137

Hearing Research, 45 (1990) 137-144 Elsevier

HEARES

01350

The effect of upper pontine transections on normal cochlear responses and on the protective effects of contralateral acoustic stimulation in barbiturate-anaesthetized normal-hearing guinea pigs R. Rajan Department

of Physiologv,

University of Western Australia, Perth, Western Australia, Australia

(Received

24 July 1989; accepted

19 November

1989)

In barbiturate-anaesthetized guinea pigs with normal cochlear neural sensitivities, upper pontine transections were made to totally isolate the cell bodies of the olivocochlear neurons in the lower brainstem from all higher centres. The effects of this procedure were examined at the cochlea on normal compound action potential (CAP) thresholds and amplitudes, on the temporary threshold shifts (TTS) in CAP sensitivity caused by monaural loud sound exposures, and on the protective effects of low-level contralateral acoustic stimulation (Cody and Johnstone, 1982; Rajan and Johnstone, 1983a, 1988). The transection had no effects on any of these responses. These results suggest that centres above the metencephalon do not exert any tonic effects on the cell bodies of the olivocochlear pathways that result in tonic effects at the cochlea. Further, these results also suggest that the protective effects of contralateral acoustic stimulation are exercised solely through lower brainstem pathways.

Pontine

transection;

Descending

influences;

Oliv-hlear;

Cochlea;

Introduction Combining a loud sound exposure to one cochlea with either acoustic stimulation at (Cody and Johnstone, 1982; Rajan and Johnstone, 1983a, 1988) or destruction of (Rajan and Johnstone, 1983a, 1989) the other cochlea activates the crossed olivocochlear efferent bundle (COCB) that then reduces the neural threshold losses caused by the exposure in the traumatised cochlea. The contralateral cochlear manipulations did not appear to directly activate the COCB (Rajan and Johnstone, 1988, 1989); rather, they were suggested to provide a facilitatory influence at the COCB cell bodies that allowed the loud sound to activate the COCB where the exposure alone would not have been able to do so (Rajan and Johnstone, 1988, 1989).

Correspondence to: R. Rajan, Department of Psychology, Monash University, Clayton, Victoria 3168, Australia. 0378-5955/90/$03.50

0 1990 Elsevier Science Publishers

Auditory

The inferior colliculus (IC) can also act through the COCB to reduce threshold losses caused by a monaural loud sound exposure at the contralateral cochlea (Rajan, 1990). Rather than directly activating the COCB, IC stimulation also appears to provide a facilitation at the COCB cell bodies to allow the exposure to activate the COCB to the traumatised cochlea (Rajan, 1990). It is possible therefore that the two peripheral manipulations detailed above exercise their facilitatory effects not directly at the COCB but through the IC, leading to facilitation then being exercised, by the IC, at the COCB. The present study examines this possibility by testing the effect of isolating the brainstem from more central structures on the protective effects of contralateral acoustic stimulation. Another aim of the study was to determine if, in the barbiturateanaesthetized guinea pig with normal cochlear neural threshold sensitivities, the olivocochlear pathways were under any tonic descending influence from higher centres to determine normal

B.V. (Biomedical

Division)

