Control of bilateral seminal emissions from ejaculatory ducts by a lumbar splanchnic nerve

1993 ◽  
Vol 265 (4) ◽  
pp. R743-R748 ◽  
Author(s):  
K. Kihara ◽  
K. Sato ◽  
M. Ando ◽  
T. Morita ◽  
H. Oshima
Keyword(s):  
Electrical Stimulation ◽  
Splanchnic Nerve ◽  
Contralateral Side ◽  
The Other ◽  
Hypogastric Nerve ◽  
Splanchnic Nerves ◽  
Posterior Urethra ◽  
Stimulation Of

To investigate the route of efferent signals for seminal emissions from ejaculatory ducts (SEEDs), canine lumbar splanchnic nerves (LSNs) were electrically stimulated. SEED was confirmed by visual verification of seminal flow into the exposed posterior urethra. In intact dogs, electrical stimulation of an LSN caused bilateral SEEDs in 13 of 16 dogs examined, with a greater volume at the stimulated side. After transection of a unilateral hypogastric nerve, bilateral SEEDs occurred by electrical stimulation of the contralateral LSN in 11 of 14 dogs with a greater volume at the stimulated side and by the stimulation of the ipsilateral LSN in 13 of 15 dogs with a greater volume at the contralateral side. Contraction pressure of the epididymal tail under the same conditions harmonized with the above results. We conclude that each LSN generates bilateral SEEDs by sending signals to bilateral epididymal tails and that some of the signals through each LSN cross to the other side at the caudal mesenteric plexus and/or the prostatic plexus.

scholarly journals Submicroscopic Changes of the Nerve Endings in the Adrenal Medulla after Stimulation of the Splanchnic Nerve

1957 ◽  
Vol 3 (4) ◽  
pp. 611-614 ◽  
Author(s):  
Eduardo De Robertis ◽  
Alberto Vaz Ferreira
Keyword(s):  
Electrical Stimulation ◽  
Electron Microscope ◽  
Adrenal Medulla ◽  
Synaptic Vesicles ◽  
Splanchnic Nerve ◽  
The Other ◽  
Nerve Endings ◽  
The Mean ◽  
Increased Activity ◽  
Stimulation Of

The nerve endings of the adrenal medulla of the rabbit were studied under the electron microscope in the normal condition and after prolonged electrical stimulation of the splanchnic nerve. With a stimulus of 100 pulses per second for 10 minutes, there is an increase in the number of synaptic vesicles in the nerve ending. The mean number is of 82.6 vesicles per square micron in the normal and of 132.7 per square micron in the stimulated glands. With a stimulus of 400 pulses per second for 10 minutes, there is a considerable depletion of synaptic vesicles and other changes occur in the nerve endings. The mean number of vesicles is of 29.2 per square micron. These results are interpreted as indicative of an increased activity of the ending in one case, and as a diminished activity and fatigue of the synaptic junction in the other.

Pre- and postganglionic sympathetic activity in splanchnic nerves of rats

1981 ◽  
Vol 241 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
B. G. Celler ◽  
L. P. Schramm
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Wistar Rats ◽  
Splanchnic Nerve ◽  
Ganglionic Blockade ◽  
Splanchnic Nerves ◽  
Before And After ◽  
Evoked Activity ◽  
Greater Splanchnic Nerve ◽  
Stimulation Of

Integrated sympathetic activity was recorded on anterior or posterior divisions of the greater splanchnic nerve (GSN) in anesthetized, acutely spinalized, artificially respired Wistar rats before and after ganglionic blockade by hexamethonium. Focal electrical stimulation of spinal sympathoexcitatory pathways elicited large increases in splanchnic sympathetic activity. Ganglionic blockade showed that the anterior and posterior divisions of the GSN are predominantly preganglionic and postganglionic, respectively. Histological examination of excised splanchnic nerves and sympathetic chains indicated that splanchnic postganglionic cell bodies must lie in the chain ganglia rather than within the GSN. Postganglionic responses were calculated for each rat by subtracting responses recorded after ganglionic blockade from responses recorded before ganglionic blockade. As expected, postganglionic responses exhibited longer onset latencies than preganglionic responses. However, evoked activity increased and decreased more rapidly in postganglionic fibers than in preganglionic fibers. Responses to stimulus trains were also better maintained in postganglionic than in preganglionic fibers.

