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1 Biology Department, University of Michigan-Flint, Flint, 48502-2186; and 2 Department of Otolaryngology, Wayne State University, Detroit, Michigan 48202
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ABSTRACT |
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 Abstract
 Introduction
Methods
Results
Discussion
References
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Myers, S. F., H. H. Salem, and J. A. Kaltenbach. Efferent neurons and vestibular cross talk in the frog. J. Neurophysiol. 77: 2061-2070, 1997. A galvanic stimulus (30- to 120-s, 0.3-mA constant current pulse) was used to depolarize the spike-generating region of horizontal and anterior canal afferent neurons. The galvanically induced spike activity from these neurons served as a driving input to the efferent vestibular system in the bullfrog. Efferent-mediated effects were assessed by intracellular recordings of posterior canal afferent spike activity, either ipsilateral or contralateral to the driving stimulus. Ipsilateral to the driving stimulus, efferent-mediated spike rate changes occurred in 62 (39%) of 158 posterior canal afferent neurons. Ipsilateral efferent-mediated effects were overwhelmingly excitatory (92%). Of responding units, 3% were inhibited during stimulus application and 5% showed mixed responses involving 3-20 s of inhibition followed by facilitation. Contralateral to the driving stimulus, efferent-mediated spike rate changes occurred in 18 (23%) of 77 posterior canal afferent neurons. Contralateral efferent-mediated effects were overwhelmingly inhibitory (95%). Only one unit was facilitated during stimulation and no mixed responses to contralateral stimulation were observed. Analysis of the coefficient of variation in interspike intervals (CV) before and during stimulation showed no significant efferent-mediated effects on spike train noise. Comparisons of resting spike rates between units showing efferent-mediated effects and those that did not were in general agreement with previous studies. Responding units had a lower mean spike rate (6.8 ± 0.70 spikes/s, mean ± SE) than did nonresponding units (10.7 ± 0.42 spikes/s, mean ± SE; P < 0.001; 2-tailed t-test of log-normalized data). Comparison between groups in the regularity of their resting spike rates, as quantified by CV, showed considerable overlap. When responding and nonresponding units with similar resting spike rates were compared, responding units had more irregular resting spike rates than did nonresponding units (P < 0.004; 2-tailed, paired t-test). In most cases (77%) the temporal pattern and general shapes of efferent-mediated responses mirrored the driving input of the galvanically activated afferent neurons. The other 23% of efferent-mediated responses exhibited a marked adaptation of the response. Adapting and nonadapting units were not significantly different in their mean resting spike rates or in the regularity of their resting spike rates.
The efferent vestibular system provides a means by which the CNS can modify sensory operations of the inner ear motion and gravity sensors. A major function of the efferent vestibular system is believed to involve adjustments of the operating range of the vestibular sensors in anticipation of a voluntary movement (Boyle and Highstein 1990 Surgical procedure
Bullfrogs (Rana catesbiana) weighing 50-180 g were anesthetized with pentobarbital sodium and ketamine hydrochloride (35 µg/g body wt of each anesthetic via intramuscular injections), with supplemental injections as necessary. During surgery and throughout the physiological experiment, the frog was covered with damp gauze to facilitate cutaneous respiration. The VIIIth nerve was approached through the roof of the mouth by removal of a small patch of mucosa and drilling through the underlying bone and cartilage with a dental drill bit to expose the dura directly over the VIIIth nerve in the cranial cavity. The otic capsule was opened posteromedially to expose the course of the posterior division of the VIIIth nerve to the branch innervating the posterior semicircular canal. Care was used when excising dura or perichondrium to avoid damage to branches of the labyrinthine artery. At the end of experimentation, the animal was killed by decapitation under deep pentobarbital anesthesia.
Experimental procedure
With the frog positioned ventral side up, the influence of efferent vestibular system on posterior canal afferent neuronal activity was investigated by galvanic activation of anterior and horizontal canal afferent neurons. Stimulating electrodes comprised paired electrodes (either tungsten or silver wire, insulated to within 1 mm of the tip with parylene or Teflon, respectively). Two sets of paired electrodes were used; one pair for each ear, placed in the otic capsule. The standard positioning was to place the cathodal electrode just anterior to the anterior canal ampulla. The anodal electrode was then placed ~8 mm posterior to the anodal electrode either within the cartilage of the otic capsule or submucosally within the middle ear. The intent of the electrode placement was to place the anterior and horizontal canal ampullae in the current path of the electrodes but in closer proximity to the cathodal electrode. Stimuli comprised long-duration (20-120 s) constant current pulses (0.1-0.45 mA) generated by an isolated pulse stimulator (AM systems model 2100).