138

cochlear responses. In this case changes at the cochlea should follow the transection of the metencephalon and the isolation of the cell bodies of the olivocochlear pathways from any influences from higher centres. Methods Preliminary surgery and testing Ten pigmented guinea pigs (150-300 g), pre-treated sub-cutaneously with Atropine Sulphate (0.65 mg/kg), were anaesthetized with 30 mg/ kg Nembutal (sodium pentobarbitone) intraperitoneally and 0.4 mg Innovar-Vet (fentanyl citrate, Droperidol) intramuscularly. They were tracheostomized, artificially ventilated on Carbogen (95% O,, 5% CO,) and administered a muscle relaxant, Alloferin (alcuronium chloride), intramuscularly at 5 mg/kg. Body temperature was maintained at 38.5 + 1°C by a thermostaticallycontrolled warming blanket and monitored continuously by a rectal probe. The heart rates were also continuously monitored. Supplementary doses of 0.1 ml Innovar-Vet were delivered hourly and 10 mg/kg Nembutal every 2 h. The animals were mounted between hollow ear bars and the cochleas exposed to place electrodes to measure threshold sensitivities to pure tones, as described previously (Rajan and Johnstone, 1983a,b). N, audiograms from 2-30 kHz were constructed for each animal and only animals with threshold sensitivities within 5 dB of normative laboratory data (Johnstone et al., 1979; Cody et al., 1980; Rajan, 1989; Rajan and Johnstone, 1983b) at each frequency were used. In addition, in two test (see below) and two control animals, input-output functions for the N, to 10 kHz and to 14 kHz tone bursts were also measured in the test cochlea to be subsequently presented a loud sound exposure. Amplitudes to 32 presentations of the tone bursts at various intensities from 5510 dB > N, threshold to about 110 dB SPL, in 10 dB steps, were averaged. Sectioning procedure In all 10 animals, using a scalpel posterior craniotomy was performed cerebellum and the occipital cortex. were carefully cut with iris scissors

blade a large to expose the The meninges and the cere-

Fig. 1. Schematic illustration of the upper pontine transection made to isolate the cell bodies of the olivocochlear neurons in the lower brainstem from any descending influences. The section was made across the entire pons from the bone margin on one side of the head across to the other side. Ventrally it extended to the base of the skull without cutting the basilar artery.

bellum gently retracted caudally to expose the midbrain and upper brainstem. The entire area was saturated with thrombin powder and tissue wicks saturated with thrombin were placed around the exposed area. Then the scalpel blade was inserted between the cerebellum and the occipital cortex to cut across the upper pons at a level below the inferior colliculi. The location of the lesion is illustrated schematically in Fig. 1. The blade was moved from the bone margin on one side of the head through the brainstem across to the bone margin on the other side of the head. Ventrally the cut extended to the base of the skull, but care was taken to ensure that the basilar artery on the ventral surface of the brainstem was not severed. In the next 7 min, N, threshold sensitivities from 2-30 kHz in both cochleas were re-measured in all animals as were the input-output functions to 10 kHz and to 14 kHz tone bursts in the test cochlea of the two test and the two control animals in which these latter measurements were previously made. None of these measures were ever altered from the initial values (see Results). Heart rates and body temperatures were also not affected by the pontine transection. Testing on TTS In five of the animals (control group) a monaural loud sound exposure at 10 kHz was then presented at 103 dB SPL for 1 min to the test cochlea. In the other five animals (test group) the

same exposure was presented to the test cochlea simultaneously with a protective acoustic stimulus (Cody and Johnstone, 1982; Rajan and Johnstone, 1983a, 1988) at 10 kHz, 80 dB SPL for 1 min, to the contralateral ear. Following the exposure N, threshold losses were monitored as described previously (Rajan and Johnstone, 1983a, 1988, 1989). Results are presented as mean threshold losses for the particular group at the designated frequency and post-exposure recording time. Student’s t-tests were used to determine statistical significances. To confirm that the pontine transection itself did not prejudice the effects of the exposure, the results of the present study are compared to the results (from Rajan and Johnstone, 1988) for groups with experimental conditions equivalent to those of this study but without any pontine sectioning, i.e., (a) the same monaural exposure alone as in the present control group, and (b) the same ipsilateral exposure combined with the same simultaneous contralateral acoustic stimulus as in the present test group. Results Effect on normal cochlear responses and monaural TTS Isolating the brainstem from higher structures

‘“:

30 FREQUENCY

CkHz 1

Fig. 2. Effect of upper pontine transection on N, audiograms in a typical control animal (upper panel) and in a typical test animal (lower panel). The open circles represent values recorded prior to the upper pontine section while the filled circles represent values recorded after sectioning. For clarity, overlapping values are represented by half-filled circles. The full line represents the mean N, audiogram from 109 barbiturate-anaesthetised normal-hearing animals while the broken lines on either side of this mean audiogram indicates 1 SD. (Rajan, 1989).

