scholarly journals Stomach Region Stimulated Determines Effects on Duodenal Motility in Rats

2021 ◽  
Author(s):  
Zhenjun T TAN ◽  
Matthew Ward ◽  
Robert J Phillips ◽  
Xueguo Zhang ◽  
Deborah M Jaffey ◽  
...  
Keyword(s):  
Electrode Site ◽  
Vagal Afferents ◽  
Male Rats ◽  
Motor Responses ◽  
Duodenal Motility ◽  
Serosal Surface ◽  
Stretch Receptors ◽  
Excitatory Responses ◽  
Post Hoc ◽  
Stimulation Of

Gastric electrical stimulation (GES) is used clinically to promote proximal GI emptying and motility. In acute experiments, we measured duodenal motor responses elicited by GES applied at 141 randomly chosen electrode sites on the stomach serosal surface. Overnight-fasted (H2O available) anesthetized male rats (n = 81) received intermittent biphasic GES for 5 min (20s-on/40s-off cycles; I = 0.3mA; pw = 0.2ms; 10 Hz). A strain gauge on the serosal surface of the proximal duodenum of each animal was used to evaluate baseline motor activity and the effect of GES. Using ratios of time blocks compared to a 15-min pre-stimulation baseline, we evaluated the effects of the 5-min stimulation on concurrent activity; on the 10-min immediately after the stimulation, and on the 15-min period beginning with the onset of stimulation. We mapped the magnitude of the duodenal response (3 different motility indices) elicited from the 141 stomach sites. Post hoc electrode site maps associated with duodenal responses suggested three zones similar to the classic regions of forestomach, corpus and antrum. Maximal excitatory duodenal motor responses were elicited from forestomach sites, whereas inhibitory responses occurred with stimulation of the corpus. Moderate excitatory duodenal responses occurred with stimulation of the antrum. Complex, weak inhibitory/excitatory responses were produced by stimulation at boundaries between stomach regions. Patterns of GES efficacies coincided with distributions of previously mapped vagal afferents, suggesting that excitation of the duodenum is strongest when GES electrodes are situated over stomach concentrations of vagal intramuscular arrays, putative stretch receptors in the muscle wall.

Responses and Afferent Pathways of Superficial and Deeper C1–C2 Spinal Cells to Intrapericardial Algogenic Chemicals in Rats

2001 ◽  
Vol 85 (4) ◽  
pp. 1522-1532 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman
Keyword(s):  
Afferent Input ◽  
Vagal Afferents ◽  
Male Rats ◽  
Prostaglandin E ◽  
Joint Movement ◽  
Spinal Neurons ◽  
Afferent Pathways ◽  
Bilateral Vagotomy ◽  
Cardiac Afferents ◽  
Stimulation Of

Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C1–C2spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C1–C2 spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C1–C2 neurons. Extracellular potentials of single C1–C2 neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10− 3 M), bradykinin, histamine, serotonin, and prostaglandin E2(10− 5 M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C1–C2 spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input ( P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C1–C2 spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C6–C7 segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C1–C2 superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.

Role of the medullary lateral tegmental field in reflex-mediated sympathoexcitation in cats

2004 ◽  
Vol 286 (3) ◽  
pp. R451-R464 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Shaun W. Phillips ◽  
Susan M. Barman
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Sympathetic Nerve Activity ◽  
Nmda Receptor Antagonist ◽  
Vagal Afferents ◽  
Reflex Pathways ◽  
Excitatory Responses ◽  
Stimulation Of

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

Responses of medullary raphe neurons to electrical and chemical activation of vagal afferent nerve fibers

1993 ◽  
Vol 70 (5) ◽  
pp. 1950-1961 ◽  
Author(s):  
A. R. Evans ◽  
R. W. Blair
Keyword(s):  
Electrical Stimulation ◽  
Chemical Activation ◽  
Vagal Afferents ◽  
Frequency Dependent ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Mixed Responses ◽  
Excitatory Responses ◽  
Dose Dependent ◽  
Stimulation Of

