Characterization of circular muscle motor neurons of the duodenum and distal colon in the Australian brush-tailed possum

2001 ◽  
Vol 443 (1) ◽  
pp. 15-26 ◽  
Author(s):  
Hiroyuki Konomi ◽  
Adrian C.B. Meedeniya ◽  
Maria E. Simula ◽  
James Toouli ◽  
Gino T.P. Saccone
Keyword(s):  
Motor Neurons ◽  
Circular Muscle ◽  
Distal Colon

Stretch-activated neuronal pathways to longitudinal and circular muscle in guinea pig distal colon

2003 ◽  
Vol 284 (2) ◽  
pp. G231-G241 ◽  
Author(s):  
Nick J. Spencer ◽  
Grant W. Hennig ◽  
Terence K. Smith
Keyword(s):  
Guinea Pig ◽  
Motor Neurons ◽  
Circular Muscle ◽  
Distal Colon ◽  
Intracellular Recordings ◽  
Excitatory Junction Potentials ◽  
Descending Interneurons ◽  
Electrical Activities ◽  
Small And Large Intestine

The role of the longitudinal muscle (LM) layer during the peristaltic reflex in the small and large intestine is unclear. In this study, we have made double and quadruple simultaneous intracellular recordings from LM and circular muscle (CM) cells of guinea pig distal colon to correlate the electrical activities in the two different muscle layers during circumferential stretch. Simultaneous recordings from LM and CM cells (<200 μm apart) at the oral region of the colon showed that excitatory junction potentials (EJPs) discharged synchronously in both muscle layers for periods of up to 6 h. Similarly, at the anal region of the colon, inhibitory junction potentials (IJPs) discharged synchronously in the two muscle layers. Quadruple recordings from LM and CM orally at the same time as from the LM and CM anally revealed that IJPs occurred synchronously in the LM and CM anally at the same time as EJPs in LM and CM located 20 mm orally. Oral EJPs and anal IJPs were linearly related in amplitude between the two muscle layers. Spatiotemporal maps generated from simultaneous video imaging of the movements of the colon, combined with intracellular recordings, revealed that some LM contractions orally could be correlated in time with IJPs in CM cells anally. N ω-nitro-l-arginine (l-NA; 100 μM) abolished the IJP in LM, whereas a prominent l-NA-resistant “fast” IJP was always observed in CM. In summary, in stretched preparations, synchronized EJPs in both LM and CM orally are generated by synchronized firing of many ascending interneurons, which simultaneously activate excitatory motor neurons to both muscle layers. Similarly, synchronized IJPs in both LM and CM anally are generated by synchronized firing of many descending interneurons, which simultaneously activate inhibitory motor neurons to both muscle layers. This synchronized motor activity ensures that both muscles around the entire circumference are excited orally at the same time as inhibited anally, thus producing net aboral propulsion.

Role of opioid neurons in the regulation of intestinal peristalsis

1987 ◽  
Vol 253 (2) ◽  
pp. G226-G231 ◽  
Author(s):  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Motor Neurons ◽  
Neural Activity ◽  
Opioid Peptides ◽  
Muscle Tone ◽  
Circular Muscle ◽  
Peristaltic Reflex ◽  
Intestinal Peristalsis ◽  
Subsequent Phase

The participation of opioid neurons in the regulation of peristalsis was examined in a rat colonic segment that permits separate characterization of the components of the peristaltic reflex (ascending contraction and descending relaxation). Naloxone increased descending relaxation and decreased ascending contraction; opioid peptides [methionine-enkephalin (Met-Enk), dynorphin-13, and morphiceptin] had opposite effects. Naloxone increased, and Met-Enk decreased, vasoactive intestinal peptide (VIP) release during each component of the reflex. The changes in VIP release reinforced the direct effects of naloxone and opioid peptides on circular muscle tone, providing an explanation for the effects of these agents on the two components of the peristaltic reflex. Dynorphin release decreased during descending relaxation and increased during ascending contraction, reflecting corresponding changes in opioid neural activity. Based on these results a model is proposed, according to which a decrease in opioid neural activity during the initial phase (i.e., descending relaxation) results in direct and VIP-mediated decrease in circular muscle tone. Restoration of opioid neural activity during the subsequent phase (i.e., ascending contraction) increases circular muscle tone and reinforces the action of tachykinin and cholinergic motor neurons, which are the direct mediators of ascending contraction.