Galvanic stimulation of anterior and horizontal canal afferent neurons
Basic experimental protocols are illustrated in Fig. 1. The anterior and horizontal canal afferent responses shown in Fig 2. provide an indication of the "driving" input to the efferent vestibular system. Long-duration, constant current pulses (30-120 s, 0.3 mA) applied to the otic capsule in the vicinity of the anterior and horizontal canal ampullae caused a two- to eightfold increase in spike rates (increase of 6-30 spikes/s over resting spike rate) of afferent nerve fibers innervating those same ampullae (Fig. 2). Spike rate changes occurred abruptly at the onset and termination of the galvanic stimulus. Partial response declines during stimulation as well as poststimulus depression of spike rates were common but not evident in all cases (compare Fig. 2, A and B, with Fig. 2C).
Comparison of ipsilateral and contralateral stimulation effects on posterior canal afferent spike rates
In paradigm 1 (Fig. 1), galvanic activation of vestibular afferent neurons of the anterior and horizontal canal ampullae was used to provide input drive to the efferent vestibular system. The influence of the efferent vestibular system on posterior canal afferent activity was examined in the presence and absence of this input drive. The incidence of efferent-mediated responses and the response types (facilitated, inhibited, or mixed) are summarized in Fig. 3. Single-unit recordings of posterior canal afferent neurons identified 62 of 158 units (39%) that changed spike rate during 0.3-mA galvanic stimulation. Ninety-two percent (57 of 62) responded with increased spike rates (prestimulus spike rate: 7.0 ± 0.72 spikes/s, mean ± SE; during-stimulus spike rate: 11.9 ± 0.91 spikes/s, mean ± SE; increase of 4-839% or 0.8-21 spikes/s; mean = 5.0 ± 3.8 spikes/s, mean ± SD). Two units (3%) responded with decreased spike rates (24% and 88%; 3 and 2 spikes/s). Three units (5%) had mixed responses involving an initial 3-20 s of reduced spike rate followed by an elevated spike rate.
Control experiments
To verify that the efferent vestibular system was responsible for the observed modulations of posterior canal afferent spike rates, three sets of control experiments were conducted (3 frogs per set). The first set involved transection of the VIIIth nerve root ipsilateral to the stimulating electrodes, but contralateral to the recording electrode. Figure 5A shows the inhibitory response of a posterior canal unit to a contralateral galvanic stimulus. After this recording, the VIIIth nerve ipsilateral to the stimulating electrodes was carefully cut without disturbing the recording electrode. Subsequent spike activity of the same posterior canal unit as well as its lack of response to additional contralateral stimuli are shown in Fig. 5B. These experiments demonstrated that for the galvanic stimulus to modify the spike rate of a posterior canal unit of the opposite side, there must be intact vestibular afferent connections to the brain stem from the stimulated inner ear. These experiments also rule out current spread from the stimulating electrodes as well as electrical activation of general sensory nerve fibers as explanations for the observed responses to contralateral galvanic stimulation.
Comparisons between posterior canal units that did and did not respond to ipsilateral galvanic stimulation
Posterior canal units that responded to ipsilateral galvanic stimulation had a mean spike rate of 6.8 ± 0.70 (SE) spikes/s (range: 0.6-21 spikes/s; n = 62), compared with a mean spike rate of 10.7 ± 0.42 (SE) spikes/s (range: 0.5-41 spikes/s; n = 96) for nonresponding units (Fig. 6). These differences were statistically significant (P < 0.001; 2-tailed t-test of log-normalized spike rates). Responding units also had more irregular spike rates, which can be quantified in terms of CV, with higher CV values indicating a greater level of spike train noise. The mean CV value for responding units was 0.91 ± 0.12 (SE) (range: 0.43-1.26), compared with a mean CV of 0.72 ± 0.08 (SE) (range: 0.23-1.10) for nonresponding units. Valid statistical comparisons of CV values require correction for differences in mean spike rates (Goldberg et al. 1984
Adaptation of efferent-mediated responses
In most cases, the temporal pattern and general shapes of efferent-mediated responses of posterior canal afferent neurons qualitatively mirrored the driving input of the galvanically activated anterior and horizontal canal afferent neurons. Of posterior canal responses, 77% approximated a step response, sometimes with an "onset" enhancement of the response. The other 23% of posterior canal units exhibited a marked response adaptation. These units, like the one shown in Fig. 8, often showed an offset response that was more pronounced than the depression of spike activity generally seen after galvanic activation of afferent neurons (compare with Fig. 2). Mean spike rates and CV values of adapting posterior canal units (6.9 ± 1.52 spikes/s, mean ± SE; CV = 0.96 ± 0.05, mean ± SE; n = 14) and nonadapting units (7.0 ± 0.8 spikes/s, mean ± SE; CV = 0.9 ± 0.13, mean ± SE; n = 452) were not significantly different (P > 0.4; 2-tailed t-test; log-normalized spike rate data).
