5-hydroxytryptamine-mediated apnea caused by the habenular nucleus

5-hydroxytryptamine contributes to the control of activities of the dilator muscle in the upper respiratory tract, and is derived from the raphe nuclei, in which the habenular nucleus exerts a sustaJned inhibitory effect. In the present study, respiratory motion curve of the genJoglossus muscle and peripheral 5-hydroxytryptamine changes were observed following L-glutamate stimulation of the habenular nucleus of adult Wistar rats. Results showed that the rats had apnea and decreased plasma 5-hydroxytryptamine content after the neurons in habenular nucleus were excited. Genioglossus muscle electromyogram amplitude and integral were significantly reduced. The genioglossus myoelectric activity and respiratory motion curve were similar to obstructive sleep apnea syndrome, thus confirming that the habenular nucleus is the key nucleus involved in the pathogenesis of obstructive sleep apnea syndrome, and is the primary regulated center in the raphe nuclei. Stimulation of the habenular nucleus may suppress 5-hydroxytryptamine release and result in apnea, which is similar to obstructive sleep apnea syndrome.

Senegenin inhibits neuronal apoptosis after spinal cord contusion injury

Senegenin has been shown to inhibit neuronal apoptosis,thereby exerting a neuroprotective effect.In the present study,we established a rat model of spinal cord contusion injury using the modified Allen＇s method.Three hours after injury,senegenin（30 mg/g） was injected into the tail vein for 3 consecutive days.Senegenin reduced the size of syringomyelic cavities,and it substantially reduced the number of apoptotic cells in the spinal cord.At the site of injury,Bax and Caspase-3 m RNA and protein levels were decreased by senegenin,while Bcl-2 m RNA and protein levels were increased.Nerve fiber density was increased in the spinal cord proximal to the brain,and hindlimb motor function and electrophysiological properties of rat hindlimb were improved.Taken together,our results suggest that senegenin exerts a neuroprotective effect by suppressing neuronal apoptosis at the site of spinal cord injury.

Coexistent Charcot-Marie-Tooth type 1A and type 2 diabetes mellitus neuropathies in a Chinese family

Charcot-Marie-Tooth disease type 1A（CMT1A） is caused by duplication of the peripheral myelin protein 22（PMP22） gene on chromosome 17. It is the most common inherited demyelinating neuropathy. Type 2 diabetes mellitus is a common metabolic disorder that frequently causes predominantly sensory neuropathy. In this study, we report the occurrence of CMT1 A in a Chinese family affected by type 2 diabetes mellitus. In this family, seven individuals had duplication of the PMP22 gene, although only four had clinical features of polyneuropathy. All CMT1 A patients with a clinical phenotype also presented with type 2 diabetes mellitus. The other three individuals had no signs of CMT1 A or type 2 diabetes mellitus. We believe that there may be a genetic link between these two diseases.

Pathogenesis and electrodiagnosis of cubital tunnel syndrome

Background Cubital tunnel syndrome is a well-recognized clinical condition and is the second most common peripheral compression neuropathy. This study was designed to investigate the causes of cubital tunnel syndrome by surgical means and to assess the clinical value of the neurophysiological diagnosis of cubital tunnel syndrome. Methods Twenty-one patients (involving a total of 22 limbs from 16 men and 5 women, aged 22 to 63, with a mean age of 49 years) with clinical symptoms and signs indicating a problem with their ulnar nerve underwent motor conduction velocity examinations at different sites along the ulnar nerve and examinations of sensory conduction velocity in the hand, before undergoing anterior transposition of the ulnar nerve.Results Electromyographic abnormalities were seen in 21 of 22 limbs [motor nerve conduction velocity (MCV) range (15.9-47.5) m/s, mean 32.7 m/s] who underwent motor conduction velocity examinations across the elbow segment of the ulnar nerve. Reduced velocity was observed in 13 of 22 limbs [MCV (15.7-59.6) m/s, mean 40.4 m/s] undergoing MCV tests in the forearms. An absent or abnormal sensory nerve action potential following stimulation was detected in the little finger of 14 of 22 limbs. The factors responsible for ulnar compression based on observations made during surgery were as follows: 15 cases involved compression by arcuate ligaments, muscle tendons, or bone hyperplasia; 2 involved fibrous adhesion; 3 involved compression by the venous plexus or a concurrent thick vein; 2 involved compression by cysts. Conclusions Factors inducing cubital tunnel syndrome include both common factors that have been reported and rare factors, involving the venous plexus, thick veins, and cysts. Tests of motor conduction velocity at different sites along the ulnar nerve should be helpful in diagnosis cubital tunnel syndrome, especially MCV tests indicating decreased velocity across the elbow segment of the ulnar nerve.

Nanoscience and the nano-bioelectronics frontier

This review describes work presented in the 2014 inaugural Tsinghua University Press-Springer Nano Research Award lecture, as well as current and future opportunities for nanoscience research at the interface with brain science. First, we briefly summarize some of the considerations and the research journey that has led to our focus on bottom-up nanoscale science and technology. Second, we recapitulate the motivation for and our seminal contributions to nanowire- based nanoscience and technology, including the rational design and synthesis of increasingly complex nanowire structures, and the corresponding broad range of ＂applications＂ enabled by the capability to control structure, com- position and size from the atomic level upwards. Third, we describe in more detail nanowire-based electronic devices as revolutionary tools for brain science, including （i） motivation for nanoelectronics in brain science, （ii） demonstration of nanowire nanoelectronic arrays for high-spatial/high-temporal resolution extracellular recording, （iii） the development of fundamentally-new intracellular nanoelectronic devices that approach the sizes of single ion channels, （iv） the introduction and demonstration of a new paradigm for innervating cell networks with addressable nanoelectronic arrays in three-dimensions. Last, we conclude with a brief discussion of the exciting and potentially transformative advances expected to come from work at the nanoelectronics-brain interface.