 1 nmol each, n = 7) also produced hypotension (-22.9 +/- 3.2 and -14.4 +/- 2.8 mmHg, respectively) and sympathoinhibition (-39.1 and -24.6%, respectively). Bilateral microinjection into RVLM of the alpha 2-adrenergic antagonists idazoxan (16 nmol/side, n = 6) or rauwolscine (2 nmol/side, n = 6) attenuated the sympatholytic effect of both 8-OHDPAT (13.1 micrograms/kg, iv) and clonidine (5.3 micrograms/kg iv). These results suggest that 8-OHDPAT may exert a portion of its central sympatholytic effect by activating alpha 2-adrenergic receptors in the rostroventral medulla.