scholarly journals Ocular and cervical vestibular evoked myogenic potentials elicited by air-conducted, low-frequency sound

2020 ◽  
Vol 30 (4) ◽  
pp. 235-247
Author(s):  
Vivien Nancy Luecke ◽  
Laura Buchwieser ◽  
Peter zu Eulenburg ◽  
Torsten Marquardt ◽  
Markus Drexl

BACKGROUND: Sound is not only detected by the cochlea, but also, at high intensities, by the vestibular system. Acoustic activation of the vestibular system can manifest itself in vestibular evoked myogenic potentials (VEMPs). In a clinical setting, VEMPs are usually evoked with rather high-frequency sound (500 Hz and higher), despite the fact that only a fraction of saccular and utricular hair cells in the striolar region is available for high-frequency stimulation. OBJECTIVE: As a growing proportion of the population complains about low-frequency environmental noise, including reports on vestibular symptoms, the activation of the vestibular system by low-frequency sound deserves better understanding. METHODS: We recorded growth functions of oVEMPs and cVEMPs evoked with air-conducted sound at 120 Hz and below. We estimated VEMP thresholds and tested whether phase changes of the stimulus carrier result in changes of VEMP amplitude and latency. RESULTS: The VEMP response of the otholith organs to low-frequency sound is uniform and not tuned when corrected for middle ear attenuation by A-weighting the stimulus level. Different stimulus carrier phases result in phase-correlated changes of cVEMP latencies and amplitudes. CONCLUSIONS: VEMPs can be evoked with rather low-frequency sound, but high thresholds suggest that they are unlikely to be triggered by environmental sounds.

1957 ◽  
Vol 40 (3) ◽  
pp. 435-450 ◽  
Author(s):  
David P. C. Lloyd

An assemblage of individual motoneurons constituting a synthetic motoneuron pool has been studied from the standpoint of relating monosynaptic reflex responses to frequency of afferent stimulation. Intensity of low frequency depression is not a simple function of transmitter potentiality. As frequency of stimulation increases from 3 per minute to 10 per second, low frequency depression increases in magnitude. Between 10 and approximately 60 per second low frequency depression apparently diminishes and subnormality becomes a factor in causing depression. At frequencies above 60 per second temporal summation occurs, but subnormality limits the degree of response attainable by summation. At low stimulation frequencies rhythm is determined by stimulation frequency. Interruptions of rhythmic firing depend solely upon temporal fluctuation of excitability. At high frequency of stimulation rhythm is determined by subnormality rather than inherent rhythmicity, and excitability fluctuation leads to instability of response rhythm. In short, whatever the stimulation frequency, random excitability fluctuation is the factor disrupting rhythmic response. Monosynaptic reflex response latency is stable during high frequency stimulation as it is in low frequency stimulation provided a significant extrinsic source of random bombardment is not present. In the presence of powerful random bombardment discharge may become random with respect to monosynaptic afferent excitation provided the latter is feeble. When this occurs it does so equally at low frequency and high frequency. Thus temporal summation is not a necessary factor. There is, then, no remaining evidence to suggest that the agency for temporal summation in the monosynaptic system becomes a transmitting agency in its own right.


2000 ◽  
Vol 83 (4) ◽  
pp. 2412-2420 ◽  
Author(s):  
Hiroshi Ikeda ◽  
Tatsuya Asai ◽  
Kazuyuki Murase

We investigated the neuronal plasticity in the spinal dorsal horn and its relationship with spinal inhibitory networks using an optical-imaging method that detects neuronal excitation. High-intensity single-pulse stimulation of the dorsal root activating both A and C fibers evoked an optical response in the lamina II (the substantia gelatinosa) of the dorsal horn in transverse slices of 12- to 25-day-old rat spinal cords stained with a voltage-sensitive dye, RH-482. The optical response, reflecting the net neuronal excitation along the slice-depth, was depressed by 28% for more than 1 h after a high-frequency conditioning stimulation of A fibers in the dorsal root (3 tetani of 100 Hz for 1 s with an interval of 10 s). The depression was not induced in a perfusion solution containing an NMDA antagonist,dl-2-amino-5-phosphonovaleric acid (AP5; 30 μM). In a solution containing the inhibitory amino acid antagonists bicuculline (1 μM) and strychnine (3 μM), and also in a low Cl−solution, the excitation evoked by the single-pulse stimulation was enhanced after the high-frequency stimulation by 31 and 18%, respectively. The enhanced response after conditioning was depotentiated by a low-frequency stimulation of A fibers (0.2–1 Hz for 10 min). Furthermore, once the low-frequency stimulation was applied, the high-frequency conditioning could not potentiate the excitation. Inhibitory transmissions thus regulate the mode of synaptic plasticity in the lamina II most likely at afferent terminals. The high-frequency conditioning elicits a long-term depression (LTD) of synaptic efficacy under a greater activity of inhibitory amino acids, but it results in a long-term potentiation (LTP) when inhibition is reduced. The low-frequency preconditioning inhibits the potentiation induction and maintenance by the high-frequency conditioning. These mechanisms might underlie robust changes of nociception, such as hypersensitivity after injury or inflammation and pain relief after electrical or cutaneous stimulation.


