scholarly journals Effects of vagal sensory input on the breathing rhythm of the carp

1991 ◽  
Vol 155 (1) ◽  
pp. 77-91
Author(s):  
P.J. F. DE GRAAF ◽  
B. L. Roberts
Keyword(s):  
Electrical Stimulation ◽  
Cyprinus Carpio ◽  
Sensory Input ◽  
Vagal Stimulation ◽  
Respiratory Rhythm ◽  
Cycle Period ◽  
Breathing Cycle ◽  
Marked Influence ◽  
Carp Cyprinus Carpio ◽  
Stimulation Of

Electrical stimulation of an epibranchial vagal ganglion, which innervates the gill region, had a marked influence on the respiratory rhythm of the carp Cyprinus carpio. Vagal input could initiate ventilation in fish displaying intermittent respiration. In fish breathing steadily, vagal stimuli could reset the respiratory rhythm by modifying the existing breathing cycle. An increase of stimulus intensity evoked a cough-like movement, thus delaying the onset of following cycles. Rhythmic stimulation, at intervals not more than 10° longer or shorter than the breathing cycle period, could entrain the respiratory rhythm in a one-toone ratio. Larger differences between the stimulation interval and the period of the breathing cycle resulted in either a cyclic modification of the respiratory cycle period or entrainment patterns with coupling ratios of 2:1 or 2:3. Coughing decreased in frequency or even stopped during rhythmic vagal stimulation.

An Electromyographic Study of the Adductor Mandibulae Complex of a Free-Swimming Carp (Cyprinus Carpio L.) During Feeding

1972 ◽  
Vol 57 (1) ◽  
pp. 261-283 ◽  
Author(s):  
C. M. BALLINTIJN ◽  
A. VAN DEN BURG ◽  
B. P. EGBERINK
Keyword(s):  
Electrical Stimulation ◽  
Cyprinus Carpio ◽  
Muscle Coordination ◽  
Free Swimming ◽  
Spontaneous Movements ◽  
Carp Cyprinus Carpio ◽  
Stimulation Of

1. The anatomy of the upper and lower jaws of the carp, together with the associated maxillaris and mandibularis muscles of the adductor mandibulae complex, is described. 2. From the electromyograms of the adductor mandibulae muscles, recorded simultaneously with a 16 mm film of the mouth movements in a free-swimming carp, the muscle coordination of the diverse mouth movements during feeding has been studied. 3. The interpretation of the results has been verified by electrical stimulation of the muscles, in different combinations, in a fish in which spontaneous movements were abolished by heavy anaesthesia.

Similarity of granular-induced inhibitory periods in pairs of neighboring mitral/tufted cells

1996 ◽  
Vol 76 (4) ◽  
pp. 2393-2401 ◽  
Author(s):  
N. Buonviso ◽  
M. A. Chaput ◽  
F. Berthommier
Keyword(s):  
Electrical Stimulation ◽  
Granule Cells ◽  
Anterior Commissure ◽  
Respiratory Rhythm ◽  
Control Group ◽  
Inhibitory Input ◽  
Mitral Cells ◽  
Temporal Correlations ◽  
Tufted Cells ◽  
Stimulation Of

