scholarly journals Innervation of the Human Cavum Conchae and Auditory Canal: Anatomical Basis for Transcutaneous Auricular Nerve Stimulation

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
P. Bermejo ◽  
M. López ◽  
I. Larraya ◽  
J. Chamorro ◽  
J. L. Cobo ◽  
...  

The innocuous transcutaneous stimulation of nerves supplying the outer ear has been demonstrated to be as effective as the invasive direct stimulation of the vagus nerve for the treatment of some neurological and nonneurological disturbances. Thus, the precise knowledge of external ear innervation is of maximal interest for the design of transcutaneous auricular nerve stimulation devices. We analyzed eleven outer ears, and the innervation was assessed by Masson’s trichrome staining, immunohistochemistry, or immunofluorescence (neurofilaments, S100 protein, and myelin-basic protein). In both the cavum conchae and the auditory canal, nerve profiles were identified between the cartilage and the skin and out of the cartilage. The density of nerves and of myelinated nerve fibers was higher out of the cartilage and in the auditory canal with respect to the cavum conchae. Moreover, the nerves were more numerous in the superior and posterior-inferior than in the anterior-inferior segments of the auditory canal. The present study established a precise nerve map of the human cavum conchae and the cartilaginous segment of the auditory canal demonstrating regional differences in the pattern of innervation of the human outer ear. These results may provide additional neuroanatomical basis for the accurate design of auricular transcutaneous nerve stimulation devices.

1958 ◽  
Vol 17 (2) ◽  
pp. 134-142 ◽  
Author(s):  
MARY F. LOCKETT ◽  
S. N. GANJU

SUMMARY Pretreatment of salt-maintained adrenalectomized mice for 6 days with 3–6 mg dried thyroid gland, or with 0·25 μg of either l-thyroxine or l-triiodothyronine, per mouse per day, delayed the early onset of both neuromuscular and muscular failure which are characteristic of these animals. Dose-effect curves for the action of thyroxine on the myoneural junctions and striped muscle fibres are given. A concentration of 0·05μg l-triiodothyronine/100 ml. bath fluid antagonized potassium reduction of the maximal twitch of the normal rat diaphragm in response to nerve stimulation, but not in response to direct stimulation of the curarized muscle.


1960 ◽  
Vol 38 (3) ◽  
pp. 287-295 ◽  
Author(s):  
Maurice F. Murnaghan

In the perfused anterior tibial muscle of the tick-paralyzed dog acetylcholine in excess of the control value is not liberated on stimulation of the peroneal nerve; in the normal muscle 7 μμg of acetylcholine is liberated per nerve volley. The paralysis is evidently not due to defective synthesis of acetylcholine because acetylcholine is liberated in control and high-potassium perfusates, the choline acetylase activity and the acetylcholine content of lumbar ventral roots and peroneal nerves do not differ from that in normal dogs, and the tick-paralyzed muscle differs from that in the hemicholinium-treated animal in its response to a train of nerve pulses after previous tetanization. As somatic motor nerve fibers in the paralyzed dog have previously been shown to conduct a nerve impulse and the factors required for acetylcholine release at the nerve terminal apparently are not absent in the paralyzed animal, the mechanism of the paralysis is probably due to an inability of the nerve impulse to traverse the terminal presynaptic fibers. The 'lesion' evidently extends to the end of the presynaptic fiber, i.e. more distally than in botulism, because direct stimulation of the tick-paralyzed muscle fails to liberate acetylcholine.