Gastric Secretion Following Vagosplanchnic Nerve Anastomosis

1956 ◽  
Vol 184 (2) ◽  
pp. 418-427 ◽  
Author(s):  
Anthony M. Imparato ◽  
L. Corsan Reid ◽  
J. William Hinton
Keyword(s):  
Electrical Stimulation ◽  
Gastric Secretion ◽  
Functional Relationship ◽  
Early Postoperative Period ◽  
Insulin Hypoglycemia ◽  
Splanchnic Nerves ◽  
Nerve Anastomosis ◽  
Nerve Anastomoses ◽  
Secretory Apparatus ◽  
Stimulation Of

Gastric secretion in response to insulin hypoglycemia and electrical stimulation of the vagus was studied in 18 dogs who had bilateral vagosplanchnic anastomoses in the chest. In six dogs the pattern of gastric secretory response to insulin changed from negative in the early postoperative period to positive between 85 and 613 days postanastomosis. In two, apparent return of vagus function was confirmed by electrical stimulation of the vagi. One of five dogs in whom splanchnovagal nerve anastomoses were performed showed a return of response to insulin at 63 days which was abolished by excision of the anastomoses. On the basis of a review of some of the ideas regarding interpretation of cross nerve anastomoses and some of the conflicting opinions regarding the fiber content of the sympathetic splanchnic nerves, the authors conclude the most likely explanation for the observed phenomena is that there are preganglionic cholinergic fibers in the greater splanchnic nerves whose relationship to the gastric secretory apparatus is similar to that of cholinergic fibers in the vagus. The regenerating fibers of the vagus followed the sheaths of these degenerating fibers and re-established functional relationship with the gastric secretory apparatus.

Reorganization of the innervation of the vas deferens after sympathetic decentralization

1996 ◽  
Vol 271 (6) ◽  
pp. R1481-R1488
Author(s):  
K. Kihara ◽  
H. Kakizaki ◽  
W. C. de Groat
Keyword(s):  
Electrical Stimulation ◽  
Vas Deferens ◽  
Ganglion Cells ◽  
Rat Vas Deferens ◽  
Pelvic Nerve ◽  
Hypogastric Nerve ◽  
Normal Side ◽  
Efferent Pathways ◽  
Stimulation Of

Reorganization of autonomic efferent pathways to the rat vas deferens was noted after chronic (30 days) sympathetic decentralization produced by hypogastric nerve (HGN) transection. In normal rats, electrical stimulation of the HGN elicited an increase in vasal pressure (VP) bilaterally, whereas pelvic nerve (PN) stimulation did not alter VP. However, after unilateral HGN transection, stimulation of the PN on the transected side but not on the normal side increased VP. The decentralized vas exhibited larger VP responses to stimulation of the contralateral HGN in comparison with the normal vas. After bilateral HGN transection, PN-induced VP responses were elicited at lower stimulus intensities than in rats with unilateral transections. PN-induced VP responses were blocked by hexamethonium and prazosin but were not altered by atropine. Distension of the vas lumen occurred after decentralization. PN-induced VP responses were not detectable in extremely distended vas. These data indicate that, after degeneration of sympathetic preganglionic axons, decentralized adrenergic ganglion cells are reinnervated by parasympathetic or sympathetic preganglionic pathways and that the reinnervation influences vasal function.

Upper thoracic sympathetic neuron responses to input from urinary bladder afferents

1983 ◽  
Vol 245 (3) ◽  
pp. R311-R320 ◽  
Author(s):  
R. Schondorf ◽  
W. Laskey ◽  
C. Polosa
Keyword(s):  
Electrical Stimulation ◽  
Urinary Bladder ◽  
Sympathetic Neuron ◽  
Neural Circuitry ◽  
Pelvic Nerve ◽  
Hypogastric Nerve ◽  
Bladder Afferents ◽  
Cervical Sympathetic ◽  
Upper Thoracic ◽  
Stimulation Of