1. Neighboring mitral/tufted cells have been previously shown to present temporal correlations of their firings related to the respiratory rhythm, particularly under odor stimulation. This occurs despite the existence of a powerful inhibitory control exerted by granule cells onto mitral/tufted cells. In the present study, we hypothesized that neighboring mitral cells can present granular induced inhibitory periods with similar latencies and durations and that such a similarity would preserve them from a possible suppression of their temporal correlations. 2. To test this hypothesis, we analyzed the latencies and durations of the inhibitory periods induced by granular activation in pairs of simultaneously recorded neighboring mitral cells. The activation of granule cells was achieved by electrical stimulation of the different pathways known to directly activate granule cells [lateral olfactory tract (LOT), anterior limb of the anterior commissure (AC), and piriform cortex (PC)]. Data from this group were compared with those of a control group composed of distant cells also recorded simultaneously. 3. Results first show that the latencies to onset of inhibition or to recovery were more frequently similar in neighboring cells than in control cells and that this similarity was enhanced by odor stimulation. Second, the probability that two cells exhibit similar inhibitory periods (i.e., similar latencies to both onset and to recovery) in response to electrical stimulation of LOT, AC, or PC was significantly higher in neighboring than in control cells. Third, only neighboring cells were found to present similar inhibitory periods in response to the stimulation of all of the three structures. 4. Granular activation was also found to modify the temporal patterns of individual mitral cells. However, although these patterns were not systematically modified similarly in neighboring mitral cells, they remained perfectly synchronized with zero delay if they were already synchronous without electrical stimulation. On the contrary, if patterns were spontaneously uncorrelated, electrical stimulation never produced a synchronization of their firings, even if their temporal relationships could be profoundly modified. 5. These results show that neighboring mitral cells can receive granular-induced inhibition with similar latencies and durations with a probability much higher than control cells. Such similarities allow neighboring mitral cells to preserve their temporal correlation despite the powerful inhibitory input from granule cells. Functional hypotheses about the role of the cortical feedback projections onto the bulb are discussed.

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

1991 ◽  
Vol 66 (6) ◽  
pp. 2084-2094 ◽  
Author(s):  
R. W. Blair ◽  
A. R. Evans
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Vagal Stimulation ◽  
Discharge Rate ◽  
Stellate Ganglion ◽  
Cell Activity ◽  
Conditioning Stimulus ◽  
Vagal Afferents ◽  
Early Peak ◽  
Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Cerebral-evoked potential responses following direct vagal and esophageal electrical stimulation in humans

1993 ◽  
Vol 264 (3) ◽  
pp. G486-G491 ◽  
Author(s):  
G. Tougas ◽  
P. Hudoba ◽  
D. Fitzpatrick ◽  
R. H. Hunt ◽  
A. R. Upton
Keyword(s):  
Electrical Stimulation ◽  
Evoked Potential ◽  
Vagal Stimulation ◽  
Direct Electrical Stimulation ◽  
Sensory Pathways ◽  
Afferent Fibers ◽  
Health And Disease ◽  
Esophageal Sphincter ◽  
Afferent Response ◽  
Stimulation Of

Cerebral evoked responses following direct electrical stimulation of the vagus and esophagus were compared in 8 epileptic subjects and with those recorded after esophageal stimulation in 12 healthy nonepileptic controls. Direct vagal stimulation was performed using a left cervical vagal pacemaker, which is used in the treatment of epilepsy. Esophageal stimulation was obtained with the use of an esophageal assembly incorporating two electrodes positioned 5 and 20 cm orad to the lower esophageal sphincter. Evoked potential responses were recorded with the use of 20 scalp electrodes. The evoked potential responses consisted of three distinct negative peaks and were similar with the use of either vagal or esophageal stimulation. The measured conduction velocity of the afferent response was 7.5 m/s in epileptic subjects and 10 m/s in healthy controls, suggesting that afferent conduction is through A delta-fibers rather than slower C afferent fibers. We conclude that the cortical-evoked potential responses following esophageal electrical stimulation are comparable to direct electrical stimulation of the vagus nerve and involve mostly A delta-fibers. This approach provides a method for the assessment of vagal afferent gastrointestinal sensory pathways in health and disease.

Effects of calcium channel antagonists on the vagally mediated cardiac chronotropic response in dogs

1990 ◽  
Vol 68 (10) ◽  
pp. 1363-1367 ◽  
Author(s):  
Don W. Wallick ◽  
Sherry L. Stuesse ◽  
Paul Martin
Keyword(s):  
Electrical Stimulation ◽  
Vagus Nerve ◽  
Calcium Channel ◽  
Total Dose ◽  
Cycle Length ◽  
Cardiac Cycle ◽  
Vagal Stimulation ◽  
Calcium Channel Antagonists ◽  
Chronotropic Response ◽  
Stimulation Of

