Slow potential variations of small intestine

1961 ◽  
Vol 201 (1) ◽  
pp. 203-208 ◽  
Author(s):  
Alex Bortoff
Keyword(s):  
Small Intestine ◽  
Slow Wave ◽  
Time Course ◽  
Longitudinal Muscle ◽  
Time Derivative ◽  
Slow Waves ◽  
Slow Potential ◽  
True Time ◽  
Wave Discharge ◽  
Core Conductor

The various configurations of externally recorded slow waves from the small intestine of the cat are compared to those recorded intracellularly. It is shown that the slow waves represent periodic depolarizations of longitudinal muscle cells and that the flow of current associated with these depolarizations is similar to that in a core conductor. By recording monopolarly from a segment of intestine immersed in a volume conductor, slow waves are obtained having configurations ranging from those approximating the true time course and polarity of the intracellular slow wave to those approximating its second time derivative. This is shown to be a function of the pressure exerted by the electrode on the tissue. From a consideration of these results, plus those recently obtained by others, it is suggested that both "propagation" and synchronization of slow waves are manifestations of a modulation of slow wave discharge brought about either by electrotonic spread of current via low resistance intercellular pathways, or by voltage field effects.

Effect of secretin on electrical activity of small intestine

1975 ◽  
Vol 229 (2) ◽  
pp. 484-488 ◽  
Author(s):  
AK Mukhopadhyay ◽  
LR Johnson ◽  
EM Copeland ◽  
NW Weisbrodt
Keyword(s):  
Small Intestine ◽  
Small Bowel ◽  
Electrical Activity ◽  
Slow Wave ◽  
Intravenous Infusion ◽  
Action Potentials ◽  
Slow Waves ◽  
Wave Frequency ◽  
Conscious Dogs ◽  
Total Percentage

The effect of intravenously administered secretin (0.5, 2.0, 6.0 U/kg-h) and intraduodenal acidification (13.2 meq/h HCl) on the electrical activity of the small bowel of three conscious dogs with gastric and duodenal cannulas was observed. Electrical activity was recorded in fasted as well as fed conditions through silver wire electrodes implanted along the entire length of the small bowel. Intravenous infusion of secretin in all dosages and in all dogs delayed the onset of the interdigestive myoelectric complex and reduced the total percentage of slow waves with superimposed spike potentials. Intraduodenal acidification also inhibited the interdigestive myoelectric complex, which developed incompletely with fewer action potentials on slow waves. Secretin did not produce any alteration in the fed pattern of activity, slow-wave frequency, or the caudal migration of the interdigestive myoelectric complex. The present study indicates that the nuerohumoral mechanisms responsible for initiation of the interdigestive myoelectric complex may be different from those responsible for its caudal migration.

Responses of muscles of cat small intestine to autonomic nerve stimulation

1963 ◽  
Vol 204 (2) ◽  
pp. 352-358 ◽  
Author(s):  
Gordon L. Van Harn
Keyword(s):  
Small Intestine ◽  
Muscle Contraction ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Longitudinal Muscle ◽  
Muscle Layer ◽  
Slow Waves ◽  
Intraluminal Pressure ◽  
Sympathetic Nerve Stimulation ◽  
Longitudinal Muscle Layer

The externally recorded slow waves from the cat small intestine originate in the longitudinal muscle layer. In vitro the slow waves are recorded from all layers of the intestine if the segment is not immersed in a saline bath. When the longitudinal layer is removed from one region, the magnitude of the slow-wave potential in the other intestinal layers decreases as the distance from the intact longitudinal muscle layer is increased. An active intestine, in vivo, responds to sympathetic nerve stimulation by a hyperpolarization, cessation of spikes, and inhibition of muscle contraction. During inactivity of the intestine, either vagus or sympathetic nerve stimulation results in a depolarization, initiation of spikes, and muscle contraction. The nature of the response is influenced by the frequency of nerve stimulation and by the level of activity of the intestinal muscle, which is altered by intraluminal pressure changes. The effect of drugs on the response of the intestine to vagal and sympathetic nerve stimulation is such as to indicate that both inhibitory and excitatory nerve fibers are present in each of the autonomic nerves. The duration of the latent period of the response is long and highly variable, and a response requires 50–100 nerve volleys.

