Quantitative analysis of surface EMG activity of cranial and leg muscles across sleep stages in human.

OBJECTIVE: The aim of this study was to make a quantitative analysis of the changes in cranial and limb muscle activity from wakefulness to light and deep sleep stages and during rapid eye movement (REM) sleep of normal subjects. METHODS: Polysomnographic recordings were made of the sleep of 9 healthy human subjects, including electromyograms of the suprahyoid, temporalis and masseter cranial muscles and the anterior tibialis limb muscle. Quantitative assessments of EMG activity were carried out with root mean square (RMS) and frequency-spectral analysis (FSA) methods. RESULTS: From wakefulness to sleep, a significant reduction (-25.2 to -71.2%; P < 0.01) was observed in EMG activity (for both RMS and FSA) of the 3 cranial muscles using both methods of analysis. The EMG activity of suprahyoid muscle further decreased from non-REM to REM sleep (-17.8 to -43.0%; P < 0.01). In contrast, the EMG activity of the anterior tibialis muscle was only slightly reduced across sleep stages and did not further reduce during REM sleep. During REM sleep, all the 4 muscles maintained minimal activity. CONCLUSIONS: The maintenance of muscle activity during REM sleep suggests that a minimal level of activity is required to preserve physiological functions (e.g. airway patency, posture) related to homeostasis and bodily protection. SIGNIFICANCE: This study suggests that quantitative sleep EMG analysis is important for understanding the mechanisms of sleep-related movement disorders or when objective assessment of changes in EMG activity are needed for diagnostic purposes or for the assessment of drug efficiency.     

Androgen receptor YAC transgenic mice carrying CAG 45 alleles show trinucleotide repeat instability

X-linked spinal and bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion in the first exon of the androgen receptor (AR) gene. Disease-associated alleles (37-66 CAGs) change in length when transmitted from parents to offspring, with a significantly greater tendency to shift size when inherited paternally. As transgenic mice carrying human AR cDNAs with 45 and 66 CAG repeats do not display repeat instability, we attempted to model trinucleotide repeat instability by generating transgenic mice with yeast artificial chromosomes (YACs) carrying AR CAG repeat expansions in their genomic context. Studies of independent lines of AR YAC transgenic mice with CAG 45 alleles reveal intergenerational instability at an overall rate of approximately 10%. We also find that the 45 CAG repeat tracts are significantly more unstable with maternal transmission and as the transmitting mother ages. Of all the CAG/CTG repeat transgenic mice produced to date the AR YAC CAG 45 mice are unstable with the smallest trinucleotide repeat mutations, suggesting that the length threshold for repeat instability in the mouse may be lowered by including the appropriate flanking human DNA sequences. By sequence-tagged site content analysis and long range mapping we determined that one unstable transgenic line has integrated an approximately 70 kb segment of the AR locus due to fragmentation of the AR YAC. Identification of the cis - acting elements that permit CAG tract instability and the trans -acting factors that modulate repeat instability in the AR YAC CAG 45 mice may provide insights into the molecular basis of trinucleotide repeat instability in humans.      

Topographical distribution and functional properties of cortically induced rhythmical jaw movements in the monkey (Macaca fascicularis)

1. The lateral part of the pericentral cortex of both hemispheres in three awake monkeys was explored with intracortical microstimulation (ICMS) using short trains (T/S; 200-microseconds pulses at 333 Hz for 35 ms, less than or equal to microA) and long trains (C/S; 200-microseconds pulses at 50 Hz for 3 s, less than or equal to 60 microA). In both hemispheres of one of these monkeys, the responsiveness of single cortical neurons to stimulation of the orofacial region was tested at the same intracortical sites where ICMS was applied. 2. Movements were evoked from four physiologically defined cortical regions: the primary face motor cortex (MI), the primary face somatosensory cortex (SI), the principal part of the cortical masticatory area (CMAp) which was located in the precentral gyrus lateral to MI, and a deep part of the cortical masticatory area (CMAd) which was located in the inferior face of the frontal operculum. 3. Two types of cortically induced movements were observed: a single twitch movement and EMG activity of the orofacial muscles that was evoked by T/S at a short latency (10-45 ms) and rhythmical jaw movements (RJMs) which were only evoked by C/S. 4. RJMs were evoked at C/S frequencies ranging from 20 to 300 Hz. At movement threshold, the frequency of the cortically induced RJMs varied from 0.7 to 1.5 Hz and usually increased with the increase of C/S intensity up to 2 times movement threshold. The vertical amplitude of RJMs was also stimulus dependent, and at movement threshold it ranged from 3 to 9 mm. 5. The movement patterns of the cortically induced RJMs remained constant during the course of C/S but could be differentiated in the frontal plane into ipsilateral- (RJMi), vertical-(RJMv), and contralateral- (RJMc) directed movements. These three different patterns of RJMs were associated with different patterns of masticatory muscle activity. 6. Each cortical region contained many sites from which RJMs could be induced (so-called RJM sites). The RJMi sites were more numerous than RJMc sites in all regions except SI and were located anterolateral or lateral to the RJMc sites in each region; the RJMv sites were scattered throughout each cortical region. 7. In MI, C/S elicited RJMs from 94 intracortical sites from which short-latency twitch movements could also be evoked by T/S.(ABSTRACT TRUNCATED AT 400 WORDS)