INTENSITY

fdB

SPL)

Fig. 3. Effect of upper pontine transection on N, input-output functions at 10 kHz (left hand panel) and at 14 kHz (right hand panel) in one of the animals of this study. The crosses represent values recorded prior to the sectioning and the squares represent values recorded after sectioning. N, amplitudes have been corrected for the averaging procedure used in determining the amplitudes.

140

by transecting the upper pons did not affect normal cochlear responses. Neither N, audiograms nor N, input-output functions were altered after the pontine section compared to the pre-sectioning values recorded in the same animals. This result for the N, audiogram is illustrated in Fig. 2 for one test animal and one control animal. In the figure the results for these animals are also compared to the mean N, audiogram obtained from 109 normal-hearing animals tested under the same anaesthetic regime as in this study (Rajan, 1989) to illustrate that both before and after the upper pontine transection the audiograms in the animals of the present study were not significantly different from normative laboratory data. The results for the input-output functions for the N, to 10 and 14 kHz tone bursts in the one animal are illustrated in Fig. 3 and show that the upper pontine transection also did not affect N, amplitudes at intensities up to the highest tested, about 110 dB SPL. Similar results were obtained in the other three animals in which such inputoutput functions were also determined, i.e., the upper pontine transections did not alter significantly or systematically the N, amplitudes re-

corded at either frequency over the entire intensity range tested. The upper pontine transections also did not affect the threshold losses caused by the monaural exposure alone (Fig. 4). Threshold losses in the control group of this study were similar to losses in the former control group (from Rajan and Johnstone, 1988) with the same monaural exposure but without pontine sectioning. There were no significant differences (P > 0.10) between these two groups in the 14 kHz threshold losses at all corresponding post-exposure times as well as in the losses at all corresponding frequencies from lo-24 kHz, 5 min post-exposure. Mean threshold losses at the frequency of greatest loss, 14 kHz, at four post-exposure times, are listed in Table I for these two control groups. Effect on the protective effects of contralateral acoustic stimulation As significantly, the upper pontine transections did not prevent the contralateral acoustic stimulus from reducing threshold losses due to the loud sound exposure in the ipsilateral cochlea (Fig. 4). Threshold losses in the test group of this study

4ow’-’ 30-

, -____

---__

zo- yL

*G

-

_.._ 10-

oh,,, , 8

10

14

FREOUENCY fkHz)

20

2L

-----____

L

0 60 120

- b#-==L

I

I

300

600%i+'

I300

TIME (SK) POST-EXPOSURE

Fig. 4. Effect of upper pontine transections on temporary threshold shifts (TTS) after a loud sound and on the protective effects of contralateral acoustic stimulation. Right hand panel: 14 kHz threshold losses at various times after the exposure. Left hand panel: Threshold losses from 8-24 kHz, 5 min post-exposure. Circles represent results from control groups and squares represent results from test groups. Filled symbols are results from the groups of the present study with pontine sectioning done before the appropriate control or test conditions. Open symbols are results from the equivalent control and test groups, without any pontine sectioning, from Rajan and Johnstone (1988). In the control groups only a monaural loud sound exposure (see Methods) was presented. In the test groups, the same monaural exposure was combined with a protective contralateral acoustic stimulus. Pontine sectioning did not alter the TTS caused by the monaural exposure alone (open circles) compared to the control group without pontine sectioning (filled circles). Pontine sectioning also did not prevent the contralateral stimulus (open squares) from exerting protective effects and threshold losses in this group were similar to losses in the previous test group (filled squares) but lower than losses in either control group.

141 TABLE

I

EXPERIMENTAL GROUPS AND 14 kHz N, THRESHOLD LOSSES (MEAN + 1 SD) AT FOUR POST-EXPOSURE RECORDING TIMES Recording time post exposure

loss, 14 kHz, at four post-exposure times, are listed in Table I for the two test groups. Post-mortem histology confirmed that in all cases the pontine transection had successfully isolated the lower brainstem from higher centres.