Analysis of CV
Analysis of CV values before and during efferent modulation of posterior canal spike activity was performed on nonadapting units with Afferent drive to efferent system
In this study a galvanic stimulus was used to depolarize the spike-generating region of horizontal and anterior canal afferent neurons to serve as a driving input to the efferent vestibular system. Vestibular afferent neurons can act monosynaptically on vestibular efferent neurons, but polysynaptic pathways are likely to be invoked as well (see Highstein 1991 Temporal characteristics of responses
The efferent-mediated responses in the present study had temporal characteristics that generally mirrored the driving afferent input. The galvanically induced driving afferent activity generally showed a poststimulation spike rate depression. This spike rate depression of the driving afferent activity usually was reflected in efferent-mediated responses of posterior canal afferent neurons as a postfacilitation depression or a postinhibition rebound. These extensions of the efferent response beyond the time period of the galvanic stimulus are not analogous to the poststimulation phenomena reported by Valli et al. (1986) Comparisons of responding and nonresponding afferent neurons
As a group, responding units had lower, more irregular spontaneous spike rates than nonresponding units; however, there was extensive overlap between groups in these parameters (see Fig. 7). Only the most regularly discharging units, those with CV values <0.4, were absent from the responding group. Studies in other species, such as squirrel monkey (Goldberg and Fernandez 1976), pigeon (Dickman and Correia 1993 Types of efferent-mediated responses
When direct activation of efferent fibers is used in the frog, responding afferent neurons fall into three categories on the basis of changes in their spontaneous spike rates: facilitation, inhibition, or mixed (combined inhibition/facilitation) (Bernard et al. 1985 Comparisons of inhibitory and excitatory efferent effects
That some efferent nerve fibers may mediate only inhibitory responses and others only excitatory effects is suggested by findings of Valli et al. (1986) Spike train noise
On an individual basis, responses of a few units suggested that the efferent vestibular system might influence spike train noise. Analysis of CV, a measure of spike train noise, found that CV values were marginally lower (less noisy) during nonadapting, facilitated responses compared with prestimulus periods (see RESULTS). This effect, however, can be attributed simply to the increased spike rate and not to any real increased regularity in action potential generation (Goldberg et al. 1984
INTRODUCTION
Abstract
Introduction
Methods
Results
Discussion
References
). Experiments in anesthetized as well as special unanesthetized preparations have shown that efferent activation causes many vestibular afferent neurons to exhibit higher background spike rates in combination with reduced response amplitudes (Boyle and Highstein 1990; Goldberg and Fernandez 1980). These primary afferent neurons are not so easily driven into spike rate saturation or silence by a strong acceleration. This efferent control over dynamic range of the inner ear motion sensors is seen in species as diverse as fish and monkeys (Boyle and Highstein 1990; Goldberg and Fernandez 1980), and may represent the most important function of the efferent vestibular system.
). Studies in the rat have found that 55% of efferent neurons also contain calcitonin gene-related peptide (Ohno et al. 1991). Ultrastructural studies in the rat indicate that efferent fibers with calcitonin gene-related peptide have different peripheral innervation patterns compared with those fibers without the peptide (Wackym 1993).
). Whether both sets of fibers are activated by the CNS simultaneously or differentially, depending on the inputs to the efferent vestibular system, is not known.
; Precht et al. 1974; Schmidt 1963). Dickman and Correia (1993) have demonstrated the effectiveness of vestibular afferent stimulation as a driving input for efferent-mediated effects on the opposite inner ear. Given the anatomic complexities of efferent vestibular system, it is possible that "how" the efferent vestibular system is activated may be important in determining the character of the efferent-mediated effects on vestibular afferent activity.
METHODS
Abstract
Introduction
Methods
Results
Discussion
References
.1
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FIG. 1.
