scholarly journals Underlying Mechanisms of Tinnitus: Review and Clinical Implications

2014 ◽  
Vol 25 (01) ◽  
pp. 005-022 ◽  
Author(s):  
James A. Henry ◽  
Larry E. Roberts ◽  
Donald M. Caspary ◽  
Sarah M. Theodoroff ◽  
Richard J. Salvi
Keyword(s):  
Health Care Professionals ◽  
Behavioral Interventions ◽  
Auditory Pathway ◽  
Common Denominator ◽  
Clear Understanding ◽  
Underlying Mechanisms ◽  
Normal Input ◽  
Central Auditory Pathway ◽  
The Brain

Background: The study of tinnitus mechanisms has increased tenfold in the last decade. The common denominator for all of these studies is the goal of elucidating the underlying neural mechanisms of tinnitus with the ultimate purpose of finding a cure. While these basic science findings may not be immediately applicable to the clinician who works directly with patients to assist them in managing their reactions to tinnitus, a clear understanding of these findings is needed to develop the most effective procedures for alleviating tinnitus. Purpose: The goal of this review is to provide audiologists and other health-care professionals with a basic understanding of the neurophysiological changes in the auditory system likely to be responsible for tinnitus. Results: It is increasingly clear that tinnitus is a pathology involving neuroplastic changes in central auditory structures that take place when the brain is deprived of its normal input by pathology in the cochlea. Cochlear pathology is not always expressed in the audiogram but may be detected by more sensitive measures. Neural changes can occur at the level of synapses between inner hair cells and the auditory nerve and within multiple levels of the central auditory pathway. Long-term maintenance of tinnitus is likely a function of a complex network of structures involving central auditory and nonauditory systems. Conclusions: Patients often have expectations that a treatment exists to cure their tinnitus. They should be made aware that research is increasing to discover such a cure and that their reactions to tinnitus can be mitigated through the use of evidence-based behavioral interventions.

Long-term modulation of tyrosine hydroxylase activity and expression by endothelin-1 and -3 in the rat anterior and posterior hypothalamus

2008 ◽  
Vol 294 (3) ◽  
pp. R905-R914 ◽  
Author(s):  
Guadalupe Perfume ◽  
Sabrina L. Nabhen ◽  
Karla Riquelme Barrera ◽  
María G. Otero ◽  
Liliana G. Bianciotti ◽  
...  
Keyword(s):  
Tyrosine Hydroxylase ◽  
Cardiovascular Effects ◽  
Receptor Activation ◽  
Catecholaminergic Neurons ◽  
Endothelin System ◽  
Catecholaminergic Transmission ◽  
Underlying Mechanisms ◽  
G Protein Coupled ◽  
The Brain

Brain catecholamines are involved in the regulation of biological functions, including cardiovascular activity. The hypothalamus presents areas with high density of catecholaminergic neurons and the endothelin system. Two hypothalamic regions intimately related with the cardiovascular control are distinguished: the anterior (AHR) and posterior (PHR) hypothalamus, considered to be sympathoinhibitory and sympathoexcitatory regions, respectively. We previously reported that endothelins (ETs) are involved in the short-term tyrosine hydroxylase (TH) regulation in both the AHR and PHR. TH is crucial for catecholaminergic transmission and is tightly regulated by well-characterized mechanisms. In the present study, we sought to establish the effects and underlying mechanisms of ET-1 and ET-3 on TH long-term modulation. Results showed that in the AHR, ETs decreased TH activity through ETB receptor activation coupled to the nitric oxide, phosphoinositide, and CaMK-II pathways. They also reduced total TH level and TH phosphorylated forms (Ser 19 and 40). Conversely, in the PHR, ETs increased TH activity through a G protein-coupled receptor, likely an atypical ET receptor or the ETC receptor, which stimulated the phosphoinositide and adenylyl cyclase pathways, as well as CaMK-II. ETs also increased total TH level and the Ser 19, 31, and 40 phosphorylated sites of the enzyme. These findings support that ETs are involved in the long-term regulation of TH activity, leading to reduced sympathoinhibition in the AHR and increased sympathoexcitation in the PHR. Present and previous studies may partially explain the cardiovascular effects produced by ETs when applied to the brain.

Crosstalk between Microglia and Neurons in Neurotrauma: An Overview of the Underlying Mechanisms

2021 ◽  
Vol 19 ◽  
Author(s):  
Muhammad Ali Haidar ◽  
Stanley Ibeh ◽  
Zaynab Shakkour ◽  
Mohammad Amine Reslan ◽  
Judith Nwaiwu ◽  
...  
Keyword(s):  
Brain Injury ◽  
Microglial Activation ◽  
Trauma Treatment ◽  
Cell Contact ◽  
Clear Understanding ◽  
Neuroinflammatory Response ◽  
Proinflammatory Responses ◽  
Underlying Mechanisms ◽  
The Brain ◽  
Cns Anomalies