10 s

60s

5min

30 min

Discussion

39.29 f 2.07

27.13 2.51

22.04 1.96

17.95 dB 2.14

38.40 + 1.14

27.40 0.55

22.60 1.14

17.40 dB 0.55

25.00 f 2.95

15.82 2.15

11.45 2.50

7.00 dB 1 .I6

25.00 + 0.71

15.80 1.30

10.40 1.14

6.60 dB 1.14

Pathways and binaural interactions producing the protective effects of contralateral acoustic stimulation The major result from the present study is that the protective effect of contralateral acoustic stimulation is exercised only through the lower brainstem and does not require intercession from any higher centres. We have previously shown (Rajan and Johnstone, 1988) that lesioning the crossed olivocochlear bundle (COCB) at the floor of the fourth ventricle in the brainstem prevents contralateral acoustic stimulation from protecting the ipsilateral cochlea. The results of these two studies therefore suggest that the protective action of the contralateral acoustic stimulus is exerted only through a lower brainstem ‘reflex ’ arc involving afferent input from both ears being integrated by the COCB neurons to the traumatised cochlea (Rajan, 1990; Rajan and Johnstone, 1988, 1989). The fact that the protective effect of contralateral acoustic stimulation acts through a lower brainstem integrative ‘reflex’ pathway of course does not preclude any descending influence on this action of the COCB. As demonstrated elsewhere (Rajan, 1990), low-rate electrical stimulation of the contralateral IC is also able to exert protective effects at the cochlea by providing a facilitatory influence at the COCB that allows activation by a loud sound exposure. Thus, the descending pathways from the midbrain to the olivocochlear cell bodies could exert significant modulatory effects on the protective actions of contralateral cochlear manipulations (Cody and Johnstone, 1982; Rajan and Johnstone, 1983a, 1988, 1989). Efferent neurons with cell bodies located in the brainstem contralateral to their target cochlea respond to monaural acoustic stimulation of the target cochlea rather than monaural stimulation of the non-target cochlea (Liberman and Brown, 1986; Robertson and Gummer, 1988). Then, the

1. Control Groups (a) Without pontine transection * (N =: 55) (b) With pontine transection (N ==5) 2. Test 8~00~~s (a) Without pontine transection * (N =:ll) (b) With pontine transection (N ==5)

In all groups the pure tone used to cause ‘ITS was at 10 kHz, 103 dB SPL and was presented for one minute. In the control group only this exposure was presented monaurally. In the test groups the exposure was combined with acoustic stimulation of the contralateral cochlea at 10 kHz, 80 dB SPL, for 1 min, simultaneous with the ipsilateral exposure. N = number of animals * Experimental groups from Rajan and Johnstone, 1988.

were significantly (P < 0.05) lower than losses in the control group of this study, both at 14 kHz at corresponding post-exposure times and at all corresponding frequencies from lo-24 kHz, 5 min post-exposure. In addition, there were no significant differences (P > 0.10) between the present test group and the former test group (Rajan and Johnstone, 1988) with the same binaural test conditions but without pontine transection, both for 14 kHz losses at all corresponding post-exposure times and for losses at all corresponding frequencies from lo-24 kHz, 5 min post-exposure. Threshold losses in both test groups were significantly lower (P < 0.05) than losses in the two control groups presented only the monaural exposure (without and with pontine transection), at all corresponding frequencies from 12-24 kHz at corresponding post-exposure recording times. Mean threshold losses at the frequency of greatest

142

COCB neurons (by definition located in the contralateral brainstem) to the cochlea exposed to loud sound must be responsive to monaural input from the traumatised target cochlea rather than monaural input from the non-target cochlea. However, as also suggested by Liberman (1988) and Robertson and Gummer (1988) on the basis of recordings from single efferent fibres, these neurons appear to be subject to modulatory influences from the non-target ear. In the case of protection from loud sounds, the non-target cochlea appears to provide a facilitatory influence (Rajan and Johnstone, 1983a, 1988, 1989) on to the COCB efferents. Thus ‘low-level sound in the non-target ear allows the loud sound in the target ear to activate the COCB neurons and reduce threshold losses at affected frequencies in the target cochlea (Cody and Johnstone, 1982; Rajan and Johnstone, 1988, and this study). Studies of the responses of single efferent neurons to acoustic stimuli have shown that binaural facilitation appeared to be the major type of input from the non-target ear in the cat (Liberman, 1988), or to be as common as suppressive input in the equivalent neurons in the guinea pig (the monaural-ipsi group of efferent neurons, see Robertson and Gummer, 1988).