Experimental paradigms used in this study. In paradigm 1, ipsilateral effects of vestibular afferent drive to efferent vestibular system were investigated. In paradigm 2, contralateral effects were investigated. Efferent vestibular neurons project widely throughout the labyrinth. For illustrative purposes only the efferent projection to the posterior semicircular canal is shown. Efferent-mediated effects on posterior canal afferent activity, either ipsilateral or contralateral to the driving stimulus, were recorded with the use of intracellular microelectrodes.
RESULTS
Abstract
Introduction
Methods
Results
Discussion
References
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FIG. 2.
Peristimulus spike rate histograms with 1-s spike bins demonstrate the effect of direct electrical activation of the afferent dendrites (A: horizontal canal nerve; B and C: anterior canal nerve). These responses provide an indication of the "driving" input to the efferent vestibular system. Horizontal bars: duration of galvanic stimulation (0.3-mA constant current pulse). A and B show the typical pattern with an "onset" response, then a period of relatively constant elevated spike rate, followed by a poststimulation spike rate depression. Response patterns like that shown in C, with little onset response and no poststimulus depression, also were observed.
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FIG. 3.
A: histogram showing the incidence of efferent-mediated responses by posterior canal afferent units. Responses were seen in 39% of units presented with ipsilateral stimulation, compared with 23% of units presented with contralateral stimulation. B: histogram showing incidence of response types where units responding to ipsilateral stimulation were overwhelmingly excited and units responding to contralateral stimulation were overwhelmingly inhibited. Some units responding to ipsilateral stimulation showed a mixed response with an initial 3- to 20-s period of inhibition, followed by excitation. C: histogram comparing spike rate changes of units facilitated by ipsilateral stimulation (Ipsi-Fac) with units inhibited by contralateral stimulation (Contra-Inh). Bars: SEs.
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FIG. 4.
Peristimulus spike rate histogram (1-s bins) of a posterior canal afferent neuron that responded to both ipsilateral (excitatory responses) and contralateral (inhibitory responses) applied stimuli. Horizontal bars: duration of galvanic stimulation. The 1st 2 stimulus periods were at 0.3-mA constant current; the 2nd 2 periods were at 0.4 mA. Note residual spontaneous activity during inhibitory responses.
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FIG. 5.
Peristimulus histograms of 2 units used in control studies to verify that the efferent vestibular system was responsible for observed changes in posterior canal afferent responses. A: inhibitory response of a posterior canal unit to a 120-s current pulse applied to the contralateral labyrinth. B: lack of response of the same unit as in A to 2 60-s current pulses after the contralateral VIIIth nerve was transected at the brain stem. C and D: another unit, ipsilateral to galvanic stimulation (a portion of the record was omitted in which a connector to a stimulating electrode came loose and had to be replaced). Two sets of ipsilateral electrodes were used to test for current spread from the stimulating electrodes to the posterior canal ampullae. The cathodal electrode of each set was approximately the same distance from the ipsilateral posterior canal ampulla but only 1 was close to the anterior and horizontal canal ampullae. When current was passed through this electrode, responses were observed (stimulus in C and 2nd stimulus in D). When current was passed through the other cathodal electrode, placed 6-8 mm posteriolateral to the horizontal canal ampulla, no response occurred (1st stimulus in D). See RESULTS for further discussion.
). This correction can be made by developing empirical formulae to normalize CV values to an arbitrary mean spike rate. This approach was attempted by the use of data from 20 afferent units in which galvanic stimuli were used to excite each unit for 20- to 30-s periods at several different levels of stable spike rates. However, individual variability between units was too great to determine formulas that could be used to reliably normalize CV values of other units.
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FIG. 6.
Histograms comparing posterior canal units that did (n = 62) and did not (n = 96) respond to ipsilateral stimulation. A: spike rate of 6.8 ± 0.70 (SE) spikes/s for responding units and 10.7 ± 0.42 (SE) spikes/s for nonresponding units. These differences were statistically significant (P < 0.001; 2-tailed t-test of log-normalized spike rates). B: for spike-rate-matched units (n = 39), mean values for coefficient of variation in interspike intervals (CV) were 0.87 ± 0.17 (SE) for responding units and 0.74 ± 0.2 (SE) for nonresponding units. These differences were statistically significant (P < 0.004; 2-tailed, paired t-test).
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FIG. 7.
Histograms comparing spike rate and CV distributions of responding and nonresponding posterior canal afferent units to ipsilateral stimulation. A: high degree of overlap for spike rates <21 spike/s, in spike rate distributions between responding and nonresponding units. B: responding units tend to have higher CV values than nonresponding units. C: when the influence of mean spike rate is compensated for by selecting spike-rate-matched units between the 2 groups, CV distributions have more closely placed, yet separate peaks in their distributions (see Fig. 6B and RESULTS).
