Ruili Xie, Tessa-Jonne F. Ropp, Michael R. Kasten, and Paul B. Manis
Hearing loss generally occurs in the auditory periphery but leads to changes in the central auditory system. Noise-induced hearing loss (NIHL) and age-related hearing loss (ARHL) affect neurons in the ventral cochlear nucleus (VCN) at both the cellular and systems levels. In response to a decrease in auditory nerve activity associated with hearing loss, the large synaptic endings of the auditory nerve, the endbulbs of Held, undergo simplification of their structure and the volume of the postsynaptic bushy neurons decreases. A major functional change shared by NIHL and ARHL is the development of asynchronous transmitter release at endbulb synapses during periods of high afferent firing. Compensatory adjustements in transmitter release, including changes in release probability and quantal content, have also been reported. The excitability of the bushy cells undergoes subtle changes in the long-term, although short-term, reversible changes in excitability may also occur. These changes are not consistently observed across all models of hearing loss, suggesting that the time course of hearing loss, and potential developmental effects, may influence endbulb transmission in multiple ways. NIHL can alter the representation of the loudness of tonal stimuli by VCN neurons and is accompanied by changes in spontaneous activity in VCN neurons. However, little is known about the representation of more complex stimuli. The relationship between mechanistic changes in VCN neurons with noise-induced or age-related hearing loss, the accompanying change in sensory coding, and the reversibility of changes with the reintroduction of auditory nerve activity are areas that deserve further thoughtful exploration.
Donald M. Caspary and Daniel A. Llano
As arguably the third most common malady of industrialized populations, age-related hearing loss is associated with social isolation and depression in a subset of the population that will approach 25% by 2050. Development of behavioral or pharmacotherapeutic approaches to prevent or delay the onset of age-related hearing loss and mitigate the impact of hearing loss of speech understanding requires a better understanding of age-related changes that occur in the central auditory processor. This chapter critically reviews and discusses changes that occur in the auditory brainstem and thalamus with increased age. It briefly discusses age-related cellular changes that occur de novo within the central auditory system versus deafferentation plasticity and animal models of aging. Subsections discuss the cochlear nucleus, superior olivary complex, inferior colliculus, and the medial geniculate body with an emphasis on age-related changes in neurotransmission and how these changes could underpin the observed loss of precise temporal processing with increased age.
Nina Kraus and Trent Nicol
The encoding of speech and music in the auditory brainstem is available at the human scalp via the auditory-evoked frequency following response. The FFR, primarily reflecting activity in the inferior colliculus, may be evoked by speech or music stimulation and represents the combined activity of sensorimotor, cognitive, and reward centers in the brain. Its response properties, like the inferior colliculus itself, are influenced by long-term experience with sound. The transparency, individual-level reliability, and ability to gauge neural plasticity provide the researcher and clinician a powerful probe of auditory processing in the human brainstem. With it, we have learned a great deal about how mechanisms of decline, deprivation, and enrichment affect the processing of complex signals such as music and speech in the human brainstem.
Rie Bager Hansen and Sarah Falk
Pain is a common and feared complication for many cancer patients. Cancer pain covers numerous pain syndromes; since the treatment is complex, it is essential to assess each individual patient with cancer pain thoroughly. Cancer pain includes not only elements of inflammatory and neuropathic pain, but also, importantly, cancer-specific elements. Starting with the clinical aspects of cancer pain and the current knowledge from in vivo models, this chapter provides an overview of the neurobiology known to drive cancer-induced bone pain as it evolves through the complex interplay between primary afferents, tumor cells, and bone cells. There continue to be many uncertainties and unknown mechanisms involved in cancer pain, and an effort to discover novel therapeutic targets should be emphasized as cancer pain poses an increasing clinical and socioeconomic burden.
Changes in the Inferior Colliculus Associated with Hearing Loss: Noise-Induced Hearing Loss, Age-Related Hearing Loss, Tinnitus and Hyperacusis
Alan R. Palmer and Joel I. Berger
The inferior colliculus is an important auditory relay center that undergoes fundamental changes following hearing loss, whether noise induced (NIHL) or age related (ARHL). These changes may contribute to the induction or maintenance of phenomena such as tinnitus (phantom auditory sensations) and hyperacusis (increased sensitivity to sound). Here, we outline changes that can occur in the inferior colliculus following damage to the periphery and/or as a result of the ageing process, both immediate and long-term, and attempt to disentangle which changes relate to either tinnitus or hyperacusis, as opposed to solely hearing loss. Understanding these changes is ultimately important to reversing the underlying pathology and treating these conditions.