The elimination, by upper pontine transection, of any descending influences from the midbrain or higher centres to the cell bodies of the olivoco&ear pathways in the lower brainstem did not result in any changes in N, thresholds or amplitudes, or the TTS in N, threshold sensitivities caused at the cochlea by a monaural loud sound exposure. We have recently demonstrated that lesioning one auditory efferent pathway, the COCB, in barbiturate-anaesthetized guinea pigs with normal N, threshold sensitivities had no effects on normal cochlear responses (N, thresholds, amplitudes, forward masking tuning curves and simultaneous masking tuning curves) or on the TTS caused by a monaural exposure (Rajan and Johnstone, 1988; Rajan et al., 1990). Barbiturates are known to potentiate inhibitory effects on mammalian central neurons in culture (Barker and Ransom, 1978) and barbiturate anaesthesia has been shown

to affect a variety of central auditory processes (Borbtly and Hall, 1970; Brownell et al., 1979; Church and Shucard, 1987; Dafny, 1978; Evans and Nelson, 1973; Henry, 1979; Herz et al., 1967; Kiang et al., 1961; Kuwada et al., 1989; Pradhan and Galambos, 1963; Ritz and Brownell, 1982; Shaw, 1986; Sutton et al., 1982; Teas and Kiang, 1964; Young and Brownell, 1976). It is possible therefore that the absence of co&ear changes after COCB lesioning in our previous study (Rajan et al., 1990) may have been due to a barbituratepotentiated descending inhibition on to the olivocochlear neurons. In such a case the olivocochlear pathways may indeed exercise tonic cochlear effects in unanaesthetised normal animals but these effects may have been abolished at the start of our previous experiments by induction of anaesthesia with the barbiturate and were therefore not revealed by subsequent lesioning of the COCB (Rajan et al., 1990). However, the present study shows that the olivocochlear neurons do not appear to receive any tonic descending influences (either excitatory or inhibitory) to determine the monaural cochlear responses measured here, since transection of the upper pons resulted in no cochlear changes in the responses in animals treated with the same anaesthetic regime as in our previous study (Rajan et al., 1990). It is possible that even if tonic descending influences on to the olivocochlear neurons did exist, they would not be revealed by the present experiments if the barbiturate anaesthetic had depressed the olivocochlear neurons themselves. Barbiturate anaesthesia is known to affect the centrifugal processes to the auditory periphery: the middle ear reflex is depressed under such anaesthesia (Borg and Msller, 1975) while, more importantly from the viewpoint of this study, certain response properties of olivocochlear neurons are affected (Liberman and Brown, 1986; Robertson and Gummer, 1985, 1988) or suggested to be affected (Gummer et al., 1988), and certain cochlear effects of low level acoustic stimuli that have been attributed to olivocochlear neuronal action (Brown, 1988) are depressed by such anaesthesia. Thus, it might be argued that tonic descending influences to the olivocochlear neurons exist in the unanaesthetised animal and although these were removed by the upper pontine transec-

