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Tinnitus is the sensation of a sound, not audible to others, often described as a continual ringing, buzzing or whistling in the head or ear(s). Although the noises are harmless, we know from personal experience tinnitus is sometimes very distressing (to say the least) but it is not life threatening and the quality of your life can be recovered. Sound reaches you as waves in the air and is converted by the inner parts of the ear (cochlea) to nerve signals.
Unfortunately, this natural selectivity can be disturbed by life's events, especially in sensitive people, and this wonderful facility may cause unwanted noises to dominate, at least until the system is retrained to ignore them. The hearing system can automatically turn up the volume (gain) when we want to hear something or are anxious about some sound. Tension caused by worry about your tinnitus is natural, so learning to relax is vital part of the relief process. The noises in your head often create a vicious cycle of tension and worry about the cause and the effect on your lifestyle. Remember your hearing system wakes up first, sleeps last and is always alert. Tensions cause your hearing system to go on full alert (like a violin string!). From experience we have found it is possible for the tinnitus noises to gradually recede into the background so that we are no longer aware of them.  You may find this hard to believe - we did!
Doctors call this natural habituation.  It can be enhanced using a medically prescribed sound generator or through self help using pleasant low level sounds (such as gentle sounds of the sea!) from MP3 player, Ipod, CD player or other sound source. It is important to avoid long periods of silence.  The use of comforting background sounds, either in the room or via  in-ear phones, 3-4 hours or preferably more a day and at night, focuses attention away from the tinnitus and speeds up the process of rehabilitation to the tinnitus. Be very suspicious of expensive so called cures and equipment and refer them to your doctor. This 2002 study showed remarkable results in treating three tinnitus sufferers using Neurofeedback, with EEG brainwave analysis before and after showing that the brainwaves had changed, and these changes were still present 12 months after training. Please call us today on 0207 978 0186 to discuss how Neurofeedback could help your tinnitus. Tinnitus is a perception of a ringing sound within the ear(s), when there is no actual external sound. The main symptom of Tinnitus is the ringing sound within one or both ears, although in some cases sounds are perceived differently: high-pitched whining, buzzing, hissing, humming, tinging or whistling sound, or as ticking, clicking, songs, beeping, sizzling, sounds or even as a pure steady tone. Treatment options for Tinnitus depend on the cause, work in different ways with different levels of effectiveness.
However, there is hope as studies have shown that Neurofeedback can improve difficult-to-treat Tinnitus. Please call us today on 0207 978 0186 to discuss how Neurofeedback could help your Tinnitus. About 85% of all tinnitus cases are deemed idiopathic, meaning that doctors don’t know what’s causing them, and are thus unable to stop tinnitus ear ringing. In even simpler layman terms, doctors are unable to determine exactly what tinnitus trigger is behind 85% of all cases of tinnitus. In identifying tinnitus triggers, it helps to understand about other ailments that usually accompany tinnitus ear ringing.
Tinnitus triggers aren’t causes- if they were, then doctors would be able to drop the “idiopathic” label of many cases of constant ear ringing, whooshing, or buzzing sounds. Instead, tinnitus triggers increase your chances of suffering from tinnitus, either in severity, duration, frequency, or all of the above. If (or when) your ENT, neurologist, or audiologist tells you that he can’t treat your tinnitus, he’s probably right.
For the overwhelming majority of idiopathic tinnitus sufferers, the road to wellness begins at home.
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MRI showed a right CP angle mass 20x15-mm low signal on T1W and mildly hyperintense on T2W and flair images. As is the case with most other intracranial pathology, MRI is the investigation of choice for the diagnosis and characterization of meningiomas.
Usually MRS does not play a significant role in diagnosis, but can help distinguish meningiomas from mimics. Natural remedies and holistic medicine focuses on the root of the problem.  It is the belief of holistic practitioners like myself, that if you can heal the root, then the symptoms will naturally disappear. If you are a member of Home Cures That Work, click on the image above to download your monthly issue in pdf format. Tinnitus has been defined as the perceptual correlate of altered spontaneous neural activity occurring without an external auditory stimulus. Tinnitus is a serious clinical symptom that may affect 30-40 million individuals nationally [1,2]. Our understanding of the functional biochemistry of the medial efferent olivocochlear system has advanced at a steady rate [22-24], whereas comparatively little in the way of function is known of the lateral efferent olivocochlear system. Opioid peptides and their unique receptors exhibit a widespread distribution in central and peripheral nervous system structures involved in vision, audition, olfaction, and somatic sensation. The activation of opioid receptors by endogenous opioid substances produces alterations in intercellular ionic conductances, resulting in either neural inhibition or neural excitation l50,66]. In contrast to their more widely studied inhibitory properties, opioid peptides also produce neural excitation [70,73,74). As indicated, dynorphin-and enkephalin-like immunoreactivities have been found in the terminal varicosities of lateral efferent neurons in some species, indicating the presence of these neuroactive peptides in mammalian cochleas [27]. Intravenous (IV) administration of the opioid κ-receptor drug agonist (-) pentazocine produces an enhancement in auditory sensitivity and intensitydependent amplitude changes in the auditory nerve compound action potential (CAP) in chinchillas [83).
The initiation of auditory signaling in the mammalian cochlea is highly dependent on the release of excitatory neurotransmitter from the IHCs. However, evidence supports the gene expression of NMDA receptor subunits in the adult guinea pig cochlea [106].
Approximately 40% of the radial type I afferent dendrites form two morphologically and functionally distinct groups that contact the modiolar-oriented surface of each IHC. As is well-known, peripheral tissue inflammation produces functional changes in neurons of the spinal cord dorsal horn.
