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At least 1,153 records · Page 64Linked to original sources
PubMed1997

Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans.

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an alpha adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (delta CBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after alpha blockade, after alpha and beta blockade, and after alpha and beta blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, delta CBF decrease and delta CBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between delta CBF and BPS were significant before inhibition and after inhibition of ANS. For BPS below 160 mmHg, BPS and delta CBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate: even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Adult↗
PubMed2004

Co-localization of the vanilloid capsaicin receptor and substance P in sensory nerve fibers innervating cochlear and vertebro-basilar arteries.

Evidence suggests that capsaicin-sensitive substance P (SP)-containing trigeminal ganglion neurons innervate the spiral modiolar artery (SMA), radiating arterioles, and the stria vascularis of the cochlea. Antidromic electrical or chemical stimulation of trigeminal sensory nerves results in neurogenic plasma extravasation in inner ear tissues. The primary aim of this study was to reveal the possible morphological basis of cochlear vascular changes mediated by capsaicin-sensitive sensory nerves. Therefore, the distribution of SP and capsaicin receptor (transient receptor potential vanilloid type 1-TRPV1) was investigated by double immunolabeling to demonstrate the anatomical relationships between the cochlear and vertebro-basilar blood vessels and the trigeminal sensory fiber system. Extensive TRPV1 and SP expression and co-localization were observed in axons within the adventitial layer of the basilar artery, the anterior inferior cerebellar artery, the SMA, and the radiating arterioles of the cochlea. There appears to be a functional relationship between the trigeminal ganglion and the cochlear blood vessels since electrical stimulation of the trigeminal ganglion induced significant plasma extravasation from the SMA and the radiating arterioles. The findings suggest that stimulation of paravascular afferent nerves may result in permeability changes in the basilar and cochlear vascular bed and may contribute to the mechanisms of vertebro-basilar type of headache through the release of SP and stimulation of TPVR1, respectively. We propose that vertigo, tinnitus, and hearing deficits associated with migraine may arise from perturbations of capsaicin-sensitive trigeminal sensory ganglion neurons projecting to the cochlea.

Animals↗
PubMed2005

An evoked potential study of the developmental time course of the auditory nerve and brainstem in children using cochlear implants.

Central auditory responses to electrical stimulation from a cochlear implant were studied in 75 pre-lingually deafened children and 11 adults. Electrically evoked auditory brainstem response (EABR) latencies significantly decreased with duration of cochlear implant use and were not significantly affected by the age at implant activation. Significant decreases in early latency waves and interwaves occurred within the first 1-2 months of implant use, whereas longer term changes (6-12 months) were found for eV and eIII-eV, which measure activity in the more rostral brainstem. Comparisons to acoustically evoked auditory brainstem response (ABR) in children with normal hearing suggested shorter interwave EABR latencies, reflecting either distinct neural generators or increased neural synchrony, but similar rates of change in the later latency eV and eIII-eV with time in sound. In sum, normal-like development of the rostral auditory brainstem is promoted by cochlear implant use in children of a wide range of ages.

Adolescent↗
PubMed1983

[Effect of chronic electric stimulation of the auditory nerve on the development of the cochlear nuclei in guinea pigs].

14 newborn guinea pigs have been deafened three days after birth by bilateral destruction of the organ of Corti, and among them 8 have been supplied with a chronic auditory electric stimulation by mean of an intra-cochlear implanted electrode. The histological study and the anatomical reconstructions of these animals' cochlear nuclei demonstrate that this chronic stimulation prevent at least partially these auditory pathway medullary formations from the atrophy due to the cochlear destruction.

Animals↗
PubMed1991

[The surgical approach to the cochlear nucleus area].

The stimulation of the proximal auditory nerve or the Cochlear Nuclear Complex (CNC) situated in the lateral recess of the fourth ventricle is a possibility of hearing rehabilitation for patients suffering from bilateral deafness by bilateral cerebellopontine-angle tumors or by transsections of cochlear nerves on both sides. Using such anatomical landmarks as proximal cochlear nerve, flocculus, choroid plexus and taenia the surgeon can locate exactly the CNC for this stimulation. We investigated location, diameter and surrounding structures of the CNC on 10 human brains fixed in 10% formalin-solution and on 9 histological series of these subjects.

Acoustic Stimulation↗
PubMed1997

Microstimulation of auditory nerve for estimating cochlear place of single fibers in a deaf ear.