143

tions in the present study, no changes were observed at the cochlea because the olivocochlear neurons themselves were depressed under barbiturate anaesthesia. Counter to this argument is the fact that under the same anaesthetic regime as used in this study, one efferent pathway, the COCB, has been shown to exert tonic effects at the cochlea, albeit in animals with idiopathic losses in auditory sensitivity (Rajan, 1989; Thompson et al., 1989). Thus, COCB neurons appear to be capable of being tonically active even under barbiturate anaesthesia. In Sudan, since all descending influences from centres above the metencephalon to the cochlea must ultimately be exercised through the olivocochlear pathways, the results of this study suggest that in barbiturate-anaesthetised guinea pigs with normal hearing sensitivities, the crossed and uncrossed olivocochlear pathways do not receive any tonic descending influences that determine the cochlear responses measured here. This result is consistent with our recent studies on the effects of COCB lesions in barbiturate-anaesthetised normal-hearing animals (Rajan, 1989; Rajan et al., 1990). As noted above, tonic activity of the COCB has been observed in barbiturate-anaesthetised animals with idiopathic hearing losses (Rajan, 1989; Thompson et al., 1989). In these cases it is possible that such hyperactivity may have been due to tonic resetting of the excitability levels either at the cell bodies of the efferent neurons themselves, or at some higher centre that then expressed tonic excitatory effects on to the cell bodies of the efferents in the lower brainstem and thereby at the cochlea (Rajan, 1989; Thompson et al., 1989). Acknowledgements This work was supported by grants from the National Health and Medical Research Council of Australia and the Australian Research Grants Scheme, and by the laboratory facilities of Dr. B. M. Johnstone. References Barker, J.L. and Ransom, B.R. (1978) Pentobarbitone pharmacology of mammalian central neurones grown in tissue culture. J. Physiol. 280, 3.55-372.

Borbely, A.A. and Hall, R.D. (1970) Effects of pentobarbitone and chlorpromazine on acoustically evoked potentials in the rat. Neuropharm. 9, 575-586. Borg, E. and Melier, A.R. (1975) Effects of central depressants on the acoustic middle ear reflex in rabbit. Acta Physiol. Stand. 94, 327-338. Brown, A.M. (1988) ~ntinuous low level sound alters cochlear mechanics: an efferent effect? Hear. Res. 34, 27-38. Brownell, W.E., Manis, P.B. and Ritz, L.A. (1979) Ipsilateral inhibitory responses in the cat lateral superior olive. Brain Res. 177, 189-193. Dafny, N. (1978) Neurophysiological approach as a tool to study the effects of drugs on the central nervous system: dose effect of pentobarbital. Exp. Neurol. 59, 263-274. Church, M.W. and Shucard, D.W. (1987) Pentobarbit~-induced changes in the mouse brainstem auditory evoked potential as a function of click repetition rate and time postdrug. Brain Res. 403, 72-81. Cody, A.R. and Johnstone, B.M. (1982). Temporary threshold shift modified by binaural acoustic stimulation. Hear. Res. 6, 199-206. Cody, A.R., Robertson, D., Bredberg, G. and Johnstone, B.M. (1980) Electrophysiological and morphological changes in the guinea pig cochlea following mechanical trauma to the organ of Corn. Acta Otolaryngol. 89, 440-452. Evans, E.F. and Nelson, P.G. (1973) The responses of single neurons in the cochlear nucleus of the cat as a function of their location and anaesthetic state. Exp. Brain Res. 17, 402-427. Gummer, M., Yates, G.K. and Johnstone, B.M. (1988) Modulation transfer function of efferent neurones in the guinea pig co&lea. Hear. Res. 36, 41-52. Henry, K.R. (1979) Differential changes of auditory nerve and brainstem short latency evoked potentials in the laboratory mouse. Electroenceph. Clin. Neurophysiol. 46, 452-459. Herz, A., Frahng, F., Niedner, I. and Farber, G. (1967) Pharmacologically induced alterations of cortical and subcortical evoked potentials compared wih physiological changes during the awake-sleep cycle in cats. Electroenceph. Clin. Neurophysiol. 26, 164-176. Johnstone, J.R., Alder, V.A., Johnstone, J&M., Robertson, D. and Yates, G.K. (1979) C&blear action potential and single unit thresholds. J. Acoust. Sot. Am. 65, 254-257. Kiang, N.Y.S., Neame, J.H. and Clark, L.F. (1961) Evoked cortical activity from auditory cortex in anaesthetized and unanaesthetized cats. Science 133, 1927-1928. Kuwada, S., Batra, R. and Stanford, T.R. (1989) Monaural and binaural response properties of neurons in the inferior colliculus of the rabbit: effects of sodium pentobarbital. J. Neurophysiol. 61, 269-282. Liberman, M.C. (1988) Response properties of cochlear efferent neurons: monaural vs. binaural stimulation and the effects of noise. J. Neurophysiol. 60, 1779-1798. Liberman, M.C. and Brown, M.C. (1986) Physiology and anatomy of single olivocochlear neurons in the cat. Hear. Res. 24, 17-36. Pradhan, S.N. and Galambos, R. (1963) Some effects of anaesthetics on the evoked responses in the auditory cortex of cats. J. Pharm. Exp. Therap. 139, 97-106.