1981 ◽  
Vol 51 (2) ◽  
pp. 317-320 ◽  
Author(s):  
S. R. Garfin ◽  
C. M. Tipton ◽  
S. J. Mubarak ◽  
S. L. Woo ◽  
A. R. Hargens ◽  
...  

The effect of fasciotomy on muscle tension (measured by a force transducer attached to the tendon) and interstitial fluid pressure (measured by Wick catheters in the muscle belly) was studied in the anterolateral compartments of 13 dog hindlimbs. Muscle tension and pressure were monitored in the tibialis cranialis muscle after low- and high-frequency stimulation of the peroneal nerve to produce twitch- and tetanic-type contractions. Fasciotomy decreased muscle force during the low-frequency stimulation by 16% (35.3 +/- 4.9 to 28.4 +/- 3.9 N) and during the high-frequency stimulation by 10% (60.8 %/- 4.9 to 54.8 +/- 3.9 N). Muscle pressure decreased 50% after fasciotomy under both conditions, 15 +/- 2 to 6 +/- 1 mmHg and 84 +/- 17 to 41 +/- 8 mmHg), respectively. Repeated functional evaluations during the testing procedure indicated that muscle fatigue was not a major factor in these results. It was concluded that fascia is important in the development of muscle tension and changes in interstitial pressure. Furthermore, the results raised questions concerning the merits of performing a fasciotomy for athletes with a compartment syndrome.


2019 ◽  
Vol 116 (13) ◽  
pp. 6397-6406 ◽  
Author(s):  
Xi Chen ◽  
Xiao Li ◽  
Yin Ting Wong ◽  
Xuejiao Zheng ◽  
Haitao Wang ◽  
...  

Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK−/−mice lacked neocortical LTP and showed deficits in a cue–cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue–cue associative memory.


2021 ◽  
Vol 15 ◽  
Author(s):  
Carlos Silva ◽  
Blake S. Porter ◽  
Kristin L. Hillman

When performing tasks, animals must continually assess how much effort is being expended, and gage this against ever-changing physiological states. As effort costs mount, persisting in the task may be unwise. The anterior cingulate cortex (ACC) and the anterior insular cortex are implicated in this process of cost-benefit decision-making, yet their precise contributions toward driving effortful persistence are not well understood. Here we investigated whether electrical stimulation of the ACC or insular cortex would alter effortful persistence in a novel weightlifting task (WLT). In the WLT an animal is challenged to pull a rope 30 cm to trigger food reward dispensing. To make the action increasingly effortful, 45 g of weight is progressively added to the rope after every 10 successful pulls. The animal can quit the task at any point – with the rope weight at the time of quitting taken as the “break weight.” Ten male Sprague-Dawley rats were implanted with stimulating electrodes in either the ACC [cingulate cortex area 1 (Cg1) in rodent] or anterior insula and then assessed in the WLT during stimulation. Low-frequency (10 Hz), high-frequency (130 Hz), and sham stimulations were performed. We predicted that low-frequency stimulation (LFS) of Cg1 in particular would increase persistence in the WLT. Contrary to our predictions, LFS of Cg1 resulted in shorter session duration, lower break weights, and fewer attempts on the break weight. High-frequency stimulation of Cg1 led to an increase in time spent off-task. LFS of the anterior insula was associated with a marginal increase in attempts on the break weight. Taken together our data suggest that stimulation of the rodent Cg1 during an effortful task alters certain aspects of effortful behavior, while insula stimulation has little effect.