: Microglia are the resident immune cells of the brain and play a crucial role in housekeeping and maintaining homeostasis of the brain microenvironment. Upon injury or disease, microglial cells become activated, at least partly, via signals initiated by injured neurons. Activated microglia, thereby, contribute to both neuroprotection and neuroinflammation. However, sustained microglial activation initiates a chronic neuroinflammatory response which can disturb neuronal health and disrupt communications between neurons and microglia. Thus, microglia-neuron crosstalk is critical in a healthy brain as well as during states of injury or disease. As most studies focus on how neurons and microglia act in isolation during neurotrauma, there is a need to understand the interplay between these cells in brain pathophysiology. This review highlights how neurons and microglia reciprocally communicate under physiological conditions and during brain injury and disease. Furthermore, the modes of microglia-neuron communication are exposed, focusing on cell-contact dependent signaling and communication by the secretion of soluble factors like cytokines and growth factors. In addition, how microglia-neuron interactions could exert either beneficial neurotrophic effects or pathologic proinflammatory responses are discussed. We further explore how aberrations in microglia-neuron crosstalk may be involved in central nervous system (CNS) anomalies, namely: traumatic brain injury (TBI), neurodegeneration, and ischemic stroke. A clear understanding of how the microglia-neuron crosstalk contributes to the pathogenesis of brain pathologies may offer novel therapeutic avenues of brain trauma treatment.

Molecular and Structural Changes in the Cochlear Nucleus in Response to Hearing Loss

2018 ◽  
pp. 142-162
Author(s):  
Maria E. Rubio
Keyword(s):  
Hearing Loss ◽  
Cochlear Nucleus ◽  
Structural Changes ◽  
Auditory Pathway ◽  
The United States ◽  
Cellular Mechanisms ◽  
Auditory Experience ◽  
Central Auditory Pathway ◽  
The Brain

Hearing loss is the third most common health problem in the United States. It can affect the quality of life and relationships. About 48 million Americans have lost some hearing. Age, illness, and genetics contribute to the generation of hearing loss. During development, auditory synaptic circuitries are highly plastic and able to adapt to fluctuations in auditory experience. Whether this is so for mature auditory nerve synapses and circuitries within nuclei along the central auditory pathway is less understood. Daily fluctuations in auditory experience can lead to hearing deficits, including hearing loss and/or deafness, Therefore, understanding the cellular mechanisms that occur in mature central auditory synaptic circuitries that lead and/or contribute to hearing loss is important. This chapter focuses on published studies using animal models describing structural and molecular changes that occur in the cochlear nucleus in response to hearing loss, the first gateway of sound processing in the brain.

scholarly journals Microglia: A Potential Therapeutic Target for Sepsis-Associated Encephalopathy and Sepsis-Associated Chronic Pain

2020 ◽  
Vol 11 ◽  
Author(s):  
Yi Li ◽  
Lu Yin ◽  
Zhongmin Fan ◽  
Binxiao Su ◽  
Yu Chen ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Immune Cell ◽  
Treatment Strategies ◽  
Neurological Dysfunction ◽  
Potential Therapeutic Target ◽  
The Central Nervous System ◽  
Underlying Mechanisms ◽  
The Relationship ◽  
The Brain

Neurological dysfunction, one of the severe manifestations of sepsis in patients, is closely related to increased mortality and long-term complications in intensive care units, including sepsis-associated encephalopathy (SAE) and chronic pain. The underlying mechanisms of these sepsis-induced neurological dysfunctions are elusive. However, it has been well established that microglia, the dominant resident immune cell in the central nervous system, play essential roles in the initiation and development of SAE and chronic pain. Microglia can be activated by inflammatory mediators, adjacent cells and neurotransmitters in the acute phase of sepsis and then induce neuronal dysfunction in the brain. With the spotlight focused on the relationship between microglia and sepsis, a deeper understanding of microglia in SAE and chronic pain can be achieved. More importantly, clarifying the mechanisms of sepsis-associated signaling pathways in microglia would shed new light on treatment strategies for SAE and chronic pain.

scholarly journals Adaptive and multifunctional hydrogel hybrid probes for long-term sensing and modulation of neural activity

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Seongjun Park ◽  
Hyunwoo Yuk ◽  
Ruike Zhao ◽  
Yeong Shin Yim ◽  
Eyob W. Woldeghebriel ◽  
...  
Keyword(s):  
Foreign Body ◽  
Brain Regions ◽  
Foreign Body Response ◽  
Behavioral Studies ◽  
Hydrogel Matrix ◽  
Underlying Mechanisms ◽  
Hybrid Devices ◽  
The Brain ◽  
Body Response

AbstractTo understand the underlying mechanisms of progressive neurophysiological phenomena, neural interfaces should interact bi-directionally with brain circuits over extended periods of time. However, such interfaces remain limited by the foreign body response that stems from the chemo-mechanical mismatch between the probes and the neural tissues. To address this challenge, we developed a multifunctional sensing and actuation platform consisting of multimaterial fibers intimately integrated within a soft hydrogel matrix mimicking the brain tissue. These hybrid devices possess adaptive bending stiffness determined by the hydration states of the hydrogel matrix. This enables their direct insertion into the deep brain regions, while minimizing tissue damage associated with the brain micromotion after implantation. The hydrogel hybrid devices permit electrophysiological, optogenetic, and behavioral studies of neural circuits with minimal foreign body responses and tracking of stable isolated single neuron potentials in freely moving mice over 6 months following implantation.