144 Rajan, R. (1989) Tonic activity of the crossed olivocochlear bundle in guinea pigs with idiopathic losses in auditory sensitivity. Hear. Res. 39, 299-308. Rajan, R. (1990) Electrical stimulation of the inferior colliculus at low rates protects the cochlea from auditory desensitization. Brain Res. (in press). Rajan, R. and Johnstone, B.M. (1983a) Crossed cochlear influences on monaural temporary threshold shifts. Hear. Res. 9, 219-294. Rajan, R. and Johnstone, B.M. (1983b) Residual effects in monaural temporary threshold shifts. Hear. Res. 12, 185-197. Rajan, R. and Johnstone, B.M. (1988) Binaural acoustic stimulation exercises protective effects at the cochlea that mimic the effects of electrical stimulation of an auditory efferent pathway. Brain Res. 459, 241-255. Rajan, R. and Johnstone, B.M. (1989) Contralateral cochlear destruction mediates protection from monaural loud sound exposures through the crossed olivocochlear bundle. Hear. Res. 39, 263-278. Rajan, R., Robertson, D. and Johnstone, B.M. (1990) Absence of tonic activity of the crossed olivocochlear bundle in determining compound action potential thresholds, amplitudes and masking phenomena in anaesthetised guinea pigs with normal hearing sensitivities. Hear. Res. 44, 195-208.

Ritz, L.A. and Brownell, W.E. (1982) Single unit analysis of the posteroventral cochlear nucleus of the decerebrate cat. Neuroscience 7, 1995-2010. Robertson, D. and Gummer, M. (1985) Physiological and morphological characterization of efferent neurones in the guinea pig cochlea. Hear. Res. 20, 63-77. Robertson, D. and Gummer, M. (1988) Physiology of cochlear efferents in the mammal. In: J. Syka and R.B. Masterton (Eds.), Auditory Pathway, Plenum Publishing Corp., New York, pp. 269-278. Shaw, N.A. (1986) The effect of pentobarbital on the auditory evoked response in the brainstem of the rat. Neuropharmacology 25, 63-69. Sutton, L.M., Frewen, T., Marsh, R., Jaggi J. and Bruce, D.A. (1982) The effects of deep barbiturate coma on multimodal evoked potentials. J. Neurosurg. 57, 178-185. Teas, D.C. and Kiang, N.Y.S. (1964) Evoked responses from the auditory cortex. Exp. Neurol. 10. 91-119. Thompson, M., Robertson, D. and Johnstone, B.M. (1989) Evidence for tonic inhibitory effects of olivocochlear efferents in anaesthetized guinea pigs. Proc. Aust. Neurosci. Sot., Neurosci. Letts. Suppl. 34, S158. Young, E.D. and Brownell, W.E. (1976) Responses to tones and noise of single cells in the dorsal cochlear nucleus of unanesthetised cats. J. Neurophysiol. 39, 282-300.

The effect of upper pontine transections on normal cochlear responses and on the protective effects of contralateral acoustic stimulation in barbiturate-anaesthetized normal-hearing guinea pigs.

In barbiturate-anaesthetized guinea pigs with normal cochlear neural sensitivities, upper pontine transections were made to totally isolate the cell b...
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