Recently, a pathophysiological analogy was constructed between chronic nociception (pain) and chronic tinnitus [124]. Overstimulation of NMDA receptors constitutes a major mechanism in glutamate-induced neurotoxicity; for this reason, NMDA receptor antagonists have been used as neuroprotectants in the prevention of excitotoxic cell injury [120,121]. Higher-than-normal levels of reactive anxiety have been reported in tinnitus sufferers, and some speculate that certain individuals may have a greater psychological predisposition or susceptibility to tinnitus than do others [134,135]. Therefore, how might endogenous dynorphins be used in the auditory periphery to modulate or maintain the aversive qualities of excessive (or even abnormally synchronous) auditory neural activity? Type I afferent dendrites innervating cochlear IHCs are themselves innervated by lateral efferent axons [31,32] and, as indicated, some evidence suggests that the lateral efferent system modulates auditory neural sensitivity [36,37]. Peripheral inflammation also is associated with peripheral (and central) receptive field enlargement [116]. Intracochlear perfusion of glutamate or aspartate at high doses has been reported to reduce the discharge of auditory units during the presentation of sound [150]. Consistent with this hypothesis are the intensitydependent biphasic changes in neural amplitude recently observed after a cochlear RW administration of the κ-receptor ligands U-50488H (see Fig. Similar intensity-dependent changes in neural amplitude have been observed consistently after IV administrations of (-) pentazocine [79,80,83]. As indicated, some 80% of tinnitus sufferers have problems that can be traced to, or associated with, changes occurring in the inner ear [1]. Tinnitus may, in some cases, be the immediate source of a stressful experience, though many individuals report that they begin to notice their tinnitus only during periods of high stress [167].
Results from an early investigation of cochlear neurotransmitter candidates in guinea pig perilymph (though excluding an analysis of perilymphatic dynorphin-like neuropeptides) indicated that exposure to intense and presumably stressful wide-band noise (80-115 dB SPL) significantly elevates levels of [Met5]-enkephalin-like opioid peptides, relative to control values obtained in quiet [168,169]. A physiological shift of the auditory periphery into a temporary state of vigilance is, in our view, synonymous with the production of a " hyperacusic" state, whereby most auditory stimuli are amplified. Alternatively, depending on NMDA receptor sensitivity (or susceptibility) or on the reactivity of the lateral efferent system to the stressor, dynorphins released into an uncompromised cochlea nevertheless could result in the generation of spectral alterations in the ensemble spontaneous discharge (Fig.
At higher levels of the neuraxis, of course, response selection would become advantageously limited or narrowed, as all the enhanced signals from the auditory periphery, including the aberrant activity interpreted as tinnitus, are assigned a significant though equal motivational saliency. A detailed account of the NMDA receptor-dynorphin peptide distribution in the central nervous system is beyond the scope and intent of this article. First is the evidence supporting the existence of lateral efferent projections to the cochlear nuclear complex [31].
Furthermore, both pharmacological [174,175] and in situ hybridization investigations [176,177] have provided evidence for the existence of NMDA and nonNMDA receptors in the mammalian cochlear nuclear complex.
Finally, a likely certainty is that the mechanisms involved in the generation and maintenance of tinnitus are represented neither simply nor narrowly in central auditory pathways or in the auditory periphery (or in both). In a pilot study involving cochlear whole-mount preparations, we have observed dense immunohistochemical staining for CGRP in the IHC region of the organ of Corti in this species.
We have presented a biochemical model to explain one possible cause of the phenomenon called tinnitus. Portions of this manuscript were presented at the Second International Tinnitus Think Tank: The Neurochemistry of Tinnitus, Martha Entenmann Tinnitus Research Center and The State University of New York Health Sciences Center at Brooklyn, NY, November 5-6, 1998.
These minute electrical signals pass up the hearing nerve to the first part of the brain which sorts out what is immediately important and usually ignores most unwanted sound. We learn to ignore mother's heartbeat and other bodily noises in the womb because we are in a cosy trouble-free place and the noises are soon familiar, unimportant and not a threat!
You can practice quiet relaxation at any time because it helps if you keep each part of your body as calm as possible. With Neurofeedback, Tinnitus is considered as too much ‘excitability’ in specific brain areas, which leads to uncontrolled activity and brain instability.
Out of the millions of people around the world who experience chronic ear ringing, headaches, and ear pressure, an astonishing number of cases are labeled “idiopathic tinnitus,” meaning that doctors can’t explain (or stop) the symptoms of tinnitus, which pretty much sums the situation up for the majority of tinnitus patients.
With a bit of detective work and determination, many people are able to alienate tinnitus triggers and utilize the many conventional and natural therapies available for their needs. Hyperacusis, defined as a collapse of tolerance to sound, is present in 40-86% of those who suffer from disabling forms of tinnitus.
In approximately 10 million individuals, the symptom is severe enough to compromise the quality of life significantly [1].
Dynorphin-like and enkephalin-like opioid peptides are codistributed within lateral efferent brainstem nuclei, in their descending fiber bundles and, in lateral efferent terminal varicosities, in the cochlea of such species as the guinea pig and rat [25-27]. The axons of descending, lateral efferent brainstem neurons [30] are well-known to terminate on the auditory spiral ganglion type I dendrites that, in turn, innervate the cochlear in-ner hair cells [31,32]. These three identified peptide families are (1) proopiomelanocortin (2) proenkephalin (proenkephalin A), and (3) prodynorphin (proenkephalin B).
This fact has underscored their neurotransmitter-neuromodulatory role in the filtering of sensory information and in the enhancement and fine tuning of the regulatory functions exerted by other neurotransmitters or hormones [53-58]. As with most neuropeptides, the receptor-activated ion-channel properties of opioid peptides are mediated by a class of membranebound, pertussis toxin-sensitive "G" -proteins [50,61,66]. As is often the case in the central nervous system [69], the ion channel actions of opioid-receptor linked G-proteins are mediated by the regulation of adenylate cyclase that catalyzes the synthesis of the second messenger, cyclic adenosine 3',5'-monophosphate (cAMP) [47,6 1). For instance, opioid receptors can be linked to a Gs-protein that, when stimulated, activates adenylate cyclase and increases cAMP [61,67].