Characterization of duodenal circular muscle motor neurons in the australian brush-tailed possum

2000 ◽  
Vol 118 (4) ◽  
pp. A403
Author(s):  
Hiroyuki Konomi ◽  
Adrian C. Meedeniya ◽  
Maria E. Simula ◽  
Jim Toouli ◽  
Gino T. Saccone
Keyword(s):  
Motor Neurons ◽  
Circular Muscle

Characterization of Myoelectric Signals Using System Identification Techniques

2004 ◽  
Author(s):  
Jeffrey T. Bingham ◽  
Marco P. Schoen
Keyword(s):  
System Identification ◽  
Motor Neurons ◽  
Current System ◽  
Electrical Potential ◽  
Computer Software ◽  
The Body ◽  
Myoelectric Signals ◽  
Hand Motion ◽  
The Central Nervous System

Human muscle motion is initiated in the central nervous system where a nervous signal travels through the body and the motor neurons excite the muscles to move. These signals, termed myoelectric signals, can be measured on the surface of the skin as an electrical potential. By analyzing these signals it is possible to determine the muscle actions the signals elicit, and thus can be used in manipulating smart prostheses and teleoperation of machinery. Due to the randomness of myoelectric signals, identification of the signals is not complete, therefore the goal of this project is to complete a study of the characterization of one set of hand motions using current system identification methods. The gripping motion of the hand and the corresponding myoelectric signals are measured and the data captured with a personal computer. Using computer software the captured data are processed and finally subjected to several system identification routines. Using this technique it is possible to construct a mathematical model that correlates the myoelectric signals with the matching hand motion.

scholarly journals AAV9-mediated delivery of miR-23a reduces disease severity in Smn2B/−SMA model mice

2019 ◽  
Vol 28 (19) ◽  
pp. 3199-3210 ◽  
Author(s):  
Kevin A Kaifer ◽  
Eric Villalón ◽  
Benjamin S O'Brien ◽  
Samantha L Sison ◽  
Caley E Smith ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Motor Neurons ◽  
Molecular Mechanisms ◽  
Viral Vector ◽  
Muscular Atrophy ◽  
Induced Pluripotent Stem Cell ◽  
Survival Motor Neuron ◽  
Virus Serotype

Abstract Spinal muscular atrophy (SMA) is a neuromuscular disease caused by deletions or mutations in survival motor neuron 1 (SMN1). The molecular mechanisms underlying motor neuron degeneration in SMA remain elusive, as global cellular dysfunction obscures the identification and characterization of disease-relevant pathways and potential therapeutic targets. Recent reports have implicated microRNA (miRNA) dysregulation as a potential contributor to the pathological mechanism in SMA. To characterize miRNAs that are differentially regulated in SMA, we profiled miRNA levels in SMA induced pluripotent stem cell (iPSC)-derived motor neurons. From this array, miR-23a downregulation was identified selectively in SMA motor neurons, consistent with previous reports where miR-23a functioned in neuroprotective and muscle atrophy-antagonizing roles. Reintroduction of miR-23a expression in SMA patient iPSC-derived motor neurons protected against degeneration, suggesting a potential miR-23a-specific disease-modifying effect. To assess this activity in vivo, miR-23a was expressed using a self-complementary adeno-associated virus serotype 9 (scAAV9) viral vector in the Smn2B/− SMA mouse model. scAAV9-miR-23a significantly reduced the pathology in SMA mice, including increased motor neuron size, reduced neuromuscular junction pathology, increased muscle fiber area, and extended survival. These experiments demonstrate that miR-23a is a novel protective modifier of SMA, warranting further characterization of miRNA dysfunction in SMA.

scholarly journals Characterization of the [125 I]-neurokinin A binding site in the circular muscle of human colon

1999 ◽  
Vol 127 (5) ◽  
pp. 1105-1110 ◽  
Author(s):  
Fiona J Warner ◽  
Alfio Comis ◽  
Robert C Miller ◽  
Elizabeth Burcher
Keyword(s):  
Binding Site ◽  
Circular Muscle ◽  
Human Colon ◽  
Neurokinin A
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