1996 ◽  
Vol 80 (2) ◽  
pp. 464-471 ◽  
Author(s):  
K. J. Ayre ◽  
A. J. Hulbert

The effects of manipulating dietary levels of essential polyunsaturated fatty acids on the function of isolated skeletal muscles in male Wistar rats were examined. Three isoenergetic diets were used: an essential fatty acid-deficient diet (EFAD), a diet high in essential (n-6) fatty acids [High (n-6)], and a diet enriched with essential (n-3) fatty acids [High (n-3)]. After 9 wk, groups of rats on each test diet were fed a stock diet of laboratory chow for a further 6 wk. Muscle function was examined by using a battery of five tests for soleus (slow twitch) and extensor digitorum longus (EDL; fast twitch). Tests included single muscle twitches, sustained tetanic contractions, posttetanic potentiation, sustained high-frequency stimulation, and intermittent low-frequency stimulation. Results for muscles from the High (n-6) and High (n-3) groups were very similar. However, the EFAD diet resulted in significantly lower muscular tensions and reduced response times compared with the High (n-6) and High (n-3) diets. Peak twitch tension in soleus muscles was 16-21% less in the EFAD group than in the High (n-6) and High (n-3) groups, respectively [analysis of variance (ANOVA), P < 0.01). During high-frequency stimulation, EDL muscles from the EFAD rats fatigued 32% more quickly (ANOVA, P < 0.01)]. Also, twitch contraction and half-relaxation times were significantly 5-7% reduced in the EFAD group (ANOVA, P < 0.01). During intermittent low-frequency stimulation, soleus muscles from the EFAD group generated 25-28% less tension than did the other groups (ANOVA, P < 0.01), but in EDL muscles from the EFAD group, endurance was 20% greater than in the High (n-6) group (ANOVA, P < 0.05). After 6 wk on the stock diet, there were no longer any differences between the dietary groups. Manipulation of dietary fatty acids results in significant, but reversible, effects in muscles of rats fed an EFAD diet.


1991 ◽  
Vol 65 (6) ◽  
pp. 1313-1320 ◽  
Author(s):  
H. R. Koerber ◽  
L. M. Mendell

1. Monosynaptic excitatory postsynaptic potentials (EPSPs) were evoked in medial gastrocnemius motoneurons by maximal group Ia stimulation of the heteronymous lateral gastrocnemius-soleus nerve in anesthetized cats. Three different patterns of high-frequency stimulation were delivered to the nerve, and the EPSPs were averaged in register (1, 2, . . ., n) for each. 2. One pattern ("Burst") consisted of 32 shocks delivered every 2 s at an interstimulus interval of 6 ms (167 Hz). The second pattern ("Stepping") was a frequency-modulated burst of 52 shocks derived from a recording of a spindle during stepping and was delivered every 2 s. The third pattern ("Paw Shake") was from an extensor spindle afferent recorded during rapid paw shake and was delivered in groups of six bursts with an interburst interval of 75 ms and a 3-s pause between groups of six bursts. The EPSPs in each burst were averaged in register (1, 2, . . ., n) so that the relative amplitude of each EPSP in the burst could be ascertained. The EPSP produced by low-frequency stimulation of the nerve (18 Hz) was also recorded for each motoneuron. 3. The initial EPSP in most bursts was larger than the EPSP measured as a result of low-frequency stimulation. This potentiation, defined as the ratio of the amplitude of the initial EPSP of the response to that of the low-frequency control, was found to vary systematically as a function of amplitude of the control EPSP as well as the stimulus paradigm used.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 258 (5) ◽  
pp. H1334-H1338 ◽  
Author(s):  
A. Ohlen ◽  
M. G. Persson ◽  
L. Lindbom ◽  
L. E. Gustafsson ◽  
P. Hedqvist

Intravital microscopy was used to study the effect of motor nerve stimulation on microvessel diameters in the rabbit tenuissimus muscle. Stimulation of the motor nerve (0.5-5 ms, 2-20 Hz, 5-15 V) evoked pulse duration- and frequency-dependent constriction of transverse and terminal arterioles. The vasoconstriction induced by low-frequency stimulation (2 Hz) was abolished by the alpha-adrenoceptor antagonist phentolamine, whereas high-frequency stimulation (10-20 Hz) resulted in a response that was only partially inhibited by phentolamine. However, desensitization of the tissue to the vasoconstrictor effects of neuropeptide Y (NPY) changed the response remaining after phentolamine into vasodilatation. Independent of stimulation parameters, pretreatment of the tissue with the adrenergic neuron blocker guanethidine reversed the constriction into dilatation that was resistant to propranolol, atropine, and indomethacin. The results document the functional presence of both vasoconstrictor and vasodilator fibers in the rabbit tenuissimus muscle motor nerve, and they suggest that part of the nerve-induced vasoconstriction at higher stimulation frequencies is caused by neuronally released NPY.


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