Mechanisms underlying nutrient-induced segmentation in isolated guinea pig small intestine

2007 ◽  
Vol 292 (4) ◽  
pp. G1162-G1172 ◽  
Author(s):  
R. M. Gwynne ◽  
J. C. Bornstein
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Motor Neurons ◽  
Slow Wave ◽  
Neural Circuit ◽  
Circular Muscle ◽  
Decanoic Acid ◽  
Slow Waves ◽  
Longitudinal Position

Mechanisms underlying nutrient-induced segmentation within the gut are not well understood. We have shown that decanoic acid and some amino acids induce neurally dependent segmentation in guinea pig small intestine in vitro. This study examined the neural mechanisms underlying segmentation in the circular muscle and whether the timing of segmentation contractions also depends on slow waves. Decanoic acid (1 mM) was infused into the lumen of guinea pig duodenum and jejunum. Video imaging was used to monitor intestinal diameter as a function of both longitudinal position and time. Circular muscle electrical activity was recorded by using suction electrodes. Recordings from sites of segmenting contractions showed they are always associated with excitatory junction potentials leading to action potentials. Recordings from sites oral and anal to segmenting contractions revealed inhibitory junction potentials that were time locked to those contractions. Slow waves were never observed underlying segmenting contractions. In paralyzed preparations, intracellular recording revealed that slow-wave frequency was highly consistent at 19.5 (SD 1.4) cycles per minute (c/min) in duodenum and 16.6 (SD 1.1) c/min in jejunum. By contrast, the frequencies of segmenting contractions varied widely (duodenum: 3.6–28.8 c/min, median 10.8 c/min; jejunum: 3.0–27.0 c/min, median 7.8 c/min) and sometimes exceeded slow-wave frequencies for that region. Thus nutrient-induced segmentation contractions in guinea pig small intestine do not depend on slow-wave activity. Rather they result from a neural circuit producing rhythmic localized activity in excitatory motor neurons, while simultaneously activating surrounding inhibitory motor neurons.

scholarly journals Conditional genetic deletion of Ano1 in interstitial cells of Cajal impairs Ca2+ transients and slow waves in adult mouse small intestine

2017 ◽  
Vol 312 (3) ◽  
pp. G228-G245 ◽  
Author(s):  
John Malysz ◽  
Simon J. Gibbons ◽  
Siva A. Saravanaperumal ◽  
Peng Du ◽  
Seth T. Eisenman ◽  
...  
Keyword(s):  
Small Intestine ◽  
Slow Wave ◽  
Interstitial Cells Of Cajal ◽  
Adult Mouse ◽  
Rank Order ◽  
Interstitial Cells ◽  
Slow Waves ◽  
Functional Reserve ◽  
Mouse Small Intestine ◽  
Cells Of Cajal