In that investigation, the nonopioid (+) pentazocine, administered at an equivalent IV dose and concentration, was without effect (Fig. Biphasic intensity-dependent amplitude changes after administration of the κ-receptor drug agonist U-50488H (50 mM) delivered to the cochlear round window (RW) in five animals. Though some uncertainty still exists [99], many investigators have argued that glutamate is the afferent neurotransmitter in the mammalian cochlea [27,100-104]. In addition, alpha-amino-3 hydroxy-5-methyl-isoxazol-propionic acid-induced excitotoxicity and degeneration of cochlear spiral ganglion neurons is accompanied by a neurotropic NMDA receptor action of glutamate in this species [100]. Here, the overall synaptic density of afferents generally is greater as compared to the density of dendrites on the pillar surfaces of the THCs. These changes consist of alterations in SDR, a lowering of thresholds, and an enlargement of receptive fields, producing an increased sensitivity to both noxious and innocuous stimuli [73,114-116]. More specifically, it was constructed between the wind-up phenomena and the associated hyperalgesia observed in chronic pain, and the auditory symptoms of hyperacusis and chronic tinnitus [125]. Noteworthy is that nonNMDA receptors also can mediate neurotoxicity, especially during prolonged or widespread insults [120,132]. A reasonable assumption is that constitutional differences exist with respect to individual reactivities to environmental and physical stress. The opioid effects of μ-receptor ligands, however, often are accompanied by emotional states of dysphoria, disorientation, or depersonalization [59,98,138], and whether dynorphins are capable of producing any form of antinociception is questionable [74,139]. Does any evidence support that a neuropharmacological link exists between endogenous μ-receptor-sensitive dynorphins (or enkephalins) and neural excitability? The preceding review seems to clarify that only a few studies have investigated the potential effects of specific opioid receptor agonist-antagonist substances on the discharge of the auditory nerve.
Endogenous dynorphins have been reported to interact with glutamate-sensitive NMDA receptors in rat cortical neurons [143], though the precise mechanism is not yet understood [144].
In addition, peripheral inflammation leads to a large increase in prodynorphin gene expression (increased mRNA) in dorsal horn neurons, and this central nervous system increase parallels the development of hyperalgesia [74,146].
However, in these investigations, neural suppression never was observed at higher stimulus levels. Endogenous opioids have been suggested to modulate excitation at NMDA receptors [147] by (1) increasing the affinity of the ligand for the receptor (2) decreasing the degree of dissociation of the ligand from the receptor, or (3) by producing a change in the second messenger response to receptor activation. However, as with all perceptions (and especially those that involve aversion), the experience of tinnitus certainly must involve central auditory pathways and cortical regions and non auditory cortical-subcortical regions. According to one view, tinnitus results from the stress-induced central enhancement and magnification of abnormal but weak triggering signals passing from the auditory periphery to the auditory cortex, where they are perceived [1]. Intense emotional stress has been reported also to improve auditory thresholds temporarily in guinea pigs [l70], and we have observed improved auditory thresholds after the cochlear administration of opioid κ-receptor ligands [19]. The amplitude enhancement of weak auditory patterns characterizing tinnitus and hyperacusis has been suggested to be part of an evolutionary survival reflex [171]. Individual constitutional differences naturally would dictate the degree to which peripheral (and central) dynorphin systems are activated (and consequently the severity of the subjective hyperacusis).
In the long term, the consequence of this prolonged vigilant state is expected to produce a vicious feed-forward cycle.
Investigations designed to determine the distribution of κ-receptors and dynorphins in specific brainstem auditory pathways and in cell layers of critical auditory nuclei have yet to be performed.
Opioid prodynorphin (and proenkephalin) derivatives have been detected throughout the medullary brainstem, in regions that have included the separate divisions of this nuclear complex [54,172,173]. Additionally, a considerable number of prodynorphin-positive neurons have been detected within the inferior colliculus [173]. For instance, the release of excitatory amino acids (and therefore the observed hyperexcitability at NMDA receptors in neurons of the spinal cord dorsal horn) is facilitated by the release of the calcitonin gene-related peptide (CGRP) [73]. Such evidence raises the possibility that a dynorphin modulation of neural excitability through, perhaps, an enhancement of glutamate effects at NMDA receptors may occur at serial locations along the auditory pathway. Recognizing that this symptom represents a broad spectrum of auditory experiences, we acknowledge the possibility of an equally broad spectrum of auditory generators. Monaghan DT, Bridges RJ, Cotman CWo The excitatory amino acid receptors:their classes, pharmacology, and distinct properties in the function of the central nervous system. Some people find aromatherapy, massage, reflexology or learning the Alexander technique, Yoga or Tai Chi to be helpful.

When referring to tinnitus, people often report ‘ringing ears’, although different sounds are reported as well. In more severe cases of Tinnitus, treatment could consist of electrical stimulation, sound therapy, sound treatment (e.g.
This information and products described are not recommended for pregnant women or children. Tinnitus has been described as the perceptual correlate of altered spontaneous neural activity occurring in the absence of an external auditory stimulus [3-6].
Though the existence of prodynorphin peptides has yet to be shown in the human auditory system, products of proenkephalin synthesis have been detected in the lateral efferent terminal varicosities of the human cochlea [28].
The axodendritic innervation pattern of these dynorphin-containing terminals suggests that the lateral efferent system participates in modulating auditory neural sensitivity [33-35].
Neuroactive opioid peptides modulate sensory input through separate and often distinct opioid receptors. Antinociception (analgesia) is the most familiar and most intensively investigated property of such opioid substances as morphine; by definition, all opioids are analgesics [49,59]. The G-proteins derive their name from the fact that they bind the guanine nucleotides, guanosine triphosphate, and guanosine diphosphate [67]. Therefore, the binding of opioid ligands to their respective receptors often activates a Gi-protein that inhibits adenylate cyclase and decreases cAMP [61,67). Nevertheless, specific receptor subtypes that bind endogenous enkephalins and dynorphins (a and κ, respectively) have yet to be identified in the cochlea of any mammalian species. Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) obtained during each of six 30-minute recording periods.
Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) for the two dependent measures, obtained during each of six 30-minute recording periods. 3) produces increased auditory sensitivity and intensity-dependent amplitude changes in the auditory nerve CAP when administered intracochlearly [93,19]. Each plotted point represents the mean percentage of amplitude change relative to a grand baseline amplitude mean (±SE) obtained during each of six 30-minute recording periods recorded at the six stimulus intensities indicated. Adding to the complexity is the fact of even less certainty regarding the receptor type activated by putative excitatory afferent neurotransmitters in the cochlea [99].
Furthermore, a significant body of pharmacological evidence supports a functional auditory role for glutamate-sensitive NMDA receptors in the adult guinea pig cochlea [101-104, 107-109]. Tn general, the modiolar-oriented units are characterized by relatively lower spontaneous discharge rates (SDRs), higher auditory thresholds, smaller fiber diameters, and lower mitochondrial densities [33,110-112]. According to Moller [125], both pain and tinnitus involve neural sensitization that leads to a reduction in threshold or increased levels of neural excitability (or both).
Characteristically, NMDA receptor-gated activity produces an influx of extracellular Ca++, which in excess activates a variety of potentially destructive processes [120,121]. Equally reasonable is the expectation of individual differences with regard to the degree to which certain endogenous biochemical systems are likely to become activated during stressful events. Also endogenous dynorphins have been demonstrated to potentiate, rather than to suppress, behavioral changes induced by stressful events [63]. The results of those investigations indirectly have supported the existence of opioid receptor subtypes in the cochlea. Unlike previously reported δ-receptor ligand effects [142], dynorphins do not appear to interact with excitatory non-NMDA receptors [143], though potential interactions between these substances and glutamate-sensitive NMDA and non-NMDA receptors have yet to be demonstrated in the mammalian cochlea. Dynorphins have been implicated also in the wind-up-like activation of NMDA receptors, leading ultimately to neurotoxicity [147].
A tempting speculation is to envision the changes that high concentrations of cochlearly administered κ-receptor drug agonists would produce on auditory neural discharge as an auditory stimulus is progressively increased in intensity from threshold. At threshold and at relatively lower stimulus levels, these substances each promoted or enhanced neural excitation. Whether these changes reflect actions at glutamate-sensitive NMDA, non-NMDA, or both receptor types, or at some other nonopioid receptor requires further investigation. Nevertheless, a peripherally generated tinnitus can result from any number of insults to the inner ear, ranging from advancing age to excessive noise exposure [2,151]. Our position however, is that during stressful episodes, these abnormal signals (triggers) are not weak but are in fact abnormally amplified in the periphery. Therefore, we are proposing that a stress-induced release of neuroactive dynorphin-like opioid peptides from the lateral efferent terminals located beneath the IHCs contributes to an increase in auditory neural sensitivity and to spectral alterations in the ensemble spontaneous discharge activity of the auditory nerve.
However, those auditory (type I) neurons innervating a cochlea having sustained weakened or damaged OHCs (and therefore preordained to generate aberrant spectral discharge patterns) would be additionally susceptible to stress.
Therefore, under certain stressful conditions, dynorphins alone may serve as a trigger for tinnitus. Step 1: Excitatory neurotransmitter (glutamate) is released by the inner hair cell (A) during the presentation of a stimulus or (B) spontaneously during periods of quiet and binds to glutamate-sensitive (possibly N-methyl-D aspartate) receptors located postsynaptically on the type I auditory dendrites. This hypothesized feedforward cycle is similar conceptually to the wind-up phenomenon, which could serve to advance the organism to a state of peripheral and central auditory neural excitotoxicity and neurotoxicity. However, an important note is that though the focus of this article has been the auditory periphery, the possibility also exists for concurrent interactions of endogenous dynorphins with NMDA receptors at locations within the central auditory system. We have found CGRP immunoreactivity in a significant number of cells in the dorsal cochlear nucleus and in neurons of the ventromedial region of the lateral superior olive (LSO) [178]. This possibility and the precise relationship of κ-receptor ligands to NMDA receptor-activated neural discharge in the inner ear will be the focus of future investigations. However, we are compelled to conclude that when a human organism is confronted with any number of stressful events, conditions are optimal for the overall release of neuroactive opioid substances and the generation and perception of tinnitus. Neural mechanisms of tinnitus: the pathological ensemble spontaneous activity of the auditory system.
Changes in the auditory neural response following cochlear administration of U-50488H and (-) pentazocine.
Modulation of synaptic efficacy as a basis for tinnitus:hints suggested from the effects of quinine and aspirin on cochlear neurotransmission.
Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers: I. Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers:II.
Coexistence of putative neuroactive substances in lateral olivocochlear neurons in guinea pig and rat. Prodynorphin peptides are co-localized within auditory structures of the Chinchilla brainstem. Efferent innervation of the inner hair cell region:origins and terminations of two lateral olivocochlear systems. Efferent synapses in the inner hair cell area of the cat cochlea:an electron-microscopic study of serial sections.
Physiology of cochlear efferent and afferent neurons:direct comparisons in the same animal. Acetylcholine potentiation of glutamate-induced response in guinea pig spiral ganglion cells. Long-term physiological consequences of cutting the olivocochlear bundle (OCB) in neonatal animals. Partial characterization of the mRNA that codes for enkephalins in bovine adrenal medulla and human pheochromocytoma. Molecular cloning establishes proenkephalin as precursor of enkephalin-containing peptides.
Cloning and sequence analysis of cON A for porcine β-neoendorphinl dynorphin precursor.