A brief electrical stimulation of the vagus nerve may elicit a triphasic response comprising (i) an initial prolongation of the same or the next cardiac cycle, (ii) a return of the subsequent cardiac cycle to about the level prior to vagal stimulation, and (iii) a secondary prolongation of cardiac cycle length that lasts several beats. We compared the effects of two calcium channel antagonists, verapamil and nifedipine, on this triphasic response to vagal stimulation in chloralose-anesthetized, open-chest dogs. In the absence of vagal stimulation, nifedipine (doses of 10, 40, and 50 μg/kg for a total dose of 100 μg/kg, i.v.) and verapamil (two doses of 100 μg/kg each, i.v.) increased the cardiac cycle length (A–A interval) by 16% (429 ± 20 to 496 ± 21 ms) and 29% (470 ± 33 to 605 ± 54 ms), respectively. Nifedipine (100 μg/kg total) attenuated the initial vagally mediated prolongation of the A–A interval, from 474 ± 19 to 369 ± 42 ms above the basal A–A interval. Following the initial prolongation of the vagal effect, other A–A intervals were not affected. In contrast, verapamil potentiated the vagally mediated initial prolongation in cardiac cycle length at the first dose administered (100 μg/kg) from 492 ± 17 to 561 ± 14 ms, but other increases in dosages had no further effect. Thus these two calcium channel antagonists have different effects on the sinoatrial chronotropic responses caused by brief vagal stimulation.Key words: autonomic control, parasympathetic, heart, calcium.

scholarly journals Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

1976 ◽  
Vol 29 (4) ◽  
pp. 351 ◽  
Author(s):  
MichaeI Pass ◽  
Trevor Heath
Keyword(s):  
Electrical Stimulation ◽  
Bile Salt ◽  
Maximum Rate ◽  
Vagal Stimulation ◽  
Bile Secretion ◽  
Vagus Nerves ◽  
Bile Formation ◽  
Vagal Innervation ◽  
Bicarbonate Output ◽  
Stimulation Of

Bile was collected before and during electrical stimulation of the vagus nerves in acute experiments on sheep with ligated cystic ducts. Most stimuli caused no change in: bile formation, but a 10-V, 10-Hz stimulus caused a slight increase in bicarbonate output. Neither the response to infused secretin nor the maximum rate of bile salt transpoit by liver cells changed during vagal stimulation; It was concluded that the vagal innervation of the liver is not likely to playa major role in the regulation of bile formation in sheep.

Interactions between Respiratory, Cardiac and Stepping Rhythms in Decerebrated Cats: Functional Hierarchical Structures of Biological Oscillators

1994 ◽  
Vol 33 (01) ◽  
pp. 129-133 ◽  
Author(s):  
K. Kawahara ◽  
Y. Yamauchi ◽  
K. Niizeki ◽  
T. Yoshioka
Keyword(s):  
Electrical Stimulation ◽  
Respiratory Rhythm ◽  
Hierarchical Structures ◽  
Heart Beat ◽  
Fictive Locomotion ◽  
Lateral Gastrocnemius ◽  
Mesencephalic Locomotor Region ◽  
Biological Oscillators ◽  
Central Origin ◽  
Stimulation Of

Abstract:Interactions are described of central origin between respiratory, cardiac and stepping rhythms during fictive locomotion in paralyzed, vagotomized, and decerebrated cats. Fictive locomotion was induced by tonic electrical stimulation of the mesencephalic locomotor region (MLR). The coherence between heart beat fluctuation, the efferent discharges of the phrenic, and the lateral gastrocnemius nerves was used to evaluate the strength of the coupling between those three rhythms. The heart beat rhythm was modulated by the centrally generated respiratory and stepping rhythms. The central respiratory rhythm was modulated by the centrally generated stepping rhythm. Based on the present findings, we have proposed a new model concerning the functional hierarchical structures of the three biological oscillators.

Vagal regulation of GRP, gastric somatostatin, and gastrin secretion in vitro

1985 ◽  
Vol 248 (4) ◽  
pp. E425-E431 ◽  
Author(s):  
S. Nishi ◽  
Y. Seino ◽  
J. Takemura ◽  
H. Ishida ◽  
M. Seno ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Inhibitory Neuron ◽  
Atropine Sulfate ◽  
Vagus Nerves ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.

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