Myenteric plexus interstitial cells of Cajal (ICC-MY) in the small intestine are Kit+ electrical pacemakers that express the Ano1/TMEM16A Ca2+-activated Cl– channel, whose functions in the gastrointestinal tract remain incompletely understood. In this study, an inducible Cre-LoxP-based approach was used to advance the understanding of Ano1 in ICC-MY of adult mouse small intestine. KitCreERT2/+;Ano1Fl/Fl mice were treated with tamoxifen or vehicle, and small intestines (mucosa free) were examined. Quantitative RT-PCR demonstrated ~50% reduction in Ano1 mRNA in intestines of conditional knockouts (cKOs) compared with vehicle-treated controls. Whole mount immunohistochemistry showed a mosaic/patchy pattern loss of Ano1 protein in ICC networks. Ca2+ transients in ICC-MY network of cKOs displayed reduced duration compared with highly synchronized controls and showed synchronized and desynchronized profiles. When matched, the rank order for Ano1 expression in Ca2+ signal imaged fields of view was as follows: vehicle controls>>>cKO(synchronized)>cKO(desynchronized). Maintenance of Ca2+ transients’ synchronicity despite high loss of Ano1 indicates a large functional reserve of Ano1 in the ICC-MY network. Slow waves in cKOs displayed reduced duration and increased inter-slow-wave interval and occurred in regular- and irregular-amplitude oscillating patterns. The latter activity suggested ongoing interaction by independent interacting oscillators. Lack of slow waves and depolarization, previously reported for neonatal constitutive knockouts, were also seen. In summary, Ano1 in adults regulates gastrointestinal function by determining Ca2+ transients and electrical activity depending on the level of Ano1 expression. Partial Ano1 loss results in Ca2+ transients and slow waves displaying reduced duration, while complete and widespread absence of Ano1 in ICC-MY causes lack of slow wave and desynchronized Ca2+ transients. NEW & NOTEWORTHY The Ca2+-activated Cl− channel, Ano1, in interstitial cells of Cajal (ICC) is necessary for normal gastrointestinal motility. We knocked out Ano1 to varying degrees in ICC of adult mice. Partial knockout of Ano1 shortened the widths of electrical slow waves and Ca2+ transients in myenteric ICC but Ca2+ transient synchronicity was preserved. Near-complete knockout was necessary for transient desynchronization and loss of slow waves, indicating a large functional reserve of Ano1 in ICC. View this article's corresponding video summary at https://youtu.be/cyPtDP0KLY4 .

scholarly journals Broadband slow-wave modulation in posterior and anterior cortex tracks distinct states of propofol-induced unconsciousness

2019 ◽  
Author(s):  
Emily P. Stephen ◽  
Gladia C. Hotan ◽  
Eric T. Pierce ◽  
P. Grace Harrell ◽  
John L. Walsh ◽  
...  
Keyword(s):  
Frontal Cortex ◽  
Slow Wave ◽  
Time Course ◽  
Wave Activity ◽  
Slow Waves ◽  
Brain State ◽  
Posterior Cortex ◽  
Anterior Cortex ◽  
Wave Modulation ◽  
Up And Down States

A controversy 5 has developed in recent years over the role that frontal and posterior cortices play in mediating consciousness and unconsciousness. One hypothesis proposes that posterior sensory and association cortices are the principal mediators of consciousness, citing evidence that strong slow-wave activity over posterior cortex during sleep disrupts the contents of dreaming. A competing hypothesis proposes that frontal-posterior interactions are critical to ignite a conscious percept, since activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. In both cases, EEG slow-waves (< 1 Hz) are considered evidence that up- and down-states are disrupting cortical activity necessary for consciousness. Here, we used anesthesia to study the interaction between the slow-wave and higher frequency activity in humans. If slow-waves are derived from underlying up and down-states, then they should modulate activity across a broad range of frequencies. We found that this broadband slow-wave modulation does occur: broadband slow-wave modulation occurs over posterior cortex when subjects initially become unconscious, but later encompasses both frontal and posterior cortex when subjects are more deeply anesthetized and likely unarousable. Based on these results, we argue that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the sensory contents of consciousness distinct from arousal and awareness of those contents.Significance StatementThe roles of frontal and posterior cortices in mediating consciousness and unconsciousness are controversial. Disruption of posterior cortex during sleep appears to suppress the contents of dreaming, yet activation of frontal cortex appears necessary for perception and can reverse unconsciousness under anesthesia. We studied the time course of regional cortical disruption, as mediated by slow-wave modulation of broadband activity, during anesthesia-induced unconsciousness in humans. We found that broadband slow-wave modulation covered posterior cortex when subjects initially became unconscious, but later encompassed both frontal and posterior cortex when subjects were deeply anesthetized and likely unarousable. This suggests that unconsciousness under anesthesia comprises several shifts in brain state that disrupt the contents of consciousness distinct from arousal and awareness of those contents.