Immunohistochemical localization of the cloned κl receptor in the rat CNS and pituitary. Endogenous opioid peptides acting at μ-opioid receptors in the dorsal horn contribute to midbrain modulation of spinal nociceptive neurons. Opioid peptide modulation of circulatory and endocrine response to mental stress in humans. Behavioral changes induced by stressful situations:effects of enkephalins, dynorphin, and their interactions. Modulatory effects of Gs-coupled excitatory opioid receptor functions on opioid analgesia, tolerance, and dependence. Dual opioid modulation of the action potential duration of mouse dorsal root ganglion neurons in culture. Dynorphin prolongs the action potential duration of mouse sensory ganglion neurons by decreasing a K+ conductance whereas the specific kappa opioid, U-50, 488H does so by increasing a Ca2+ conductance.
Dynorphin prolongs the action potential of mouse sensory ganglion neurons by decreasing a potassium conductance whereas another specific kappa opioid does so by increasing a calcium conductance.
Mu, delta, and kappa opioid receptor mRNA expression in the rat CNS:an in situ hybridization study. Improvement in auditory function following pentazocine suggests a role for dynorphins in auditory sensitivity.
Effects of opioid drugs on auditory evoked potentials suggest a role of lateral efferent olivocochlear dynorphins in auditory function. Binaltorphimine-related bivalent ligands and their K opioid receptor antagonist selectivity.
Implication of NMDA type glutamate receptors in neural regeneration and neoformation of synapses after excitotoxic injury in the guinea pig cochlea. Receptor pharmacological models for inner ear therapies with emphasis on glutamate receptors:a survey. The role of glutamate at the afferent synapses of mammalian inner hair cells:a microiontophoretic study.
A microiontophoretic study of the role of excitatory amino acids at the afferent synapses of mammalian inner hair cells. N-methyl-D-aspartate-induced oscillations in excitatory afferent neurotransmission in the guinea pig cochlea. Transient expression of NMDA receptors during rearrangement of AMPA-receptor expressing fibers in the developing ear. Electrophysiological evidence for the presence of NMDA receptors in the guinea pig cochlea. Morphological differences among radial afferent fibers in the cat cochlea:an electron-microscopic study of serial sections.
Morphometry of intracellularly labeled neurons of the auditory nerve:correlations with functional properties. Response properties of cochlear efferent neurons:monaural vs binaural stimulation and the effects of noise. Contribution of central neuroplasticity to pathological pain:review of clinical and experimental evidence. A comparative study of the changes in receptive-field properties of multireceptive and nociceptive rat dorsal hom neurons following noxious mechanical stimulation. The induction and maintenance of central sensitization is dependent on N-methylD-aspartic acid receptor activation; implications for the treatment of post-injury pain hypersensitivity states.
The relation between net calcium, alkali cation and chloride movements in red cells exposed to salicylate.
Concomitant salicylate-induced alterations of outer hair cell subsurface cisternae and electromotility.
Mu agonist induced euphoria as opposed to dysphoria elicited by κ-agonists in humans and experimental animals. Intrathecal dynorphin 1-13 results in an irreversible loss of the tail-flick reflex in rats. A direct non-opiate interaction of dynorphin 1-13 with the N-methyl-D-aspartate NMDA receptor.
The influence of sustained opioid receptor blockade in a model of long-term, localized inflammatory pain in rats.
In situ hybridization cytochemistry and immunocytochemistry reveal an increase in spinal dynorphin biosynthesis in a rat model of peripheral inflammation and hyperalgesia.
Selective potentiation of NMDA-induced activity and release of excitatory amino acids by dynorphin:possible roles in paralysis and neurotoxicity.
Norbinaltorphimine protection against N-methyl-D-aspartic acid-induced convulsions and mortality.
Acute ultrastructural changes in acollstic trauma:serial-section reconstruction of stereocilia and cuticular plates.
Effect of sound stimulation at several levels on concentrations of primary amines, including neurotransmitter candidates, in perilymph of the guinea pig inner ear. Immunocytochemicallocalization of glycine in a subset of cartwheel cells of the dorsal cochlear nucleus in rats. Differential expression of N-methyl-D-aspartate receptor in the cochlear nucleus of the mouse. Localization of calcitonin gene-related peptide (CGRP) within auditory structures of the chinchilla brainstem. A visit to your doctor will usually reassure you that there are no underlying medical conditions you may be worrying about. We can distinguish familiar sounds in a great hubbub of other sounds such as our name in a crowd or baby's cry above the telly or even a single musical instrument in a full orchestra.
In time the resulting acute perception of sounds, either the tinnitus or external sounds (hyperacusis) or both, subsides naturally but sometimes the acute phase persists and therapy is necessary to assist retraining of the system to to regain its autonomic skill. The key is to find what helps you the most and practice it often, at least daily. At HUSH we find that improving posture can also help with some forms of tinnitus.
The sound can appear as a quiet background sound or as a sound even louder that external sounds. During Neurofeedback training we aim to calm the brain again and to stabilise auditory processing and sensitivity.
Please note that we have a material financial connection to the provider of the goods and services from links on the website in that we receive payment for each qualified sale or potential customer referral.
Biological systems known to regulate the body's overall response to stress use and release endogenous neuroactive opioid peptides. Some 80% of tinnitus sufferers have problems that can be traced to or are associated with changes in the inner ear [1].
Preliminary work has indicated also that dynorph in-related derivatives are codistributed within lateral efferent brain stem nuclei of the chinchilla [29], though it remains to be determined whether the descending axons that project into the cochlea also contain dynorphins in this species. Data from recent pharmacologic studies [36,37] and developmental studies [38,39] also suggest an important role for this system in modulating auditory sensitivity. Also well-known is that opioid peptides function as neurotransmitters or neuromodulators and that they play an important role in modulating nociceptive sensory input [59-61].
In many other instances, the opioid receptor-linked stimulation of a G-protein may regulate a specific type of ion channel directly, such as a potassium (K+) or a calcium (Ca++) channel, independent of adenylate cyclase-cAMP. Furthermore, results of a subsequent investigation [79] indicated that large auditory neural amplitude changes at twice the dose were naloxone-reversible and occurred with no corresponding changes in the hair cell-generated cochlear microphonic potential (Fig.
