scholarly journals MECHANISMS OF BIOELECTRIC ACTIVITY IN ELECTRIC TISSUE

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).

1990 ◽  
Vol 63 (2) ◽  
pp. 303-318 ◽  
Author(s):  
C. C. Bell

1. Physiologically and morphologically identified primary afferent fibers from mormyromast electroreceptor organs were recorded intracellularly. The fiber recordings were made from the nerve root of the posterior lateral line nerve, where the fibers enter the brain, and from the electrosensory lateral line lobe (ELL), near the central terminals of the fibers. 2. The intracellular recordings reveal a variety of potentials, synaptic and nonsynaptic, in addition to the large orthodromic action potentials from the periphery. The goal of the present study was to describe and interpret these various potentials in mormyromast afferent fibers as a first step in understanding the processing of electrosensory information in ELL. 3. Three types of synaptic potentials were recorded inside mormyromast afferent fibers: 1) electric organ corollary discharge (EOCD) excitatory postsynaptic potentials (EPSPs), driven by the motor command that elicits the electric organ discharge (EOD); 2) EPSPs evoked by electrosensory stimulation of electroreceptors in the skin near the electroreceptor from which the recorded fiber originates or by direct stimulation of an electrosensory nerve; and 3) inhibitory postsynaptic potentials (IPSPs) evoked by electrosensory stimulation of more distant electroreceptors. These synaptic potentials can be attributed to synaptic input to postsynaptic cells in ELL that is observed inside the afferent fibers because of electrical synapses between the fibers and the postsynaptic cells. 4. The peripherally evoked EPSPs could frequently be shown to be unitary. The unitary EPSPs were identical to the orthodromic spikes in originating from a single electroreceptor, in threshold, and in latency shift with increasing stimulus intensity. These similarities suggest that the unitary EPSPs are electrotonic EPSPs caused by impulses in other mormyromast afferent fibers that terminate on some of the same postsynaptic cells as the recorded fiber. The peripherally evoked IPSPs had a longer latency than the EPSPs or orthodromic spikes, requiring the presence of an inhibitory interneuron. 5. The peripherally evoked EPSPs, both unitary and nonunitary, show absolute refractory periods of 3-8 ms, followed by relative refractory periods of approximately 8 ms, when tested with two identical stimuli to a nerve. These refractory periods are interpreted as because of refractoriness in the fine preterminal branches of the axonal arbor. 6. A depolarizing afterpotential is commonly associated with the orthodromic spike and probably results from the successful propagation of the spike into the entire terminal arbor. The depolarizing afterpotential has a refractory period that is similar to that of the peripherally evoked EPSPs and that is also interpreted as refractoriness in the fine preterminal branches.(ABSTRACT TRUNCATED AT 400 WORDS)


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.


1984 ◽  
Vol 56 (4) ◽  
pp. 922-929 ◽  
Author(s):  
M. Aubier ◽  
N. Viires ◽  
D. Murciano ◽  
G. Medrano ◽  
Y. Lecocguic ◽  
...  

We studied the effects of intravenously administered terbutaline on diaphragmatic force and fatigue during electrical stimulation of the diaphragm in 17 anesthetized dogs. The diaphragm was stimulated indirectly through the phrenic nerves with electrodes placed around the fifth roots and directly with electrodes surgically implanted in the abdominal side of each hemidiaphragm. Transdiaphragmatic pressure (Pdi) during direct or indirect supramaximal 2-s stimulation applied over a frequency range of 10–100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. In seven dogs the administration of terbutaline (0.5 mg) had no effect on Pdi at any stimulation frequency applied directly or indirectly. The effect of terbutaline (0.5 mg) on diaphragmatic fatigue was then tested in 10 other dogs. Diaphragmatic fatigue was produced by continuous 20-Hz electrical supramaxial stimulation of the phrenic nerves during 30 min. At the end of the fatigue procedure Pdi decreased by 50 +/- 5 and 30 +/- 8% of control values at 10 and 100 Hz, respectively, for either direct or indirect stimulation. The decrease in Pdi for low frequencies of stimulation (10 and 20 Hz) lasted 100 +/- 18 min, whereas it lasted only 40 +/- 10 min for the high frequencies (50 and 100 Hz). When terbutaline (0.5 mg) was administered after the fatiguing procedure, Pdi increased within 15 min by 20 +/- 4% at 10 Hz and by 12 +/- 3% at 100 Hz for either direct or indirect stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)


1956 ◽  
Vol 186 (3) ◽  
pp. 475-482 ◽  
Author(s):  
Lawrence Kruger

The afferent evoked electrical response in precentral and postcentral cerebral cortex was studied in anesthetized and unanesthetized monkeys. Responses to nerve volleys were obtained on both sides of the central sulcus, tactile evoked responses were limited to the contralateral postcentral gyrus. Precentral responses were evoked by stimulation of the fast cutaneous and slow muscle afferent fibers. The amplitude and distribution of precentral responses varied with the number of peripheral nerve fibers synchronously activated. The latency of precentral responses increased as a function of distance from the central sulcus. Precentral and postcentral potentials were altered in the same manner by topical application of Novocaine and strychnine and the spreading depression of Leão. The nature of the afferent precentral electrical response, the anesthetic conditions for its study and the possible functional role of this projection are discussed.


