scholarly journals AUDITORY THRESHOLD CHANGE IN SINGING CICADAS

1994 ◽  
Vol 187 (1) ◽  
pp. 45-55 ◽  
Author(s):  
R Hennig ◽  
T Weber ◽  
F Huber ◽  
H Kleindienst ◽  
T Moore ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Sound Production ◽  
Auditory Threshold ◽  
Electrophysiological Recording ◽  
Frequency Range ◽  
Auditory Thresholds ◽  
Hearing Sensitivity ◽  
Auditory Nerves ◽  
Stimulation Of

The hearing sensitivity in singing cicadas is reduced during sound production by a folding of the tympanal membranes. Using electrophysiological recording and nerve stimulation techniques, we have shown an effect of the folded tympanum on the auditory threshold of two species of cicadas, Tibicen linnei and Okanagana rimosa. Auditory thresholds of both species increased by about 20 dB when the tympana folded during singing. In T. linnei the increase in threshold affected the whole frequency range, from 1 to 16 kHz, in a similar way. Electrical stimulation of one or both auditory nerves resulted in a folding of both tympanal membranes in a way very similar to that seen in singing animals. We have demonstrated that a cicada male is able to adjust its auditory threshold within a range of about 20 dB by the tympanal folding mechanism.

Noncholinergic vasodilator innervation in the feet of ducks

1979 ◽  
Vol 237 (2) ◽  
pp. H112-H117
Author(s):  
D. D. McGregor
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Anas Platyrhynchos ◽  
Gallus Domesticus ◽  
Krebs Solution ◽  
Vasomotor Responses ◽  
Pekin Ducks ◽  
Stimulation Of

Vasomotor responses to nerve stimulation were studied in the feet of Pekin ducks (Anas platyrhynchos) and domestic chickens (Gallus domesticus). The birds were killed and the feet isolated and perfused with a Krebs solution. Electrical stimulation of pedal nerves gave vasoconstrictor responses that were abolished by injecting guanethidine and by treating birds with reserpine. After guanethidine or reserpine, nerve stimulation resulted only in vasodilatation, which was unaffected by hexamethonium. Vasodilator responses to nerve stimulation were not blocked by hyoscine or atropine, which blocked responses to acetylcholine, nor by metiamide, which blocked vasodilatation in response to histamine. Responses to nerve stimulation were blocked by tetrodotoxin. Isoprenaline produced vasoconstriction that was blocked by phentolamine and also weak vasodilator responses that were antagonized by propranolol. It is concluded that the vasoconstrictor innervation is adrenergic. The identy of the vasodilator neurotransmitter is unknown; it is apparently not acetylcholine, a catecholamine, or histamine.

Magnetically Evoked Facial Nerve Potential

1989 ◽  
Vol 100 (4) ◽  
pp. 345-347 ◽  
Author(s):  
Ian M. Windmill ◽  
Serge A. Martinez ◽  
Christopher B. Shields ◽  
Markku Paloheimo
Keyword(s):  
Electrical Stimulation ◽  
Facial Nerve ◽  
Nerve Stimulation ◽  
Magnetic Stimulation ◽  
Electrical Current ◽  
Facial Muscle ◽  
Facial Nerve Stimulation ◽  
Muscle Responses ◽  
Stimulation Of

Facial nerve stimulation by electrical current is painful and tends to discourage serial studies. Transcutaneous magnetic stimulation of the facial nerve is painless, easily reproducible, and elicits facial muscle responses identical to electrical stimulation.

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

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.

scholarly journals Phasic action of the tensor muscle modulates the calling song in cicadas

1996 ◽  
Vol 199 (7) ◽  
pp. 1535-1544
Author(s):  
P Fonseca ◽  
R Hennig
Keyword(s):  
Electrical Stimulation ◽  
Sound Production ◽  
Time Window ◽  
Time Lag ◽  
Motor Units ◽  
Pulse Amplitude ◽  
Time Correlation ◽  
Calling Song ◽  
Sound Pulse ◽  
Stimulation Of

The effect of tensor muscle contraction on sound production by the tymbal was investigated in three species of cicadas (Tettigetta josei, Tettigetta argentata and Tympanistalna gastrica). All species showed a strict time correlation between the activity of the tymbal motoneurone and the discharge of motor units in the tensor nerve during the calling song. Lesion of the tensor nerve abolished the amplitude modulation of the calling song, but this modulation was restored by electrical stimulation of the tensor nerve or by mechanically pushing the tensor sclerite. Electrical stimulation of the tensor nerve at frequencies higher than 30­40 Hz changed the sound amplitude. In Tett. josei and Tett. argentata there was a gradual increase in sound amplitude with increasing frequency of tensor nerve stimulation, while in Tymp. gastrica there was a sudden reduction in sound amplitude at stimulation frequencies higher than 30 Hz. This contrasting effect in Tymp. gastrica was due to a bistable tymbal frame. Changes in sound pulse amplitude were positively correlated with changes in the time lag measured from tymbal motoneurone stimulation to the sound pulse. The tensor muscle acted phasically because electrical stimulation of the tensor nerve during a time window (0­10 ms) before electrical stimulation of the tymbal motoneurone was most effective in eliciting amplitude modulations. In all species, the tensor muscle action visibly changed the shape of the tymbal. Despite the opposite effects of the tensor muscle on sound pulse amplitude observed between Tettigetta and Tympanistalna species, the tensor muscle of both acts by modulating the shape of the tymbal, which changes the force required for the tymbal muscle to buckle the tymbal.

scholarly journals In vivo Photonic Stimulation of Sciatic Nerve with a 1470 nm Laser

2016 ◽  
Vol 26 (3) ◽  
Author(s):  
Marie Dautrebande ◽  
Pascal Doguet ◽  
Simon-Pierre Gorza ◽  
Jean Delbeke ◽  
Yohan Botquin ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Muscle Activation ◽  
Radiant Exposure ◽  
Stimulation Of

Photonic stimulation is a new modality of nerve stimulation, which could overcome some of the electrical stimulation limitations. In this paper, we present the results of photonic stimulation of rodent sciatic nerve with a 1470 nm laser. Muscle activation was observed with radiant exposure of 0.084 J/cm<sup>2</sup>.

