Abstract
Peripheral axons from auditory spiral ganglion neurons project to the organ of Corti and synapse with both inner and outer hair cells prior to the onset of hearing. The developmental processes that determine axon outgrowth are largely unknown, though it is thought that a combination of axon guidance molecules and neurotrophic factors determine the fate of the projections. Here, we use immunofluorescence to show that the P2X3 receptor is expressed in both spiral ganglion neurons and hair cells during cochlear development. Furthermore, we demonstrate that P2X3 expression is nearly ubiquitous among spiral ganglion neurons at E16.5. These results support previous work on the spatial expression of P2X3 during development and serve as a foundation for future examination of the developmental function of P2X3.
Introduction
The mammalian cochlea is located within the inner ear and is responsible for the transduction of auditory stimuli from an organism’s external environment to the brain. The neurons that mediate this signal transduction are spiral ganglion neurons (SGN), a bipolar cell type with peripheral axons extending to mechanically sensitive hair cells (HC) in the organ of Corti (OC) and central axons that bifurcate and project to the dorsal and ventral cochlear nuclei (DCN, VCN) (Coate, et al., 2013). SGNs are divided into two classes determined by the hair cells to which they project: 90-95% of SGNs innervate inner hair cells (IHCs), whereas the remaining 5-10%
* Interneurons or Pseudopolare (Spelling) cells form all the neural wiring within the CNS. These have two axons (instead of an axon and a dendrite). One axon communicates with the spinal cord; one with either the skin or muscle. These neurons have two processes. (Examples are dorsal root ganglia cells.)
(2005) neurofibromatosis type II is a rare condition with an incidence of 1 in 25,000 persons and a penetrance of nearly 100% by age sixty. NFII is an autosomal dominant heritable neoplasia syndrome as defined by Asthagiri et al. (2012). The hallmark of this disorder is the development of bilateral acoustic neuromas, also known as cochleovestibular schwannomas (CVSs), on the auditory nerve. According to previous research, bilateral CVSs are present in 90-95% of NFII patients (Evans, et al., 1992). These non-cancerous tumors are a result of an NFII gene mutation specifically affecting a protein called merlin, also known as schwannomin. This protein acts as a suppressor, keeping cells from growing too rapidly. When the mutation occurs in the gene, it leads to a production of non-functioning merlin protein that cannot regulate growth and division of cells leading to acoustic neuromas. Although it is known how these neuromas form, the way that these neuromas cause hearing loss is not yet fully understood. Asthagiri et al. (2012) stated that “the most frequently cited hypothesis is that the enlarging CVS causes hearing loss through direct compression and stretching of the cochlear nerve.” Neurofibromatosis type II is characterized by bilateral acoustic neuromas, and the surgery to remove these neuromas generally results in severe damage to the auditory nerve causing deafness (Jackson, Mark, Helms, and Behr,
C. elegans is an effective model for investigation of the rationed systems that adjust sound maturing. We report that maturing C. elegans neurons can display novel neurite outgrowth from dendrites and from somata. New outgrowths can be exceedingly pervasive in maturing touch receptor neurons, with mitochondria regularly situated at branch locales. Diverse neurons display particular sorts of outgrowth, even with a solitary neuronal class. Be that as it may, not all neurons display morphological change with age, showing cell-specificity of basic decrease. In the maturing nematode sensory system, neuronal passing or potentially distinguishable loss of procedures are not promptly evident, but rather in light of the fact that dendrite
Cells in lamina I respond mainly to noxious and thermal stimuli. Lamina II is composed of many tightly packed interneurons that remain in the spinal cord and are a major postsynaptic target for primary afferents. Interneurons can be excitatory (glutamatergic) or inhibitory (GABA- or glycinergic) and are involved in modulation and transmission of sensory information [263, 268]. Aδ and C fibers synapse onto nociceptive interneurons and secondary afferent fibers (or projection neurons) in the dorsal horn. The axons of these neurons cross to the midline of the spinal cord through the anterior white commissure and ascend up the lateral white matter where they transmit somatosensory information to higher level supraspinal pain-processing centers [269, 270]. The most prominent ascending pathway is the spinothalamic tract, which transmits the discriminative components of pain (such as the quality, location, and intensity) [271, 272]. The projection neurons of the spinothalamic tract originate in laminae I, II, and V of the dorsal horn, and ascend up the ventrolateral funiculus [272]. A second ascending pathway involved in pain transmission is the spinomesencephalic tract, which also originates in laminae I, II, and V and travels up the
During normal development of the mammalian central nervous system (CNS), neural stem cells (NSC) give rise to neurons via process of neurogenesis (Kempermann et al., 2004; Zhao et al., 2008). Neurogenesis normally occurs in dentate gyrus (DG) region of the hippocampus and lateral ventricle of sub-ventricular zone (SVZ) (Zhao et al., 2008). Hippocampal neurogenesis plays pivotal role in neurologic and psychiatric disorder like epilepsy, depression, schizophrenia and mood disorders (Antonova et al., 2004; Keller and Roberts, 2008; Lucassen et al., 2006; Zhao et al., 2008). Development of the nervous system is complex, and includes multistep dynamic processes such as proliferation, differentiation, migration, expansion of axons and dendrites, synapse formation, myelination and programmed cell death (Rice and Barone, 2000). These processes required the coordinated expression of cellular and molecular events in a spatial and temporal manner during the brain development (Rice and Barone, 2000; Rodier, 1994). Several growth factors and signal transduction cascades have been implicated in controlling NSC behavior in the developing brain (Faigle and Song, 2013). Among these, members of the Wnt family of secreted glycoprotein thought to be variably influence proliferation and lineage decisions of NSC and their progeny (Clevers et al., 2014).
