Experimental investigations with electrical stimulation of the oculomotor nucleus: The effects of stimulus frequency

1966 ◽  
Author(s):  
Donald G. Pitts
Keyword(s):  
Electrical Stimulation ◽  
Stimulus Frequency ◽  
Experimental Investigations ◽  
Oculomotor Nucleus ◽  
Stimulation Of

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.

Skeletal muscle vasodilation during electrical stimulation of the preoptic recess

1986 ◽  
Vol 250 (2) ◽  
pp. H221-H225 ◽  
Author(s):  
K. G. Proctor ◽  
S. L. Bealer
Keyword(s):  
Skeletal Muscle ◽  
Electrical Stimulation ◽  
Steady State ◽  
Stimulus Frequency ◽  
Base Line ◽  
Beta Adrenergic ◽  
State Reduction ◽  
Arterial Blood ◽  
Arteriolar Diameter ◽  
Stimulation Of

Transverse (3rd-order) arterioles (diam 12 +/- 2 micron, n = 6) in rat spinotrapezius muscle were observed with video microscopy during electrical stimulation of preoptic recess in periventricular region of hypothalamus (AV3V region) to test whether active skeletal muscle vasodilation was mediated by a beta-adrenergic mechanism. Bipolar wire electrodes were implanted in AV3V 3-7 days before an experiment. Continuous superfusion of propranolol (10(-5) M) caused steady-state reduction (3 +/- 1 microns) in arteriolar diameter and reduced steady-state vasodilation (26 +/- 2 vs. 11 +/- 2 microns) caused by a continuous superfusion of isoproterenol (10(-6) M). Six arterioles were observed with and without propranolol during four frequencies of AV3V stimulation (8-15 V, 0.2-0.5 ms pulse duration; 10, 15, 20, and 25 Hz; 1 min stimulus duration). Stimulation caused frequency-related reductions in arterial blood pressure (10-20 mmHg), which were sustained and not altered by propranolol. Transient peak diameters were observed after 30 +/- 7 s; the time was not related to stimulus frequency or affected by propranolol. Peak diameters averaged 14-17 microns during vehicle and 11-12 micron during propranolol (maximum diam 32 +/- 3). Peak vasodilations were significant but identical with vehicle or propranolol (avg 3 +/- 1 microns) and not related to stimulus frequency. Diameters stabilized at steady-state values above base line only during 15 and 20 Hz with vehicle and only during 20 Hz with propranolol. We conclude that AV3V stimulation causes transient vasodilation in spinotrapezius muscle that is probably not mediated by beta-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Rise in endothelium-derived NO after stimulation of rat perivascular sympathetic mesenteric nerves

1999 ◽  
Vol 277 (3) ◽  
pp. H1027-H1035 ◽  
Author(s):  
Mauricio P. Boric ◽  
Xavier F. Figueroa ◽  
M. Verónica Donoso ◽  
Alfonso Paredes ◽  
Inés Poblete ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Sympathetic Activity ◽  
Perfusion Pressure ◽  
Stimulus Frequency ◽  
No Synthase ◽  
No Production ◽  
No Release ◽  
Perivascular Nerves ◽  
Stimulation Of

To evaluate whether sympathetic activity induces nitric oxide (NO) production, we perfused the rat arterial mesenteric bed and measured luminally accessible norepinephrine (NE), NO, and cGMP before, during, and after stimulation of perivascular nerves. Electrical stimulation (1 min, 30 Hz) raised perfusion pressure by 97 ± 7 mmHg, accompanied by peaks of 23 ± 3 pmol NE, 445 ± 48 pmol NO, and 1 pmol cGMP. Likewise, perfusion with 10 μM NE induced vasoconstriction coupled to increased NO and cGMP release. Electrically elicited NO release depended on stimulus frequency and duration. Endothelium denudation with saponin abolished the NO peak without changing NE release. Inhibition of NO synthase with 100 μM N ω-nitro-l-arginine reduced basal NO and cGMP release and blocked the electrically stimulated and exogenous NE-stimulated NO peak while enhancing vasoconstriction. Blocking either sympathetic exocytosis with 1 μM guanethidine or α1-adrenoceptors with 30 nM prazosin abolished the electrically evoked vasoconstriction and NO release. α2-Adrenoceptor blockade with 1 μM yohimbine reduced both vasoconstriction and NO peak while increasing NE release. In summary, sympathetically released NE induces vasoconstriction, which triggers a secondary release of endothelial NO coupled to cGMP production.