Considerable evidence supports the existence of excitatory non-N-methyl-D-aspartate (NMDA) receptors in the normal adult mammalian cochlea [27,99]. Cochlear NMDA receptors may, however, be restricted to the type I auditory dendrites innervating the modiolar side, as opposed to the pillar side, of the IHCs [109].
Tn approximately 70% of these units (25-30% of the total), the auditory dendrites may be innervated by a range of 1-32 lateral efferent axons (mean, 10).

The enlargement of receptive fields and the ensuing hyperalgesia occur via the facilitation of excitatory amino acid effects at NMDA receptors [73,114]. Recently, inner ear damage from overstimulation was shown to be prevented by the cochlear administration of leupeptin, an inhibitor of intracellular Ca++ -activated cytosolic proteases (calpains) [15,133]. As with pain, what is becoming clear is that tinnitus must consist of both central and peripheral components; certainly, the response of an organism to stress surely involves the entire organism, both its peripheral and central nervous systems. Furthermore, evidence suggests that the aversive motivational properties of endogenous and exogenous opioids are mediated through peripheral κ-opioid receptors [140,141]. Nevertheless, dynorphins have been proposed to playa significant role in pathologies of central and peripheral inflammation [73,115,144,145]. For example, dynorphins produce neurotoxic effects in the spinal cord [139], and the κ-receptor-induced neurotoxicity and neurological dysfunction occur through an enhanced excitotoxic activity at NMDA receptors [73,144,148]. As the stimulus level is increased, glutamate concentrations in the inner ear also would increase but would be potentiated abnormally at each level of increase as a consequence of a κ-receptor facilitation of glutamate at NMDA receptors. The OHCs appear to be the inner ear structures most susceptible to damage in general and to noise damage in particular [152-155], and often tinnitus is associated with OHC dysfunction [3,156,157]. Though signal enhancement or increased synchronicity (or both) may occur at any location in the auditory system during extreme episodes of anxiety or stress [1], the initial neural changes involved in most forms of tinnitus begin in the auditory periphery [127]. Therefore, as part of an overall response to stress during actual or perceived life-threatening situations (as in extreme anxiety), endogenous neuroactive dynorphin peptides are released into the mammalian cochlea at axodendritic synapses beneath the IHCs and are released throughout the central nervous system.
The release of dynorphins and perhaps the subsequent enhanced neural sensitivity to excitatory neurotransmitter activation [73, 148] would result in amplified spectral alterations in the ensemble spontaneous discharge activity associated with tinnitus [4], thereby exacerbating or revealing the preexisting symptom. This event might occur in a manner that perhaps is similar to that described after receipt of sodium salicylate [4,5,21], shown recently to potentiate glutamate effects at NMDA receptors in the mammalian cochlea (20). Step 2: Endogenous dynorphin-related opioid peptides released from lateral efferent terminals tonically, or during physical or emotional stress, interact with N-methyl-D-aspartate receptors located postsynaptically on the type I auditory dendrites, to potentiate the excitatory properties of glutamate. Presently unknown is whether this group of LSO neurons projects specifically to the chinchilla cochlea as palt of the lateral efferent system. In Abstracts of the Twenty-Second Midwinter Meeting of the Association for Research in Otolaryngology 836:209-210, 1999. In Abstracts of the Twenty-First Midwinter Meeting of the Associationfor Research in Otolaryngology, 447, 1998. In Abstracts of the Eighteenth Midwinter Meeting of the Associatiollfor Research in Otolaryngology, 679:170, 1995. In Abstracts of the Twentieth Midwinter Meeting of the Associationfor Research in Otolaryngology, 600:20,1997. In Abstracts of the Twentieth Midwinter Meeting of the Association for Research in Otolaryngology, 213:54, 1997. In GJ Siegel, BW Agranoff, RW Albers, SK Fisher, MD Uhler (eds), Basic Neurochemistry (6th ed). In JG Hardman, LE Limbird, PB Molinoff, et al.(eds), Goodman and Gilman's The Pharmacological Basis of Therapeutics (9th ed). In R Quirion, K Jhamandas, C Gianoulakis (eds), Progress in Clinical and Biological Research: The International Narcotics Research Conference INRC '89.
Proceedings of the Second International Tinnitus Think Tank: The Neurochemistry of Tinnitus. In AG Gilman, TW Rail, AS Nies, P Taylor (eds), Goodman and Gilman's The Pharmacological Basis of Therapeutics (8th ed).
In GE Reich, JA Vernon (eds), Proceedings of the Fifth International Tinnitus Seminar, 1995. In Abstracts of the Nineteenth Midwinter Meeting of the Associationfor Research in Otolaryngology, 469:118, 1996. This 2015 study surprised researchers by showing that the parts of the brain involved in generating tinnitus were much broader than expected.
Tinnitus can occur sporadically, as well as constantly, and causes different levels of distress. By calming the brain and training the brain to stay calm, Neurofeedback can significantly improve Tinnitus symptoms. These stress-related neuromodulators consist of products derived from three genetically distinct precursor hormones. Hyperacusis has been defined as a collapse of tolerance to sound, often occurring with no significant loss in hearing sensitivity [7,8]. Consistent with what is currently known regarding neuroactive opioid peptides is our view that auditory neural modulation occurs at axodendritic synapses beneath the IHCs and involves (at least in part) the actions of endogenous opioid substances [40].