To do this, the researchers exposed a second group of adult quail to the same hearing-damaging sound as the first and then injected them with radiolabeled thymidine. This allowed researchers to use autoradiography that produce low levels of background issues as well as being able to see 10 to 20 grains over red blood cells. The control birds were still given the injections, however, they were not exposed to the sound. The experimental group experienced the same pattern of damage as the birds in the previous experiment and thymidine was seen over hair cells and support cells in the damaged area. There was no thymidine observed outside of the damaged area. The transition zone of the basilar membrane, where tall and short hair cells are integrated, it seemed that the short cells were more often labeled than the tall cells. Tall cells do not lack the afferent auditory-nerve fiber innervation that is seen in short cells making them a more useful candidate for labeling. The researchers failed to identify location and mechanism of the activation of the precursor cells but remained hopeful that there may exist a way to restore inner ear sensory losses that are caused from injury of hair
The nerve splits into two nerve branches in the inner ear, the cochlear nerve and the vestibular nerve. The cochlear nerve is an afferent sensory nerve used for a sending auditory information from the inner ear to the brain, and the vestibular nerve is an afferent sensory nerve used for sending balance and head position information from the inner ear to the brain. Vestibular Schwannoma arises in the vestibular nerve, but the growth could affect functions of the cochlear nerve, and the other local cranial nerves including the Facial Nerve (CN VII), Trigeminal Nerve (CN V), the Glossopharyngeal Nerve (CN IX), and the Vagus Nerve (CN
It is generally accepted that tinnitus is related to the changes in neural activity and maladaptive neuroplasticity of the auditory networks due to the damage in the auditory system. However, recent evidence obtained from neuroimaging studies show that both auditory and non-auditory structures are involved in the development of tinnitus (Leaver et al., 2011;
Chapter two begins to go in depth about how the brain works and what makes a human tick . It amazes me that an average person could have up to one hundred billion neurons. Chapter two gives insight on the early discoveries of neurons, and the doubt that the brain is composed of individual cells. The discovery was made by Santiago Ramón y Cajal using a newly developed staining technique to show that a small gap separates the tips of one neuron's fibers from the surface of the next neuron thus proving that the brain is similar to the rest of the body in that is contains individual cells. Neurons share common characteristics with animal cells but more look like a spider web network all interlinking, keeping in mind there are around one hundred
Different frequencies reach their peak at different positions along the tube, which allows the cochlea to distinguish them. Researchers have found that the spiral shape significantly enhances the “vibrational motions” that translate into nerve signals. However, if the cochlear is damaged it is obvious how important the development of the cochlear implant is. Essentially the cochlear implant serves as a bypass for damaged sections of the ear, replacing the function of the ineffective hair cells.
Cochlear implants, the surgical device which the media has frequently offered as the miracle cure for deafness, has been utilized as a treatment for hearing loss since the early 1960s (Paludnevicience & Harris, 2011, p.100). In patients with a hearing loss due to damage of hair cells in the inner ear, cochlear prostheses are able to provide some degree of hearing restoration by bypassing these structures and transmitting sounds directly to the auditory nerve (Paludneviciene & Harris, 2011, p. 100). With its start in the mid twentieth century, the technological resources available to the creators of cochlear implants limited their ability to provide patients a natural hearing experience. Though they initially provided only limited gains to deaf
While sensorineural deafness can be the result of tiny hair cells being damaged, this can also occur when the auditory nerve is damaged (Better Hearing Institute, n.d.). Sensorineural deafness changes the ability of hearing faint sound and reduce the intensity of sound, creating difficulties for the person suffers from it to understand others (hearcom, n.d.). The causes of sensorineural deafness may vary, the exposure to loud noises, aging, medicines, illnesses, head trauma, or malformation in the structure of the inner ear are all potential causes (Better Hearing Institute, n.d.). Genetic also play as a role in the cause of sensorineural deafness. While sensorineural hearing loss is irreversible, researchers have found a way to help the patients to be able to hear better. Through a cochlear implant, an electronic device that replaces the function of the damaged inner ear and provide sound signal to the brain, people who suffer from sensorineural hearing loss would be able to hear (cochlear,
sensory neurons located in the head and tail sense an extensive variety of extracellular and
Many serotonergic projections from the raphe nucleus terminate in the superficial laminae of the dorsal horn, an area strongly associated with nociceptive processing (Todd, 2010). These axons can be found throughout the dorsal horn but are most numerous in the superficial laminae.
Brain alterations can be triggered not only by environmental factors, but also by injury or disease. Such alterations usually take the form of changes in the manner in which nerve cells (neurons) connect to one another. “Axonal sprouting” is the mechanism that underpins these processes and involves the development of new nerve endings on undamaged axons which help to re-establish disrupted connections between neurons. Furthermore, the new nerve endings forming on undamaged axons can also facilitate connection with other undamaged neurons, creating new neural pathways that replace the impaired function. For instance, the two brain hemispheres each fulfil clearly defined functions, but if one of them incurs damage, its functions can be transferred