The aim of the present study was to evaluate the organization of neural circuitry responsible for the intersegmental transmission of input from urinary bladder afferents to sympathetic preganglionic neurons (SPNs). The electrical activity of SPNs was recorded from axons of the cervical sympathetic trunk in anesthetized central nervous system (CNS)-intact and in unanesthetized midcollicular-decerebrate or acute C1 spinal cats. In all three preparations, tonically active SPNs were excited or inhibited by 1) electrical stimulation of myelinated afferents of the pelvic or hypogastric nerve, both of which contain bladder afferents, and 2) spontaneous contraction or distension of the urinary bladder. The SPN responses to bladder distension were abolished by pelvic nerve section. A comparison of responses of SPNs in CNS-intact and acute spinal animals to electrical stimulation of pelvic nerve afferents suggests that both propriospinal and supraspinal circuits are involved in the intersegmental transmission of input from bladder afferents to SPNs.

The release of catecholamines from the adrenal medulla and its modulation by α2-adrenoceptors in the anaesthetized dog

1987 ◽  
Vol 65 (4) ◽  
pp. 550-557 ◽  
Author(s):  
Sylvain Foucart ◽  
Réginald Nadeau ◽  
Jacques de Champlain
Keyword(s):  
Electrical Stimulation ◽  
Adrenal Medulla ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Feedback Mechanism ◽  
Adrenal Vein ◽  
Low Frequencies ◽  
Negative Feedback Mechanism ◽  
Frequency Of Stimulation ◽  
Stimulation Of

The adrenal nerve of anaesthetized and vagotomized dogs was electrically stimulated (10 V pulses of 2 ms duration for 10 min) at frequencies of 1, 3, 10, and 25 Hz. There was a correlation between the frequency of stimulation and the plasma concentrations of epinephrine, norepinephrine, and dopamine in the adrenal vein, mainly after the 1st min of stimulation and the maximal concentration was reached sooner with higher frequencies of stimulation. Moreover, the relative percentage of catecholamines released in response to the electrical stimulation was not changed by the frequency of stimulation. To test the hypothesis that a local negative feedback mechanism mediated by α2-adrenoceptors exists in the adrenal medulla, the effects of the systemic administration of clonidine (α2-agonist) and yohimbine (α2-antagonist) on the concentrations of catecholamines in the adrenal vein were evaluated during the electrical stimulation of the adrenal nerve (5 V pulses of 2 ms duration for 3 min) at 3 Hz. Moreover, the effects of the systemic injections of more specific α2-agonist and antagonist (oxymetazoline and idazoxan) were tested on the release of catecholamines in the adrenal vein in response to electrical stimulation of the splanchnic nerve at 1 and 3 Hz frequencies. The injection of 0.5 mg/kg of yohimbine caused a significant increase in the concentrations of epinephrine and norepinephrine in the adrenal vein induced by the electrical stimulation of the adrenal nerve and the injection of 15 μg/kg of clonidine had no effects. In the second series of experiments, the injection of 2 μg/kg of oxymetazoline caused a significant decrease in the release of epinephrine and norepinephrine at 1 Hz, but similarly to clonidine, there were no changes at 3 Hz. In contrast, the release of epinephrine and dopamine in response to electrical stimulation of the splanchnic nerve was increased at 3 Hz after the injection of idazoxan, but not at 1 Hz. It is concluded that the adrenal medulla catecholamines secretion appears to be partly modulated by a presynaptic inhibitory mechanism that involves α2-adrenoceptors. The observation that agonists appear to be more efficient at low frequencies of stimulation while antagonists appear to be more efficient at higher frequencies could be explained by the possibility that adrenal medullary α2-receptors would be saturated at higher frequencies of stimulation.

scholarly journals Pancreatic and extrapancreatic galanin release during sympathetic neural activation

1990 ◽  
Vol 258 (3) ◽  
pp. E436-E444 ◽  
Author(s):  
B. E. Dunning ◽  
P. J. Havel ◽  
R. C. Veith ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Splanchnic Nerve ◽  
Sympathetic Nerves ◽  
Neural Activation ◽  
Anesthetized Dogs ◽  
Basal Insulin Secretion ◽  
Peripheral Arterial ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