Multielectrode cochlear prostheses seek to approximate the cochlea's normal frequency-place mapping through spatial segregation of stimulus currents. Various electrode configurations have been employed to achieve such segregation. Direct measurements of stimulation regions among single auditory nerve (AN) fibers has been possible only when normal hearing is preserved, such that each fiber's cochlear place can be inferred from its tuning curve. This precludes measurements in deafened ears, or ears compromised by implantation of the electrodes. Data presented here demonstrate that the cochlear place of an AN fiber can be estimated without acoustic sensitivity, using electrical microstimulation through a recording pipette in the AN bundle. The procedure exploits cochleotopic projection to isofrequency laminae within the contralateral inferior colliculus (IC). Microstimulation excites a small group of fibers neighboring the recorded fiber, generating centrally propagated volleys along a narrow frequency-specific pathway. Evoked potential recordings at varying depths are made to identify the ICC lamina where the response to AN microstimulation is greatest. Preliminary data are also presented for an alternative method of identifying the lamina using a frequency domain measure of binaural interactions within the IC.

Animals↗
PubMed1996

A primary acoustic startle pathway: obligatory role of cochlear root neurons and the nucleus reticularis pontis caudalis.

Davis et al. (1982) proposed a primary acoustic startle circuit in rats consisting of the auditory nerve, posteroventral cochlear nucleus, an area near the ventrolateral lemniscus (VLL), nucleus reticularis pontis caudalis (PnC), and spinal motoneurons. Using fiber-sparing lesions, the present study reevaluated these and other structures together with the role of neurons embedded in the auditory nerve [cochlear root neurons (CRNs)], recently hypothesized to be involved in acoustic startle. Small electrolytic lesions of the VLL of ventrolateral tegmental nucleus (VLTg) failed to eliminate startle. Large electrolytic lesions including the rostral ventral nucleus of the trapezoid body (rVNTB) and ventrolateral parts of PnC or lesions of the entire PnC blocked startle. However, small NMDA-induced lesions of the rVNTB failed to block startle, making it unlikely that the rVNTB itself is part of the startle pathway. In contrast, NMDA lesions of the full extension of the ventrolateral part of the PnC blocked startle completely, suggesting that the ventrolateral part of the PnC is critically involved. Bilateral kainic acid lesions of CRNs also blocked the startle reflex completely, providing the first direct evidence for an involvement of CRNs in startle. This blockade probably was not caused by damage to the auditory nerve, because the lesioned animals showed intact compound action potentials recorded from the ventral cochlear nucleus. Hence, a primary acoustic startle pathway may involve three synapses onto (1) CRNs, (2) neurons in PnC, and (3) spinal motoneurons.

Action Potentials↗
PubMed1979

Auditory nerve activity and cochlear morphology after noise exposure.

Four chinchillas were exposed for 5 days to an octave band of noise centered at 4 kHz and having an SPL of 86 dB. After a recovery period of approximately 6 months, behavioral audiograms were obtained and auditory nerve fiber activity was recorded. The animals were killed and the cochleas embedded in plastic to obtain a surface preparation and 1 mu radial sections of the organ of Corti. Behavioral threshold shifts ranged from 5 to 20 dB at frequencies between 4 and 11 kHz. Auditory nerve fiber thresholds were elevated up to 70 dB for units with characteristic frequencies between 4 and 14 kHz. Units with higher and lower characteristic frequencies had normal thresholds. Cochleagrams showed narrow lesions of inner and/or outer hair cells over approximately a 1 mm distance. A comparison of the three realms of data revealed the following: (1) The greatest threshold shifts from the noise exposure were seen in the single nerve fiber thresholds while the smallest shifts were seen in the behavioral thresholds, (2) the greatest behavioral and neural threshold shifts and greatest cochlear damage occurred 1 octave above the center frequency of the noise exposure, and (3) based on the frequency-place map of the chinchilla cochlea, the range of fibers with elevated thresholds exceeded the extent of the OHC lesion. A number of anatomical changes were seen that effectively increased the extent of the damage found in the chochleagram. These changes included: distortions in the surface topography of the organ of Corti affecting the orientation of IHC; missing pillar cells in the presence of normal OHC and/or IHC and protrusion of the IHC cuticular plate into the subtectorial space.

Animals↗