Migrating spike complex in the small intestine of the fasting cat

1993 ◽  
Vol 265 (4) ◽  
pp. G619-G627
Author(s):  
W. C. De Vos
Keyword(s):  
Small Intestine ◽  
Action Potential ◽  
Electrical Activity ◽  
Slow Wave ◽  
Close Association ◽  
Slow Waves ◽  
Wave Frequency ◽  
Laboratory Animals ◽  
Variable Frequency ◽  
Implanted Electrodes

This study characterizes the migrating spike complex (MSC) in the small intestine of the awake fasting cat and compares the MSC with interdigestive activity in the small intestine of other species. Electrical activity in each of 12 cats with implanted electrodes showed MSCs, bands of spike potentials which attenuated slow-wave frequency and amplitude as the MSCs progressed distally. MSCs occurred at variable frequency with intervals ranging from < 1 min to > 5 h and averaged 51.2 +/- 2.8 (SE) min. MSCs migrated at 1-8 mm/s, accelerating distally; the duration decreased distally such that the length of the bowel in a burst (2-3 cm proximally) was conserved. The MSC was associated with an intense prolonged contraction of duration similar to that of the MSC. Sometimes the MSCs occurred in close association, and when an MSC period was < 5.7 min, the second MSC propagated at a slower rate than the first. Frequently, a brief series of slow wave-associated spikes preceded an MSC. MSCs were not associated with slow waves. The MSC differs in several respects from the migrating myoelectric complex of other laboratory animals and is more appropriately classified in a category that includes giant migrating spikes, prolonged propagated contractions, power contractions, and migrating action potential complexes.

scholarly journals Electrophysiological Studies of the Antrum Muscle Fibers of the Guinea Pig Stomach

1970 ◽  
Vol 55 (1) ◽  
pp. 48-62 ◽  
Author(s):  
H. Kuriyama ◽  
T. Osa ◽  
H. Tasaki
Keyword(s):  
Slow Wave ◽  
Longitudinal Muscle ◽  
Muscle Fibers ◽  
Circular Muscle ◽  
Slow Waves ◽  
The Other ◽  
Spike Generation ◽  
High K ◽  
Electrophysiological Studies ◽  
Guinea Pig Stomach

The membrane potentials of single smooth muscle fibers of various regions of the stomach were measured, and do not differ from those measured in intestinal muscle. Spontaneous slow waves with superimposed spikes could be recorded from the longitudinal and circular muscle of the antrum. The development of tension was preceded by spikes but often tension appeared only when the slow waves were generated. Contracture in high K solution developed at a critical membrane potential of -42 mv. MnCl2 blocked the spike generation, then lowered the amplitude of the slow wave. On the other hand, withdrawal of Na+, or addition of atropine and tetrodotoxin inhibited the generation of most of the slow waves but a spike could still be elicited by electrical stimulation. Prostigmine enhanced and prolonged the slow wave; acetylcholine depolarized the membrane without change in the frequency of the slow waves. Chronaxie for the spike generation in the longitudinal muscle of the antrum was 30 msec and conduction velocity was 1.2 cm/sec. The time constant of the foot of the propagated spike was 28 msec. The space constants measured from the longitudinal and circular muscles of the antrum were 1.1 mm and 1.4 mm, respectively.

Effects of alterations in calcium levels on cat small intestinal slow waves

1982 ◽  
Vol 243 (1) ◽  
pp. C7-C13 ◽  
Author(s):  
A. W. Mangel ◽  
J. A. Connor ◽  
C. L. Prosser
Keyword(s):  
Intracellular Calcium ◽  
Slow Wave ◽  
Calcium Concentration ◽  
Longitudinal Muscle ◽  
Slow Waves ◽  
Wave Frequency ◽  
Intracellular Calcium Concentration ◽  
Magnesium Concentration ◽  
Reduced Frequency ◽  
Intestinal Slow Waves