1. Various intensities, frequencies, and pulse widths of electrical stimulation of vagal afferent fibers were used to assess the responses of 87 medullary raphe neurons to vagal afferent fiber input in pentobarbital sodium-anesthetized, barodenervated paralyzed cats. Thirty-seven neurons were antidromically activated from the T2-T3 segments of the thoracic spinal cord, and 40 neurons could not be antidromically activated. Neurons were located in the nucleus raphe magnus (79%) and the nucleus raphe obscurus (15%). The remaining 6% of the neurons were not found; however, their locations were comparable in depth and position on the midline with other neurons in the same animals whose locations were identified. 2. The responses of 60 neurons to electrical stimulation of vagal afferent fibers were classified as excitatory (38%), inhibitory (24%), or mixed, (7%). The mixed responses were characterized by excitation at one frequency or intensity and inhibition at another frequency or intensity. The remaining 27 neurons did not clearly respond. 3. The excitatory responses to electrical stimulation of the cervical vagus nerve were intensity and frequency dependent. Inhibitory responses were frequency dependent at lower frequencies of stimulation and both frequency and intensity dependent at higher frequencies. The mixed responses were frequency dependent. Overall, longer pulse widths produced significantly greater responses than shorter pulse widths. 4. Thirty-three neurons were tested for responses to chemical stimulation of vagal afferents with intra-atrial injections of three doses of veratridine. Twenty-one percent were excited, 55% were inhibited, and 6% had mixed responses. For the mixed responses, excitation occurred at one dose and inhibition at another. The remaining 18% of the neurons were unresponsive to veratridine. The excitatory responses were dose dependent, but the inhibitory responses were not. Three doses of phenybiguanide (PBG) were also used to chemically activate vagal afferents in 27 neurons. Eleven percent were excited, 44% were inhibited, and 4% had mixed responses. The remaining 41% were unresponsive to PBG. The excitatory and inhibitory responses were dose dependent. 5. When comparing responses in projection and nonprojection neurons, inhibition was seen significantly more often in projection neurons and excitation in nonprojection neurons. Sixty-three percent of the neurons inhibited by electrical stimulation were raphespinal neurons, and 78% of the neurons excited by vagal stimulation were nonprojection neurons. Similar observations were made with the responses to chemical activation of the vagus. 6. Neurons with lower spontaneous discharge rates were more often excited by vagal stimulation and neurons with higher rates were more often inhibited.(ABSTRACT TRUNCATED AT 400 WORDS)

Motor reflexes of stomach elicited by phenyldiguanide in the rat

1980 ◽  
Vol 58 (4) ◽  
pp. 352-359 ◽  
Author(s):  
K. S. Rao
Keyword(s):  
Motor Activity ◽  
Motor Response ◽  
Sympathetic Nerves ◽  
Vagal Afferents ◽  
Intragastric Pressure ◽  
Motor Responses ◽  
Efferent System ◽  
Efferent Pathway ◽  
Cervical Vagotomy ◽  
Stimulation Of

Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anaesthesia. Phenyldiguanide injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.

scholarly journals Evidences of Existence of Serotoninergic Nerves, Enhancing Duodenal Motility

2015 ◽  
Vol 70 (6) ◽  
pp. 718-726
Author(s):  
Viktor Mihajlovich Smirnov ◽  
Dmitrij Sergeevich Sveshnikov ◽  
Igor Leonidovich Myasnikov ◽  
Tat'jana Evgen'evna Kuznecova ◽  
Jurij Nikolaevich Samko
Keyword(s):  
Sympathetic Nerves ◽  
The Body ◽  
Sympathetic Trunk ◽  
Thoracic Cavity ◽  
Internal Organs ◽  
Electrical Nerve Stimulation ◽  
Motor Responses ◽  
Duodenal Motility ◽  
5Ht Receptors ◽  
Stimulation Of