In addition to modulating the sensation-perception of pain, opioid peptides exert a wide spectrum of physiological-behavioral effects on autonomic function, affect, mood, attention, and physical or psychological stress [62,63]. In postnatal rats, glutamate-sensitive NMDA receptor subtypes have been reported to appear only transiently in the developing cochlea prior to the onset of hearing [105]. The remaining 33% of the modiolar-oriented units (10-15% of the total) are extremely mitochondria-poor, exhibit very low SDRs, and have the highest auditory thresholds of all the type I auditory units. In addition, chronic (prolonged) pain has been attributed to a gradual increase in action potential discharge and excitability in high-threshold spinal cord neurons in response to repeated peripheral stimulation. Moreover, patients with severe tinnitus report discomfort from intense auditory stimuli, and repeated exposure to such stimuli actually lowers their tolerance to all sounds [125-127].
Though clearly no single drug panacea exists, neuroprotective drug therapy has been proposed also for the alleviation of tinnitus [15,122,123].
As has been emphasized, endogenous opioid peptides play a role in the fine-tuning and filtering of sensory information and are released from neural systems in response to stress [53,57]. Iontophoretic application of the δ-opioid receptor ligand [Met5]-enkephalin produces a naloxone-reversible reduction in excitatory amino acidinduced auditory neural excitation in the guinea pig cochlea. For example, in the spinal cord (dorsal horn), dynorphins induce an NMDA receptor antagonist-reversible enlargement of neural receptive fields.
The excitotoxic and neurotoxic actions of dynorphins at the NMDA receptor arise through a κ-receptor mediated facilitation of NMDA receptor sensitivity to glutamate or to aspartate [114,147].
Therefore different-even oppositeeffects on neural amplitude would be predicted at each progressive increase in stimulus level from auditory neural threshold. Abnormally elevated spontaneous discharge rates within single auditory neurons often are observed when cochlear noise damage is confined to the OHCs [153,154,158]. The result is to advance an affected organism to a heightened state of auditory vigilance [40], which may be adaptive in the short-term when a rapid fight-or-flight response is required. Step 3A: Neural responses to relatively low levels of an auditory stimulus are enhanced [19]. In the rat, however, the medial limb of the LSO contains a large percentage of efferent neurons [179], suggesting that the CGRP-positive neurons observed in the chinchilla may be part of the lateral efferent system of neurons projecting to the cochlea.
Presented at the Martha Entenmann Tinnitus Research Center and the State University of New York SUNY Health Sciences Center at Brooklyn.
The cause of Tinnitus can be various factors, from wax build up, a cold, a blow to the head, or prolonged exposure to a loud noise, ear infections, objects in the ear, nasal allergies, neurological damage and stress. Hyperacusis is present in approximately 40-86% of those who suffer from disruptive forms of tinnitus; it also can compromise the quality of life in those individuals so afflicted [7-9].
Indeed, considerable evidence indicates that endogenous opioid peptides are found within, and are released from, neural systems that regulate the body 's overall biological response to stress [53,64,65].
Therefore, in many neural systems, opioid receptors are coupled to either the Gi-or Go-protein, wherein the actions of opioid ligands inhibit adenylate cyclase and K+ or Ca++ channels are regulated [61).
Such powerful IV μ-receptor agonists as fentanyl and morphine are without effect on the same auditory measures [84-87].
Tn fact, this smaller subset of modiolar-oriented units exhibits thresholds that are 20-80 dB poorer than are the thresholds of the more numerous type I units innervating the IHC pillar side [33,110,111,113]. The windup phenomenon associated with pain depends on NMDA receptor activation in high-threshold neurons [118]. Some suggested pharmacological therapies have included antianxiolytics, antioxidants, antihistamines, antidepressants, anticonvulsants, antiepileptogenics, diuretics, Ca++ channel blockers, dexamethasone, lidocaine, and (of course) glutamate-receptor antagonists [11,12,15]. Emotional or physical stress is known also to induce potent analgesic effects [53,117,136], and "stress-induced analgesia" is likely to involve multiple opioid systems [65,137].
The δ-receptor effect, however, occurs at both NMDA and glutamate-sensitive non-NMDA receptors, though enkephalin appears to exert a stronger inhibitory effect on non-NMDA receptor-induced auditory neural activity [142].
The receptive field enlargement results in a greater number of stimulated neurons and produces hyperalgesia [73,115]. Moreover, the existence of an activity-dependent neuronal plasticity in response to tissue injury has been hypothesi zed to account for the increased sensitivity and spontaneous pain associated with enhanced dorsal horn excitability at NMDA receptors by endogenous dynorphin peptides [114,73].
Normally, OHCs serve to damp activity in unstimulated regions of the cochlear partition, thereby decreasing the auditory sensitivity at (irrelevant) frequencies corresponding to those regions [153,159-161]. Alternatively, spectral anomalies in the ensemble spontaneous discharge associated with tinnitus may be amplified or generated, as illustrated in step 3B. Enkephalin and dynorphin-related peptides exist within the efferent olivocochlear systems (lateral and medial) of several mammalian species, including humans. In a large percentage of those suffering from both phenomena, the debility has been traced to the auditory periphery [10-12]. In addition to the wide range of observed behavioral responses, a wide range of neurophysiological responses also is produced by the binding of endogenous opioid ligands to their receptors.
Opioid receptor activation of the Gi-or the Go-protein has been linked to neural inhibition through an activation of voltage-or Ca++ dependent, inward-rectifying K+ channel conductances or inhibition of voltage-dependent inward Ca++ channel conductances [61,66,70-72]. From these investigations, some have argued that the observed auditory neural changes after IV (-) pentazocine reflect drug actions within the cochlea [79,80,83]. The dendrites of each of these very low SDR-very high threshold units are innervated by 7-32 lateral efferent axons (mean, 20), an amount twice the number of lateral efferent axons terminating on each of the pillar-oriented type I auditory dendrites [33]. Cochlear NMDA receptors also are activated primarily by the presentation of repetitive or relatively intense auditory stimuli [27, 108]. Therefore, an important component of an organism's response to a real or perceived life-threatening emergency is a reduction in responsiveness to pain.