SECRETION OF FSH AND LH IN THE PSEUDOPREGNANT RAT

1965 ◽  
Vol 49 (3) ◽  
pp. 370-378 ◽  
Author(s):  
G. P. van Rees ◽  
C. A. de Groot
Keyword(s):  
Electrical Stimulation ◽  
Adult Female ◽  
The Other ◽  
Female Rats ◽  
Cervix Uteri ◽  
Similar Increase ◽  
Clear Cut ◽  
Inhibiting Effect ◽  
Pituitary Glands ◽  
Stimulation Of

ABSTRACT The pituitary LH- and FSH-content was estimated in rats made pseudopregnant by electrical stimulation of the cervix uteri; serum FSH was also estimated. An increase in both FSH- and LH-content was found, which was largest in the pituitary glands collected on the 7th day of pseudopregnancy. A similar increase in pituitary LH-content could be induced in normal adult female rats by a course of injections of 5 mg of progesterone daily. Serum FSH-levels did not show any clear-cut changes during pseudopregnancy, but rose at the end of it. In the discussion a connection is made between the similarity of the result of progesterone treatment and pseudopregnancy on one hand and between the ovulation-inhibiting effect of progesterone and its ability to increase pituitary FSH-and LH-levels on the other.

Effect of Various Sensory Stimuli on Reflex Laryngeal Adduction

1977 ◽  
Vol 86 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Masafumi Suzuki ◽  
Clarence T. Sasaki
Keyword(s):  
Splanchnic Nerve ◽  
Laryngeal Nerve ◽  
Organ System ◽  
Sensory Nerves ◽  
The Other ◽  
Evoked Responses ◽  
Sensory Stimuli ◽  
Adult Cats ◽  
Repetitive Electrical Stimulation ◽  
Stimulation Of

Various types of sensory stimuli may influence reflex laryngeal adduction. The recurrent laryngeal nerve responses evoked by single shock and repetitive electrical stimulation of a number of sensory nerves have been neurophysiologically observed in twenty-five adult cats. Stimulation of major cranial afferents produces strong adductor responses. The magnitude of these evoked responses is approached only by stimulation of the splanchnic nerve in the abdomen. On the other hand, comparable stimulation of special sensory and spinal somatic sensory nerves produces rapidly attenuated evoked adductor responses. We postulate that while these latter adductor responses may be insufficient to produce strong glottic closure, they may effectively modify phonatory function of the larynx. We have, therefore, attempted to demonstrate the effects of various sensory elicitations upon reflex laryngeal adduction as they may compositely influence both protective and phonatory control of this organ system.

In vivo modulation by α2-adrenoceptors of adrenal catecholamine release in the anaesthetized dog

1988 ◽  
Vol 66 (3) ◽  
pp. 380-384 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Reginald Nadeau
Keyword(s):  
Electrical Stimulation ◽  
Splanchnic Nerve ◽  
Catecholamine Release ◽  
Agonist Stimulation ◽  
Control Stimulation ◽  
Anaesthetized Dog ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

In this study, the reversal of the potentiating effect of idazoxan, a selective α2-antagonist, on adrenal catecholamine release elicited by splanchnic nerve stimulation in anaesthetized and vagotomized dogs, was investigated with the use of oxymetazoline, a selective α2-agonist. Stimulation of the left splanchnic nerve (5.0-V pulses of 2 ms duration for 3 min at a frequency of 2 Hz) was applied before and 20 min after the i. v. injection of each drug. Blood samples were collected in the adrenal vein before and at the end of each stimulation. The results show that the release of catecholamines induced by electrical stimulation was potentiated by 50% after idazoxan injection (0.1 mg/kg). This enhanced response was significantly antagonized by the subsequent injection of oxymetazoline (2 μg/kg). The α2-modulating effect appears to be related to the amount of catecholamines released during the stimulation, since by subgrouping of the data on the basis of the degree of potentiation by idazoxan, it was observed that this drug was more efficient when catecholamine release was higher during control stimulation. In contrast, the reversing effect of oxymetazoline was found to be more pronounced when catecholamine release was lower. These results thus suggest that the sensitivity of the α2-adrenoceptor mechanism may depend upon the in situ concentration of adrenal catecholamine release during electrical stimulation and that the potentiating effect of α2-blockade can be reversed by activation of those receptors by a selective α2-agonist.

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