1960 ◽  
Vol 38 (1) ◽  
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.


1924 ◽  
Vol 6 (5) ◽  
pp. 615-624 ◽  
Author(s):  
Charles L. Wible

1. In Mnemiopsis veratrin shows two stages of veratrin poisoning. First, inhibition of the beats of the plates which disappears on cutting them away either singly or in small groups. Second, after half an hour mechanical stimulation excites the beat of the plates in the intact veratrinized animal. It is concluded that veratrin acts on nervous tissue and not on the substance of the swimming plates. 2. In Lumbricus, veratrin acts on the ventral nerve cord alone, and not on the muscles and peripheral nerves. 3. In Musca, veratrin first causes opisthotonos, then spasms and extreme flexion of the legs. Decapitation causes these effects to disappear hence veratrin acts on the cerebral ganglia of the fly. 4. Veratrin applied to the sciatic nerve of the frog causes, after a latent period of 20 minutes, irregular contractions of the gastrocnemius which persist for an hour or more. Veratrin is thus a neurophil alkaloid of the first class as well as second and in this way resembles tetraethyl ammonium chloride. 5. If the end of a sciatic nerve is dipped into veratrin solution, then direct stimulation of the gastrocnemius muscle results in contraction with delayed relaxation, although the muscle itself is not subject to the action of veratrin. 6. By means of preparations of the sartorius muscle of the frog it is shown that veratrin acts not on the muscle cells directly but on the nerve fibers. Hence veratrin produces the characteristic muscle curve showing delayed relaxation by its action on the nervous elements.


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.


2005 ◽  
Vol 93 (6) ◽  
pp. 3463-3478 ◽  
Author(s):  
Sarah J. Griffin ◽  
Leslie R. Bernstein ◽  
Neil J. Ingham ◽  
David McAlpine

Interaural time differences (ITDs) are important cues for mammalian sound localization. At high frequencies, sensitivity to ITDs, which are conveyed only by the envelope of the waveforms, has been shown to be poorer than sensitivity to ITDs at low frequencies, which are conveyed primarily by the fine structure of the waveforms. Recently, human psychophysical experiments have demonstrated that sensitivity to envelope-based ITDs in high-frequency transposed tones can be equivalent to low-frequency fine-structure–based ITD sensitivity. Transposed tones are designed to provide high-frequency auditory nerve fibers (ANFs) with similar temporal information to that provided by low-frequency tones. We investigated neural sensitivity to ITDs in high-frequency transposed and sinusoidally amplitude modulated (SAM) tones, in the inferior colliculus of the guinea pig. Neural sensitivity to ITDs in transposed tones was found to be greater than that to ITDs in SAM tones; in response to transposed tones, neural firing rates were more modulated as a function of ITD and discrimination thresholds were found to be lower than those in response to SAM tones. Similar to psychophysical findings, ITD discrimination of single neurons in response to transposed tones for rates of modulation <250 Hz was comparable to neural discrimination of ITDs in low-frequency tones. This suggests that the neural mechanisms that mediate sensitivity to ITDs at high and low frequencies are functionally equivalent, provided that the stimuli result in appropriate temporal patterns of action potentials in ANFs.


1973 ◽  
Vol 82 (4) ◽  
pp. 464-472 ◽  
Author(s):  
Merle Lawrence ◽  
Lars-Göran Johnsson

An analysis of the contribution to hearing made by the presence of a normal organ of Corti as compared to direct electric stimulation of the nerve leads to the following conclusions: The portion of the basal turn of the cochlea which can be stimulated contains activity regions primarily limited to frequencies above 5000 Hz. Electrical stimulation of sensory afferent nerve fibers gives rise to sensations of very limited dynamic range compared to normal adequate stimulation through the organ of Corti. Following destruction of the organ of Corti, the speed of nerve degeneration in man is not known, but appears to be slow. Some ganglion cells almost always persist but it is doubtful that these are excitable. The severe nerve degeneration known to be present in most cases of human deafness raises critical questions about the feasibility and logic of a direct stimulation of the auditory nerve in these patients. The unavoidable damage to the capillaries and endosteum of the walls of the scala tympani by insertion of a wire is certain to produce further degeneration and new bone formation.


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