Regional responsiveness of renal perfusion to activation of the renal nerves

2002 ◽  
Vol 283 (5) ◽  
pp. R1177-R1186 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Gabriela A. Eppel ◽  
Simon C. Malpas ◽  
Niwanthi W. Rajapakse ◽  
Alistair Stewart ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Stimulus Frequency ◽  
Renal Medulla ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Vascular Elements ◽  
Doppler Flux ◽  
Stimulation Of

We tested for regional differences in perfusion responses, within the renal medulla and cortex, to renal nerve stimulation in pentobarbital sodium-anesthetized rabbits. Laser-Doppler flux (LDF) was monitored at various depths below the cortical surface (1–15 mm). Basal cortical LDF (1–3 mm, ∼200–450 U) was greater than medullary LDF (5–15 mm, ∼70–160 U), but there were no statistically significant differences in basal LDF within these regions. The background LDF signal during aortic occlusion was similar in the cortex (2 mm, 31 U) and outer medulla (7 mm, 31 U), but slightly greater in the inner medulla (12 mm, 44 U). During electrical stimulation of the renal nerves (0.5–8 Hz), cortical LDF and total renal blood flow were similarly progressively reduced with increasing stimulus frequency. Medullary LDF (measured between 5 and 15 mm) was overall less responsive than cortical LDF. For example, 4-Hz stimulation reduced inner medullary LDF (9 mm) by 19 ± 6% but reduced cortical LDF (1 mm) by 54 ± 11%. However, medullary LDF responses to nerve stimulation were similar at all depths measured. Our results indicate that while the vascular elements controlling medullary perfusion are less sensitive to the effects of electrical stimulation of the renal nerves than are those controlling cortical perfusion, sensitivity within these vascular territories appears to be relatively homogeneous.

Electrical stimulation of peripheral and central pathways for the relief of musculoskeletal pain

1991 ◽  
Vol 69 (5) ◽  
pp. 697-703 ◽  
Author(s):  
M. Catherine Bushnell ◽  
Serge Marchand ◽  
Nicole Tremblay ◽  
Gary H. Duncan
Keyword(s):  
Electrical Stimulation ◽  
Deep Brain Stimulation ◽  
Musculoskeletal Pain ◽  
Nerve Stimulation ◽  
Transcutaneous Electrical Nerve Stimulation ◽  
Dorsal Column ◽  
Electrical Nerve Stimulation ◽  
Dorsal Column Stimulation ◽  
Deep Brain ◽  
Stimulation Of

One method for the treatment of chronic musculoskeletal pain involves stimulation of the peripheral or central nervous system. Such stimulation includes transcutaneous electrical nerve stimulation, dorsal column stimulation, and deep brain stimulation. This review discusses the clinical use of electrical stimulation for the relief of musculoskeletal pain, and describes the results of studies conducted in our laboratory suggesting that such stimulation reduces pain transmission along sensory-discriminative pathways.Key words: pain, nociception, transcutaneous electrical nerve stimulation, dorsal column stimulation, deep brain stimulation.

Effect and mechanism of vagal nerve stimulation on somatostatin secretion in dogs

1986 ◽  
Vol 250 (2) ◽  
pp. E212-E217 ◽  
Author(s):  
B. Ahren ◽  
T. L. Paquette ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Base Line ◽  
Anesthetized Dogs ◽  
Arterial Plasma ◽  
Stimulation Of

To investigate the effect of vagal nerve stimulation on the release of pancreatic somatostatin, we electrically stimulated (10 Hz, 5 ms, 13.5 mA, and 10 min) the thoracic vagi just below the heart in halothane anesthetized dogs (n = 15). The stimulation increased the pancreatic output of somatostatinlike immunoreactivity (SLI) (delta = +248 +/- 81 fmol/min, P less than 0.005; base-line levels = 455 +/- 150 fmol/min). min). Arterial plasma SLI levels increased as well (delta = +16 +/- 3 fmol/ml, P less than 0.001; base-line levels = 65 +/- 3 fmol/ml), reflecting stimulation of extrapancreatic SLI secretion. Significant vagal activation was verified by a fivefold increase of pancreatic output of pancreatic polypeptide (PP) (delta = +31.4 +/- 5.9 ng/min, P less than 0.001; base-line levels = 7.8 +/- 0.9 ng/min). Atropine pretreatment (n = 6) inhibited partially both the PP response (delta = +7.9 +/- 3.8 ng/min after atropine) and the pancreatic SLI response (delta = +92 +/- 29 fmol/min) to vagal nerve stimulation. However, atropine pretreatment did not modify the arterial SLI response (delta = +20 +/- 7 fmol/ml). Hexamethonium pretreatment (n = 9) completely abolished all three responses. We conclude that 1) electrical stimulation of the vagus stimulates pancreatic SLI, extrapancreatic SLI, and PP release in vivo in the dog; 2) both muscarinic and nonmuscarinic mechanisms mediate the PP and pancreatic SLI responses; 3) a nonmuscarinic mechanism mediates the extrapancreatic SLI response; and 4) all three responses are mediated via ganglionic nicotinic receptors.

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