Donata Oertel, Xiao-Jie Cao, and Alberto Recio-Spinoso
Plasticity in neuronal circuits is essential for optimizing connections as animals develop and for adapting to injuries and aging, but it can also distort the processing, as well as compromise the conveyance of ongoing sensory information. This chapter summarizes evidence from electrophysiological studies in slices and in vivo that shows how remarkably robust signaling is in principal cells of the ventral cochlear nucleus. Even in the face of short-term plasticity, these neurons signal rapidly and with temporal precision. They can relay ongoing acoustic information from the cochlea to the brain largely independently of sounds to which they were exposed previously.
J.A. Kaltenbach and D.A. Godfrey
Tinnitus most commonly begins with alterations of input from the ear resulting from cochlear trauma or overstimulation of the ear. Because the cochlear nucleus is the first processing center in the brain receiving cochlear input, it is the first brainstem station to adjust to this modified input from the cochlea. Research published over the last 30 years demonstrates changes in neural circuitry and activity in the cochlear nucleus that are associated with and may be the origin of the signals that give rise to tinnitus percepts at the cortical level. This chapter summarizes what is known about these disturbances and their relationships to tinnitus. It also summarizes the mechanisms that trigger tinnitus-related disturbances and the anatomical, chemical, neurophysiological, and biophysical defects that underlie them. It concludes by highlighting some major controversies that research findings have generated and discussing the clinical implications the findings have for the future treatment of tinnitus.
Roy E. Ritzmann and Sasha N. Zill
This article discusses legged locomotion in insects. It describes the basic patterns of coordinated movement both within each leg and among the various legs. The nervous system controls these actions through groups of joint pattern generators coupled through interneurons and interjoint reflexes in a range of insect species. These local control systems within the thoracic ganglia rely on leg proprioceptors that monitor joint movement and cuticular strain interacting with central pattern generation interneurons. The local control systems can change quantitatively and qualitatively as needed to generate turns or more forceful movements. In dealing with substantial obstacles or changes in navigational movements, more profound changes are required. These rely on sensory information processed in the brain that projects to the multimodal sensorimotor neuropils collectively referred to as the central complex. The central complex affects descending commands that alter local control circuits to accomplish appropriate redirected movements.
Brett R. Schofield and Nichole L. Beebe
Descending auditory pathways originate from multiple levels of the auditory system and use a variety of neurotransmitters, including glutamate, GABA, glycine, acetylcholine, and dopamine. Targets of descending projections include cells that project to higher or lower centers, setting up circuit loops and chains that provide top-down modulation of many ascending and descending circuits in the auditory system. Descending pathways from the auditory cortex can evoke plasticity in subcortical centers. Such plasticity relies, at least in part, on brainstem cholinergic systems that are closely tied to descending cortical projections. Finally, the ventral nucleus of the trapezoid body, a component of the superior olivary complex, is a major target of descending projections from the cortex and midbrain. Through its complement of different neurotransmitter phenotypes, and its wide array of projections, the ventral nucleus of the trapezoid body is positioned to serve as a hub in the descending auditory system.
Nanna Brix Finnerup and Nadine Attal
The present chapter presents an update of the current classification, diagnosis, assessment, mechanisms, and treatment of neuropathic pain. Neuropathic pain, which is defined as pain associated with a lesion or disease of the somatosensory nervous system, may be caused by a variety of conditions, such as diabetic neuropathy, herpes zoster, surgical trauma, spinal cord injury, and stroke. The diagnostic criteria for neuropathic pain are a history of a nervous system disease or lesion and pain distribution and sensory signs in a neuroanatomically plausible distribution. The treatment of neuropathic pain is often multidisciplinary and involves specific drugs. Recent progress in the diagnosis, assessment, and understanding of its mechanisms offers the perspective of a more rational therapeutic management, which should result in better therapeutic outcome.