Intact segments of cat intestinal muscle and strips of isolated longitudinal muscle were treated with agents that reduce intracellular calcium concentration: incubation in 0-calcium saline, treatment with calcium conductance blockers, elevated extracellular magnesium concentration, or alkalinization with NH4Cl. These treatments reduced amplitude and frequency of slow waves in intact segments but only reduced frequency in isolated longitudinal muscle. The reduction in frequency was characterized by prolongation of the hyperpolarized phase of the slow waves. Treatments that would moderately increase intracellular calcium concentration, i.e., increasing external calcium to four times normal levels or lowering pH by CO2, increased slow-wave frequency. Increased frequency was associated with reduced amplitude and shortening of the hyperpolarized phase of the slow waves. Greater than four times normal calcium levels and intense spiking reduced slow-wave frequency. Chlorotetracycline fluorescence, an indicator of intracellular calcium concentration, showed fluctuations synchronous with slow waves. It is concluded that the reactions that pace the generation of slow waves are dependent on the level of intracellular calcium.

Electrical activity of the longitudinal muscle of dog small intestine studied in vivo using microelectrodes

1960 ◽  
Vol 198 (1) ◽  
pp. 113-118 ◽  
Author(s):  
E. E. Daniel ◽  
A. J. Honour ◽  
A. Bogoch
Keyword(s):  
Small Intestine ◽  
Body Temperature ◽  
Action Potential ◽  
Electrical Activity ◽  
Longitudinal Muscle ◽  
Muscle Cells ◽  
Slow Waves

The electrical activity of longitudinal muscle cells of the small intestine of the dog have been recorded in vivo using microelectrodes. This activity is characterized by periodic slow depolarizations of from 3 to 15 mv starting from potentials of 35–50 mv. The frequency of these slow depolarizations is less in the ileum than in the jejunum and is diminished by reduction in body temperature. Asphyxia diminishes both frequency and amplitude of these slow depolarizations without affecting the resting potentials. Action potential spikes arise from the larger slow depolarizations. The records obtained in this study are compared with previously recorded monopolar extracellular records. It is concluded that the slow waves recorded using extracellular electrodes arise from slow depolarizations of intestinal muscle cells. It is proposed that these slow depolarizations are a coordinating mechanism for motility of the longitudinal muscle of the dog intestine. The mechanism of synchronization of the slow waves themselves remains to be elucidated.

scholarly journals The myogenic component in distention-induced peristalsis in the guinea pig small intestine

2001 ◽  
Vol 280 (3) ◽  
pp. G491-G500 ◽  
Author(s):  
Graeme Donnelly ◽  
Timothy D. Jackson ◽  
Krista Ambrous ◽  
Jing Ye ◽  
Adeel Safdar ◽  
...  
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Slow Wave ◽  
Action Potentials ◽  
Slow Waves ◽  
Intraluminal Pressure ◽  
Control Activity ◽  
Potential Oscillations ◽  
Frequency Gradient

In an in vitro model for distention-induced peristalsis in the guinea pig small intestine, the electrical activity, intraluminal pressure, and outflow of contents were studied simultaneously to search for evidence of myogenic control activity. Intraluminal distention induced periods of nifedipine-sensitive slow wave activity with superimposed action potentials, alternating with periods of quiescence. Slow waves and associated high intraluminal pressure transients propagated aborally, causing outflow of content. In the proximal small intestine, a frequency gradient of distention-induced slow waves was observed, with a frequency of 19 cycles/min in the first 1 cm and 11 cycles/min 10 cm distally. Intracellular recording revealed that the guinea pig small intestinal musculature, in response to carbachol, generated slow waves with superimposed action potentials, both sensitive to nifedipine. These slow waves also exhibited a frequency gradient. In addition, distention and cholinergic stimulation induced high-frequency membrane potential oscillations (∼55 cycles/min) that were not associated with distention-induced peristalsis. Continuous distention produced excitation of the musculature, in part neurally mediated, that resulted in periodic occurrence of bursts of distally propagating nifedipine-sensitive slow waves with superimposed action potentials associated with propagating intraluminal pressure waves that caused pulsatile outflow of content at the slow wave frequency.

Sign in / Sign up

Export Citation Format

Share Document