1986 ◽  
Vol 64 (2) ◽  
pp. 206-212 ◽  
Author(s):  
Yasuyuki Furukawa ◽  
Paul Martin

In the isolated, blood-perfused canine right atrium, which was pretreated with propranolol, negative chronotropic and inotropic responses were evoked by stimulation of the intramural parasympathetic nerve fibers or by intra-arterial infusion of acetylcholine (ACh). Successive cholinergic interventions were applied; first, a conditioning intervention for 2 min was given, then this was followed by a test intervention for 4 min. The two interventions were separated by a rest period that varied from 15 to 240 s. The cardiac responses to the conditioning parasympathetic nerve stimulation quickly reached maximum levels, and then they "faded" or progressively diminished back toward the control level. The inotropic responses to the conditioning infusion of ACh (1 μg/min) faded slightly but the chronotropic response did not. After the rest period, the test nerve stimulation evoked responses that also gradually faded with time. The maximal amplitude of the responses to the test simuli were less than those to the conditioning stimuli. This reduction in the maximal amplitude of the cardiac responses to the test stimuli was more pronounced with high frequency stimulation (30 Hz) than with low frequency stimulation (5 Hz). The decrement was also more pronounced the shorter the rest period, and it was greater at earlier times after beginning the stimulation. Conversely, the maximal cardiac responses to test infusions of ACh were not appreciably less than the responses to the conditioning infusions. We conclude, therefore, that the diminution of the cardiac responses to the second test stimulation of the parasympathetic nerve fibers was mainly ascribable to a prejunctional rather than to a postjunctional mechanism.


1989 ◽  
Vol 256 (6) ◽  
pp. R1331-R1339
Author(s):  
K. H. Pitetti ◽  
G. A. Iwamoto ◽  
J. H. Mitchell ◽  
G. A. Ordway

We used a constant flow preparation to study the changes in left circumflex coronary arterial (LCCA) pressure and resistance evoked by electrical stimulation of branches of muscle, cutaneous, and mixed nerves in the hindlimb of anesthetized dogs. Stimulation (20 Hz) of all three nerve types at 20, 70, 100, and 200 times the voltage threshold that evoked compound action potentials significantly (P less than 0.05) increased LCCA resistance. Stimulation at three and five times threshold had no effect on this same variable. Cooling the nerve to 2-4 degrees C, temperatures that block myelinated nerve fibers, attenuated but did not abolish the increase in LCCA resistance. Combinations of beta- and alpha-adrenergic and cholinergic blockade established that the biphasic change evoked by nerve stimulation was due to an initial alpha-adrenergic vasoconstriction followed by a metabolite-induced vasodilation. These data demonstrate that stimulation of muscle, cutaneous, or mixed nerve afferent C-fibers increases coronary arterial resistance by alpha-adrenergic vasoconstriction.


1993 ◽  
Vol 264 (1) ◽  
pp. R204-R210
Author(s):  
P. J. Davies ◽  
M. S. Hedrick ◽  
D. R. Jones

The neuromuscular control of the glottis, a muscular sphincter that controls air flow to and from the swim bladder, was investigated using in vitro preparations from bowfin (Amia calva). Stimulation of the ramus intestinalis branch of the vagus nerve caused an increase in isometric tension of the glottal musculature, indicating active closure. The glottis could be actively opened only by direct stimulation of muscle bundles lying lateral to the glottis. In 19 of 24 preparations supramaximal nerve stimulation (20 Hz, 10 V) caused a two-phase increase in muscle tension. Immediately after the onset of stimulation there was a rapid increase in muscle tension. After the end of the train of stimuli, the tension decreased and then again increased briefly followed by a slow return to baseline lasting approximately 60 s. The addition of hyoscine reduced maximum tension of the response by 63 +/- 7% and abolished the second slower element of the response to vagal stimulation. The remaining faster response to nerve stimulation was abolished by tubocurarine. Applied acetylcholine or carbachol mimicked the slow response, causing a slow-onset sustained contraction that was abolished by hyoscine. Hence, the musculature showed physiological characteristics of both skeletal and smooth muscle. Histological examination of the glottis confirmed the physiological results: smooth muscle fibers were found lining the pneumatic duct and lumen of the glottis arranged in a circular fashion around the lateral margins of the glottis. Distinct skeletal muscle bundles were found lateral to the smooth muscle and also arranged in parallel with the glottal lumen, forming a skeletal muscle sphincter.(ABSTRACT TRUNCATED AT 250 WORDS)