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FIG. 8.
Peristimulus histogram of a posterior canal unit showing adaptation of efferent-mediated responses during 2 60-s ipsilateral stimulations.
50 s of stable spike rate during stimulation. Although some units had changes in CV values as large as 0.23, CV values of most units changed little or not at all during stimulation. As a group, units with excitatory responses (spike rate change: 5.7 ± 3.7 spikes/s, mean ± SD) had a mean prestimulus CV value of 0.92 ± 0.23 (SD) and a mean during-stimulation CV value of 0.87 ± 0.19 (SD). Although this difference was statistically significant (P < 0.02; 2-tailed, paired t-test; n = 24), the difference is most likely due to differences in spike rates, not spike train noise levels. Similarly, units with inhibitory responses (spike rate change: 
4.9 ± 3.2 spikes/s, mean ± SD) had statistically higher CV values in conjunction with lower spike rates(P < 0.02; 2-tailed, paired t-test; n = 14; prestimulation CV = 0.90 ± 0.11, mean ± SD; during-stimulation CV = 0.95 ± 0.14, mean ± SD).
DISCUSSION
Abstract
Introduction
Methods
Results
Discussion
References
for review). The galvanic stimuli applied may have caused one action potential per efferent axon in the vicinity of the stimulating electrode during each stimulus pulse (Highstein and Baker 1985). These single action potentials could be transmitted via efferent collateral axons to multiple ipsilateral endorgans. Early studies in the frog (Llinas and Precht 1969) suggested that single, brief electrical pulses could induce measurable efferent-mediated effects; however, the light level of anesthesia used in some of those experiments may have allowed for an arousal or behavioral activation of efferent neurons. Effective efferent stimulation requires many spikes per second (Rossi et al. 1980; Valli et al. 1986). Single efferent action potentials during a 20- to 120-s stimulus pulse would not be expected induce significant efferent-mediated changes in afferent spike activity.
. Poststimulation phenomena, seen in studies in which isolated labyrinths and direct efferent fiber activation were used, comprised 2-5 s of elevated resting spike rate after either a facilitation or an inhibition. Any such phenomena probably were obscured in the present study because of extensions of the driving afferent input (i.e., poststimulation spike rate depression) to the efferent system beyond the end of the galvanic stimulus pulse.
), and toadfish (Boyle and Highstein 1990), have also found either lower occurrence of or weaker efferent effects in regularly versus irregularly discharging vestibular afferent neurons.
; Rossi et al. 1980; Valli et al. 1986). The same categories of responses were observed in the present study; however, our use of an indirect method of efferent activation resulted in a much lower incidence of inhibitory responses. Increased vestibular afferent drive to the efferent system caused predominantly facilitation of spike rates of responding units of the ipsilateral labyrinth (92%) and predominantly inhibition of responding units of the contralateral labyrinth (95%). These findings are consistent with the study by Gribenski and Caston (1976) on the tonic influence of the efferent system on spontaneous afferent activity in the frog. The study by Dickman and Correia (1993) of bilateral communication between the vestibular labyrinths also found increased afferent activity to cause predominantly inhibition of contralateral afferent neuronal activity. This preponderance of inhibition was related to whether the responding afferent neuron had regular or irregular spontaneous spike activity. In the study by Dickman and Correia, a mechanical stimulus was used to excite canal afferent neurons of one ear during recording of afferent unit activity from the contralateral labyrinth. Of the units that responded to contralateral stimulation, 84% of the irregularly discharging units were inhibited. In contrast, 71% of regularly discharging units that responded to the contralateral stimulus were excited.
, in which a few single-unit responses shifted from inhibition to facilitation as the concentration of applied carbachol was increased to >1 µM. The current data, however, are too limited, without repeated stimulus applications, to make any meaningful inferences about underlying mechanisms.
. Those investigators identified four afferent units in which activation of different subsets of efferent fiber collaterals caused opposite effects on spontaneous spike rates (facilitation or inhibition).
). There is no evidence that efferent fibers innervate afferent dendrites in the frog. Physiological evidence from Guth et al. (1986) indicates that excitatory efferent neurons do not innervate afferent dendrites, because acetylcholine application does not cause increased spike rates when the hair cell synapse is blocked by low Ca2+ and high Mg2+ concentrations. Pharmacological studies of isolated hair cells provide good evidence that both the excitatiory and inhibitory actions of the vestibular efferent neurons are due to synapses on hair cells that modulate a calcium-dependent potassium current (Guth et al. 1994; Housley et al. 1990).