The review is devoted to the mechanism of duodenal motility activation caused by sympathetic nerves. The authors have found that stimulation of the sympathetic trunk in the thoracic cavity in dogs in most cases provide not inhibitory but excitatory motor responses of the duodenum. Excitatory effects were eliminated during 5HT-receptors blockade by promedol and lysergol. Analysis of publications showed that sympathetic trunk contains serotoninergic fibers, providing excitatory motor responses of the duodenum to electrical nerve stimulation. According to histochemical and physiological studies, amount of serotonergic fibers in the sympathetic trunk is several times more than the adrenergic. This means that the body has sertoninergic nerves. Serotoninergic nerve as well as the sympathetic is a collective notion. There are: sympathetic trunks, their ramifications and branches that innervate the internal organs. Since promedol blocks serotonergic nerves, this is plausible cause of constipation in patients after surgical treatment along with the application of this drug.

Chemical Activation of Cervical Cell Bodies: Effects on Responses to Colorectal Distension in Lumbosacral Spinal Cord of Rats

1999 ◽  
Vol 82 (6) ◽  
pp. 3423-3433 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman
Keyword(s):  
Spontaneous Activity ◽  
Chemical Activation ◽  
Male Rats ◽  
Evoked Responses ◽  
Colorectal Distension ◽  
Lumbosacral Spinal Cord ◽  
Cervical Cell ◽  
Upper Cervical ◽  
Excitatory Responses ◽  
Stimulation Of

We have shown that stimulation of cardiopulmonary sympathetic afferent fibers activates relays in upper cervical segments to suppress activity of lumbosacral spinal cells. The purpose of this study was to determine if chemical excitation (glutamate) of upper cervical cell bodies changes the spontaneous activity and evoked responses of lumbosacral spinal cells to colorectal distension (CRD). Extracellular potentials were recorded in pentobarbital-anesthetized male rats. CRD (80 mmHg) was produced by inflating a balloon inserted in the descending colon and rectum. A total of 135 cells in the lumbosacral segments (L6–S2) were activated by CRD. Seventy-five percent (95/126) of tested cells received convergent somatic input from the scrotum, perianal region, hindlimb, and tail; 99/135 (73%) cells were excited or excited/inhibited by CRD; and 36 (27%) cells were inhibited or inhibited/excited by CRD. A glutamate (1 M) pledget placed on the surface of C1–C2 segments decreased spontaneous activity and excitatory CRD responses of 33/56 cells and increased spontaneous activity of 13/19 cells inhibited by CRD. Glutamate applied to C6–C7 segments decreased activity of 10/18 cells excited by CRD, and 9 of these also were inhibited by glutamate at C1–C2 segments. Glutamate at C6–C7 increased activity of 4/6 cells inhibited by CRD and excited by glutamate at C1–C2 segments. After transection at rostral C1 segment, glutamate at C1–C2still reduced excitatory responses of 7/10 cells. Further, inhibitory effects of C6–C7 glutamate on excitatory responses to CRD still occurred after rostral C1transection but were abolished after a rostral C6transection in 4/4 cells. These data showed that C1–C2 cells activated with glutamate primarily produced inhibition of evoked responses to visceral stimulation of lumbosacral spinal cells. Inhibition resulting from activation of cells in C6–C7 segments required connections in the upper cervical segments. These results provide evidence that upper cervical cells integrate information that modulates activity of distant spinal neurons responding to visceral input.