2018 ◽  
Vol 120 (3) ◽  
pp. 1173-1185 ◽  
Author(s):  
M. Bączyk ◽  
E. Jankowska

Direct current (DC) potently increases the excitability of myelinated afferent fibers in the dorsal columns, both during DC polarization of these fibers and during a considerable (>1 h) postpolarization period. The aim of the present study was to investigate whether similarly long-lasting changes in the excitability of myelinated nerve fibers in the dorsal columns may be evoked by field potentials following stimulation of peripheral afferents and by subthreshold epidurally applied current pulses. The experiments were performed in deeply anesthetized rats. The effects were monitored by changes in nerve volleys evoked in epidurally stimulated hindlimb afferents and in the synaptic actions of these afferents. Both were found to be facilitated during as well as following stimulation of a skin nerve and during as well as following epidurally applied current pulses of 5- to 10-ms duration. The facilitation occurring ≤2 min after skin nerve stimulation could be linked to both primary afferent depolarization and large dorsal horn field potentials, whereas the subsequent changes (up to 1 h) were attributable to effects of the field potentials. The findings lead to the conclusion that the modulation of spinal activity evoked by DC does not require long-lasting polarization and that relatively short current pulses and intrinsic field potentials may contribute to plasticity in spinal activity. These results suggest the possibility of enhancing the effects of epidural stimulation in human subjects by combining it with polarizing current pulses and peripheral afferent stimulation and not only with continuous DC. NEW & NOTEWORTHY The aim of this study was to define conditions under which a long-term increase is evoked in the excitability of myelinated nerve fibers. The results demonstrate that a potent and long-lasting increase in the excitability of afferent fibers traversing the dorsal columns may be induced by synaptically evoked intrinsic field as well as by epidurally applied intermittent current pulses. They thus provide a new means for the facilitation of the effects of epidural stimulation.


1953 ◽  
Vol 37 (1) ◽  
pp. 91-110 ◽  
Author(s):  
Mario Altamirano ◽  
Christopher W. Coates ◽  
Harry Grundfest ◽  
David Nachmansohn

1. A preparation is described consisting of one or several layers of innervated cells of the electric organ of Electrophorus electricus. 2. Each plaque is multiply innervated and only at its caudal face. The nerve fibers may derive from two or more different nerve trunks. 3. During activity the innervated face becomes negative relative to the non-innervated. 4. The first electrical response of the cell to an increasing neural volley is graded and has the character of a prepotential. At a critical size of the prepotential the cell discharges with an all-or-nothing spike. 5. Both responses have durations of about 2 msec. 6. A neural volley which does not cause the spike discharge facilitates the discharge of the cell by a second subsequent volley in the same nerve (temporal facilitation). 7. The period of facilitation lasts ca. 900 msec. During the first 100 msec., the facilitation is large enough to cause a spike. In the later portion only the prepotential is facilitated. No electrical concomitant has been detected. 8. Neural volleys reaching the plaque from different trunks interact at the cell to produce a period of facilitation lasting only about 2 msec. This interaction is interpreted as spatial summation. 9. In a population of cells, simultaneous stimulation of 2 nerves causes a smaller discharge than the sum of the two isolated responses (occlusion). 10. Cells denervated for 7 weeks or more can be excited directly, but only by a current flow outward through the caudal face. 11. Weak direct stimulation causes a prepotential in the denervated plaque. On increasing the stimulus the prepotential increases to a critical size when a spike develops. The duration of both responses is about 2 msec. 12. The absolutely refractory period of the denervated cell is about 1.5 msec. and relative refractoriness lasts about 15 msec. 13. Direct stimulation causes slight facilitation lasting as long as 200 msec. 14. Repetitive stimulation of the nerve at low frequencies (2 to 3 per second) causes rapid "fatigue" of transmission. The denervated plaque, however, responds for several minutes to repetitive direct stimulation at high frequencies (25 per second).


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