; Valli et al. 1985), whereas other investigators have found a predominantly excitatory effect (~60% of responding units) (Bernard et al. 1985). Rossi et al. (1980) felt that careful dissection was necessary to obtain the consistent inhibitory effects of efferent activation. They suggested that the efferent nerve fibers mediating inhibitory effects were more susceptible to dissection damage than were nerve fibers mediating excitatory effects. Taken as a whole, studies in which direct electrical activation of efferent fibers was used indicate that at least a large proportion of vestibular afferent neurons responding do so with a decrease in spike rate. With the use of vestibular afferent activity as a driving input to the efferent vestibular system in the present study, we found only 3% of responding afferent fibers to be purely inhibited by an ipsilateral driving stimulus (5% showed a mixed, inhibited/facilitated response). This suggests that moderate vestibular afferent input to the efferent system preferentially activates excitatory efferent fibers to the ipsilateral labyrinth. If a significant resting efferent activity (tone) was present in our ketamine/pentobarbital-anesthetized frogs, an alternate explanation for predominantly excitatory responses could be that the vestibular afferent input to the efferent system preferentially inhibited the inhibitory efferent fibers to the ipsilateral labyrinth. Attempts in our laboratory to measure resting and evoked efferent activity with the use of suction electrodes have not been successful. Efferent activity in unanesthetized toadfish is low (4-5 spikes/s) when the animal is at rest (Boyle and Highstein 1990). Pentobarbital anesthesia is believed to reduce efferent vestibular activity (Schmidt 1963). Ketamine blocks N-methyl-D-aspartate glutamate receptors (Anis et al. 1983), but how this might alter vestibular efferent activity is not known. The level of ketamine/pentobarbital anesthesia in the current study was kept as low as possible but undoubtedly varied between animals. Still, resting efferent tone, if any, probably was low. Efferent-mediated responses limited to spike rate changes of a few spikes per second may have been caused by a disinhibition or disfacilitation of vestibular hair cells/afferent neurons (i.e., decreased efferent activity); however, the stronger efferent effects were more probably due to active inhibition or facilitation of vestibular hair cells/afferent neurons (i.e., increased efferent activity).
, in their pharmacological study, used primarily whole nerve, multiunit recordings, which emphasized responses of small-diameter fibers. That study showed excitatory responses to acetylcholine application with an underlying inhibitory response when muscarinic blockers were given in combination with acetylcholine. Other studies involving direct activation of efferent fibers with rapid current pulses (50 Hz) relied on single-unit recordings, which mainly select larger-diameter, more irregularly discharging afferent fibers (Rossi et al. 1980; Valli et al. 1985). The stimuli applied in these studies were reported to produce maximal activation of efferent fibers (Valli et al. 1986). Combining the results of the single-unit and multiunit studies suggests that larger-diameter afferent fibers are under a greater inhibitory influence than the more numerous small-diameter fibers (Guth et al. 1986). In the present study we used intracellular single-unit recordings and therefore mainly sampled larger-diameter afferent fibers; however, the efferent-mediated response of the ipsilateral labyrinth was predominantly facilitation and rarely inhibition. These findings suggest that how efferent fibers are activated is important in determining efferent responses, at least for large-diameter afferent fibers.
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ACKNOWLEDGEMENTS |
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This work was supported in part by a 1995 faculty development grant from the University of Michigan-Flint and by National Institute of Deafness and Other Communications Disorders Grant 5 R29 DC-00971.
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FOOTNOTES |
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1
The electrode puller used allowed control of the final taper angle of the electrode tip so that sharp electrodes could be pulled with relatively low impedances.
2
Statistics are reported for units responding to ipsilateral stimulations, excluding 3 units with mixed, inhibitory/excitatory responses.
3
Low range based on high-gain unit, 1.5 spikes·s
1·deg1·s2; 8-fold response 
15 spikes/s. High range based on low-gain unit, 0.25 spikes·s1·deg1·s2; 2-fold response 30 spikes/s.
Address for reprint requests: S. F. Myers, Biology Dept., University of Michigan-Flint, Flint, MI 48502-2186.
Received 12 August 1996; accepted in final form 16 December 1996.
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REFERENCES |
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Abstract
Introduction
Methods
Results
Discussion
References
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