Such evidence is consistent with the widely observed inhibitory properties of enkephalins, and indicates that endogenous enkephalins acting through δ-receptors modulate excitatory neural activity at glutamate-sensitive NMDA and non-NMDA receptors in the mammalian cochlea. Finally, the κ-receptor antagonist norbinaltorphimine has been found to be a potent antagonist of NMDA receptor activity, and a neuroprotective role has been suggested for this agent in the treatment of NMDA-induced convulsions and neurotoxicity [144, 149]. This property of OHCs contributes greatly to the sharp tuning of the cochlear partition [161-164]. Prodynorphin derivatives, however, may be restricted exclusively to lateral efferent neurons. For instance, in one investigation, hyperacusis was shown to involve the peripheral auditory system in 59% of cases [6].
This finding is suggested by (-) pentazocine's relatively high tissue solubility [88] and relatively low molecular weight [89,90], factors that should permit an easy passage of (-) pentazocine across the blood-labyrinthine barrier.
This anatomical array suggests that the lateral efferent system exerts relatively more influence on type I auditory neurons characterized by very low rates of spontaneous discharge and very high thresholds. NMDA receptor-linked and non-NMDA receptor-linked neurotoxic effects of glutamate or aspartate have been implicated also in a number of severe pathophysiological neurodegenerative disorders [119-121], in auditory neural excitotoxicity [15], in acute ischemia of radial auditory dendrites [27,109] and, of course, in tinnitus [10,11,15,101,122,123].
As indicated, cochlear NMDA receptors appear to be restricted to the much higher threshold, modiolar-oriented type I auditory dendrites [109].
Though such evidence argues that glutamate activation of cochlear NMDA receptors plays a substantial role in inner ear neuroexcitotoxicity and in the etiology, maintenance, or exacerbation of peripheral neural generators of tinnitus, what has become clear also is that stress-related events are more powerful triggers for tinnitus than are strictly auditory-related events [6,7,15,16]. This reaction creates little diffi-culty in envIsioning that in meeting the behavioral demands prompted by such exposure, an animal's normal reactions to pain could prove deleterious [117]. Also fairly likely is that such effects normally are initiated via the lateral efferent system.
Such evidence, taken together with more recent data [19], is consistent with the widely observed excitatory properties of dynorphins, further suggesting the possibility that endogenous dynorphins, acting through κ-receptors, facilitate the excitatory neural actions of glutamate in the inner ear.
One popular theory [157,165] is that damaged or dysfunctional OHCs decouple from the tectorial membrane, owing to a loss in their hydrostatic pressure [166] or to stereocilia damage [153]. Effects of electrical stimulation of efferent olivocochlear neurons on cat auditory-nerve fibers: III. Descending lateral efferent axons terminate solely on primary (type I) auditory dendrites innervating cochlear inner hair cells in most species.
Furthermore, both auditory phenomena are associated with or are induced or exacerbated by physical fatigue or psychological stress [2,6,13-16]. Naloxone Hel (Narcan), the antagonist drug of choice for opioid intoxication, also is known to pass easily through blood-endothelial barriers [59]. Finally, sodium salicylate, well-known for its anti nociceptive properties and its capacity to produce transient tinnitus, also increases intercellular Ca++ levels in neurons [125] and in cochlear outer hair cells (OHCs) [129].
Consequently, during threatening conditions, reactions to pain would be suppressed in favor of more adaptive behaviors, enabling an organism to escape or defend itself (fight or flight). The corresponding loss in their normal damping properties leads to an increased production of thermal noise within specified regions of the cochlear partition. This action indicates that they play an important role in modulating auditory nerve sensitivity and spontaneous discharge. An association has been drawn also between clinical depression (dysphoria) and severe forms of tinnitus, with an incidence reported as high as 60-80% [16-18]. Alternatively, the observed auditory neural changes subsequent to IV administration of (-) pentazocine or naloxone may have been, at least in part, an indirect reflection of the actions of both drugs in the brainstem, leading to the subsequent release-suppression of dynorphins, or of some other neurotransmitter-modulator at the lateral efferent-type I auditory synapse. Perhaps more important, however, was the recent demonstration that sodium salicylate potentiates the excitatory effects of glutamate at NMDA receptors in the mammalian inner ear [20], an action consistent with the observations and conclusions made by previous tinnitus investigators [3,130,131]. This added shift in the neural discharge spectra then is interpreted erroneously by the central auditory system as a genuine signal [3,4].
In a fashion similar to that exhibited by the observed excitatory mechanism of action of dynorphins in the spinal cord, sodium salicylate (aspirin) recently was shown to facilitate the excitatory effects of glutamate in the cochlea.
As discussed later, opioid κ-receptor ligands administered into the cochlea have been observed to alter auditory neural sensitivity to low-intensity sounds [19]. Whether and to what extent such effects occurred from indirect drug actions in the brainstem or from direct actions in the cochlea cannot be evaluated at present.
This article provides support for a neurochemical model in which endogenous dynorphins may induce hyperacusis and can contribute to the induction, maintenance, or exacerbation of tinnitus in the auditory periphery by altering auditory type I neural excitability to glutamate. In a fashion similar to that of the reported effects of dynorphins in the spinal cord, sodium salicylate recently was shown to facilitate the excitatory effects of glutamate in the cochlea [20]. Still unknown is whether κ-receptors exist in the chinchilla brainstem and whether IV (-) pentazocine effects are eliminated in animals, maintaining ablations to the lateral efferent pathways. Furthermore, salicylate produces tinnitus concomitant with quantifiable spectral alterations in the "ensemble spontaneous discharge activity" of the auditory nerve [4,5,21]. Our position is that endogenous dynorphin peptides are liberated into the inner hair cell (IHC) synaptic region by the lateral efferent olivocochlear system.
These neuroactive substances then interact with nearby excitatory neurotransmitter receptors, producing quantifiable alterations in stimulus-evoked and spontaneous auditory neural activity.
During periods of physical or emotional stress, this interaction may be especially pertinent. Furthermore, this hypothesized association may not be restricted only to tinnitus generated at the level of the auditory periphery.

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