Reflux mechanisms involved in cardiac arrhythmias induced by hypothalamic stimulation

1978 ◽  
Vol 234 (2) ◽  
pp. H199-H209
Author(s):  
D. E. Evans ◽  
R. A. Gillis
Keyword(s):  
Blood Pressure ◽  
Cardiac Arrhythmias ◽  
Carotid Sinus ◽  
Vagal Afferents ◽  
Vagal Activity ◽  
Vagus Nerves ◽  
Stretch Receptors ◽  
Vagal Nerve Activity ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of widespread areas in the CNS has been shown to cause cardiac arrhythmias, which occur most frequently after cessation of stimulation. To determine the reflex and autonomic mechanism responsible for the poststimulation arrhythmias, we anesthetized cats with chloralose, and recorded arterial pressure, ECG, and cardiac vagal nerve activity. Stimulation of the hypothalamus consistently caused increases in blood pressure and heart rate during stimulation and caused arrhythmias, accompanied by vagal hyperactivity, immediately following stimulation. The arrhythmias were mediated solely by the vagus nerves because vagotomy or propantheline administration prevented them, whereas propranolol did not. Administration of either phentolamine or spinal cord transection prevented both the rise in blood pressure during stimulation and the poststimulation arrhythmias, but sectioning the carotid sinus and aortic depressor nerves had no preventative effect. However, when this denervation was combined with sectioning of vagal afferents, bursts of vagal activity (used as an index of cardiac rhythm disturbances) were prevented in three of six animals. Subsequent administration of phentolamine prevented the bursts in the remaining animals. It is concluded that poststimulation arrhythmias are elicited by the rise in blood pressure occurring during stimulation causing a sudden surge in parasympathetic outflow to the heart. The reflexogenic areas involved appear to be stretch receptors innervated by afferent vagal fibers.

DER EINFLUSS VON RESERPIN AUF DIE ANTITHYREOIDALE WIRKUNG VON KALIUMPERCHLORAT

1962 ◽  
Vol 39 (3) ◽  
pp. 423-430
Author(s):  
H. L. Krüskemper ◽  
F. J. Kessler ◽  
E. Steinkrüger
Keyword(s):  
Thyroid Gland ◽  
Male Rats ◽  
Normal Male ◽  
Tissue Respiration ◽  
List Type ◽  
Morphological Alterations ◽  
Hormone Synthesis ◽  
Stimulation Of

ABSTRACT 1. Reserpine does not inhibit the tissue respiration of liver in normal male rats (in vitro). 2. The decrease of tissue respiration of the liver with simultaneous morphological stimulation of the thyroid gland after long administration of reserpine is due to a minute inhibition of the hormone synthesis in the thyroid gland. 3. The morphological alterations of the thyroid in experimental hypothyroidism due to perchlorate can not be prevented with reserpine.

OVULATORY DISCHARGE OF GONADOTROPHINS INDUCED BY HYPOTHALAMIC STIMULATION IN CASTRATED MALE RATS BEARING A TRANSPLANTED OVARY

1966 ◽  
Vol 51 (2) ◽  
pp. 281-289 ◽  
Author(s):  
J. Moll ◽  
G. H. Zeilmaker
Keyword(s):  
Electrical Stimulation ◽  
Preoptic Area ◽  
Hypothalamic Stimulation ◽  
Male Rats ◽  
Corpora Lutea ◽  
Histological Changes ◽  
Experimental Animals ◽  
Cumulus Oophorus ◽  
Dc Current ◽  
Stimulation Of

ABSTRACT Castrated young adult inbred male rats bearing ovarian transplants were subjected to electrical stimulation of the hypothalamus. This was done in order to investigate whether discharge of ovulatory amounts of gonadotrophins could be induced in such male animals by this procedure. Bilateral stimulations with unipolar electrodes and a DC current of 1.5 mA applied during 10 seconds induced in the ovarian grafts histological changes indicating the discharge of ovulatory amounts of gonadotrophins. In animals killed one day after stimulation these changes consisted of displacement of the ova towards the centre of the follicles with loosening of the cumulus oophorus. In one animal the ova had left the follicles. In animals killed three days after stimulation numerous young corpora lutea could be observed. These results were obtained with electrode tips either close to the median eminence, or in the preoptic area. Shamstimulations were ineffective. Some of the experimental animals received progesterone pretreatment. This rendered the stimulations ineffective, if continued until the day preceding stimulation, but seemed without effect on the results of stimulation, if two or three days without progesterone preceded the stimulations.

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