Effect of injury severity on lower urinary tract function after experimental spinal cord injury.

Lower urinary tract dysfunction is a serious burden for patients following spinal cord injury. Patients are usually limited to treatment with urinary drainage catheters, which can lead to repeated urinary tract infections and lower quality of life. Most of the information previously obtained regarding lower urinary tract function after spinal cord injury has been in completely transected animals.

Effect of spinal cord injury severity on alterations of the H-reflex.

The monosynaptic motoneuron response to stimulation of Ia afferents is known to be altered by spinal cord injury (SCI). Although the Hoffman (H)-reflex is a tool that is often used to measure this reflex in patients, there has not been a systematic study investigating the effect of SCI severity and time on the H-reflex. We used a clinically relevant model of spinal cord contusion (Mild and Moderate) as well as complete surgical transection to measure the H-reflex at 1, 4 and 8 weeks after injury.

Tumor necrosis factor-alpha inhibits physiologically identified dorsal motor nucleus neurons in vivo.

Our previous studies have shown that tumor necrosis factor-alpha (TNF-alpha) activates solitary nucleus neurons involved in vago-vagal reflex control of gastric motility. Here, we describe the dual role of TNF-alpha as also modulating neurons in the dorsal motor nucleus of the vagus (DMN) that respond to gastric distention. A large majority of physiologically identified DMN neurons are rapidly and completely inhibited by exposure to TNF-alpha, suggesting that TNF-alpha may induce gastric stasis by functioning as a hormone that modulates both portions of this reflex pathway during illness.

TNF-alpha-induced c-Fos generation in the nucleus of the solitary tract is blocked by NBQX and MK-801.

Previous studies have shown that identified neurons of the nucleus of the solitary tract (NST) are excited by the cytokine tumor necrosis factor-alpha (TNF-alpha). Vagal afferent connections with the NST are predominantly glutaminergic. Therefore, we hypothesized that TNF-alpha effects on NST neurons may be via modulation of glutamate neurotransmission.

c-Fos generation in the dorsal vagal complex after systemic endotoxin is not dependent on the vagus nerve.

The present study used activation of the c-Fos oncogene protein within neurons in the dorsal vagal complex (DVC) as a marker of neuronal excitation in response to systemic endotoxin challenge [i.e. , lipopolysaccharide (LPS)].