scholarly journals Stimulus-dependent changes in optical responses of the dorsal cochlear nucleus using voltage-sensitive dye

2011 ◽  
Vol 106 (1) ◽  
pp. 421-436 ◽  
Author(s):  
F. G. Licari ◽  
M. Shkoukani ◽  
J. A. Kaltenbach
Keyword(s):  
Electrical Stimulation ◽  
Cochlear Nucleus ◽  
Stimulus Frequency ◽  
Sound Level ◽  
Dorsal Cochlear Nucleus ◽  
Lateral Direction ◽  
Response Latencies ◽  
Voltage Sensitive Dye ◽  
Optical Responses ◽  
Stimulation Of

Optical imaging with voltage-sensitive dye was used to examine the spatiotemporal dynamics of stimulus-driven activity on the surface of the dorsal cochlear nucleus (DCN). Stimulation with tones at low to moderate levels produced localized regions of activation that were most commonly elongated rostrocaudally. The size of these activation areas expanded with increases in sound level, while their centers shifted from the lateral direction to the medial direction with increases in stimulus frequency. In contrast to the tonotopic patterns of activation evoked by tones, electrical stimulation of the DCN surface resulted in bands of activation that were elongated along the medial-lateral axis; response latencies increased with distance along these bands from the point of stimulation. Shifting the site of electrical stimulation from the rostral direction to the caudal direction induced corresponding shifts in the rostrocaudal location of the activation band; moving the electrode tip to subsurface depths resulted in loss of the elongated band. Transecting the DCN along the rostrocaudal axis midway between its medial and lateral extremities blocked propagation of the response to the half of the DCN distal to but not proximal to the stimulating electrode. The results suggest that the two modes of stimulation activated two distinct populations of neurons, one involving primarily tonotopically organized cells and the other crossing these tonotopic zones and likely representing the activation of parallel fibers. These results reveal a number of new features in the spatial patterns of tone-elicited activation that are not readily predicted by responses recorded electrophysiologically.

Pharyngeal branch of the glossopharyngeal nerve plays a major role in reflex swallowing from the pharynx

2002 ◽  
Vol 282 (5) ◽  
pp. R1342-R1347 ◽  
Author(s):  
Jun-Ichi Kitagawa ◽  
Tomio Shingai ◽  
Yoshihiro Takahashi ◽  
Yoshiaki Yamada
Keyword(s):  
Electrical Stimulation ◽  
Mechanical Stimulation ◽  
Stimulus Frequency ◽  
Superior Laryngeal Nerve ◽  
Posterior Pharyngeal Wall ◽  
Glossopharyngeal Nerve ◽  
Pharyngeal Wall ◽  
Swallowing Reflex ◽  
Pharyngeal Branch ◽  
Stimulation Of

Mechanical stimulation of the pharyngeal areas readily elicits reflex swallowing. However, it is much more difficult for electrical stimulation of the glossopharyngeal nerve (GPN) to evoke reflex swallowing than it is for stimulation of the superior laryngeal nerve (SLN) to do so. These paradoxical findings remain unexplained; hence, the main purpose of this study was to explain this contradiction by using a urethane-anesthetized rat. Mechanical stimulation easily elicited reflex swallowing from the pharynx. The posterior pillars, posterior pharyngeal wall, and the soft palate of the rat were extremely reflexogenic areas for swallowing. Sectioning the pharyngeal branch of the GPN (GPN-ph), however, eliminated the swallowing reflex from these areas. In contrast, sectioning the lingual branch of the GPN had no effect on the elicitation of swallowing. Electrical stimulation of the GPN-ph and SLN elicited sequentially occurring swallows. The relationship between stimulus frequency and the latency of swallowing for the GPN-ph was approximately the same as that for the SLN. These results indicate that the GPN-ph plays a major role in the initiation of reflex swallowing from the pharynx in rats.

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