scholarly journals Cerebral derailment after myocardial infarct: mechanisms and effects of the signaling from the ischemic heart to brain

2021 ◽  
Author(s):  
Paolo Gelosa ◽  
Laura Castiglioni ◽  
Joanna Rzemieniec ◽  
Majeda Muluhie ◽  
Marina Camera ◽  
...  
Keyword(s):  
Clinical Evidence ◽  
Heart Diseases ◽  
Myocardial Infarct ◽  
Cardiovascular Complications ◽  
Ischemic Heart ◽  
Underlying Mechanisms ◽  
Anxiety Depression ◽  
The Brain ◽  
A Current

AbstractMyocardial infarction (MI) is the leading cause of death among ischemic heart diseases and is associated with several long-term cardiovascular complications, such as angina, re-infarction, arrhythmias, and heart failure. However, MI is frequently accompanied by non-cardiovascular multiple comorbidities, including brain disorders such as stroke, anxiety, depression, and cognitive impairment. Accumulating experimental and clinical evidence suggests a causal relationship between MI and stroke, but the precise underlying mechanisms have not yet been elucidated. Indeed, the risk of stroke remains a current challenge in patients with MI, in spite of the improvement of medical treatment among this patient population has reduced the risk of stroke. In this review, the effects of the signaling from the ischemic heart to the brain, such as neuroinflammation, neuronal apoptosis, and neurogenesis, and the possible actors mediating these effects, such as systemic inflammation, immunoresponse, extracellular vesicles, and microRNAs, are discussed.

scholarly journals How repair-or-dispose decisions under stress can initiate disease progression

2019 ◽  
Author(s):  
Andreas Nold ◽  
Danylo Batulin ◽  
Katharina Birkner ◽  
Stefan Bittner ◽  
Tatjana Tchumatchenko
Keyword(s):  
Tissue Damage ◽  
Decision Making Process ◽  
Biological Functions ◽  
Short Term ◽  
Damage Propagation ◽  
Underlying Mechanisms ◽  
The Brain ◽  
Insight Into ◽  
Conflicting Goals

AbstractGlia, the helper cells of the brain, are essential in maintaining neural resilience across time and varying challenges: By reacting to changes in neuronal health glia carefully balance repair or disposal of injured neurons to prevent further tissue damage. Malfunction of these interactions is implicated in many neurodegenerative diseases. Reductionist models with a minimal number of parameters provide the opportunity to gain insight into biological functions and inform experimental designs. We introduce such a model that mimics long-term implications of repair-or-dispose decisions. Depending on the functionality of the decision-making process, the model assumes four distinct tissue states: healthy, challenged, primed tissue at risk of acute damage propagation, and chronic neurodegeneration. These states of the model correspond to the progression stages observed in the most common neurodegenerative conditions. The underlying mechanisms are in agreement with experimental observations of glia-neuron crosstalk and reproduce a homeostatic balance between repairing and damage-inducing reactions. The model suggests that the onset of neurodegeneration results from a tug-of-war between two conflicting goals: short-term resilience to stressors vs long-term prevention of tissue damage.

scholarly journals Role of Exosomes in Cancer-Related Cognitive Impairment

2020 ◽  
Vol 21 (8) ◽  
pp. 2755 ◽  
Author(s):  
Yong Qin Koh ◽  
Chia Jie Tan ◽  
Yi Long Toh ◽  
Siu Kwan Sze ◽  
Han Kiat Ho ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Functioning ◽  
Cell Communication ◽  
Clear Understanding ◽  
Functional Changes ◽  
Patients With Cancer ◽  
Neurological Processes ◽  
Underlying Mechanisms ◽  
Exocytic Pathway ◽  
The Brain

A decline in cognitive function following cancer treatment is one of the most commonly reported post-treatment symptoms among patients with cancer and those in remission, and include memory, processing speed, and executive function. A clear understanding of cognitive impairment as a result of cancer and its therapy can be obtained by delineating structural and functional changes using brain imaging studies and neurocognitive assessments. There is also a need to determine the underlying mechanisms and pathways that impact the brain and affect cognitive functioning in cancer survivors. Exosomes are small cell-derived vesicles formed by the inward budding of multivesicular bodies, and are released into the extracellular environment via an exocytic pathway. Growing evidence suggests that exosomes contribute to various physiological and pathological conditions, including neurological processes such as synaptic plasticity, neuronal stress response, cell-to-cell communication, and neurogenesis. In this review, we summarize the relationship between exosomes and cancer-related cognitive impairment. Unraveling exosomes’ actions and effects on the microenvironment of the brain, which impacts cognitive functioning, is critical for the development of exosome-based therapeutics for cancer-related cognitive impairment.

scholarly journals Active Life for Brain Health: A Narrative Review of the Mechanism Underlying the Protective Effects of Physical Activity on the Brain

2021 ◽  
Vol 13 ◽  
Author(s):  
Hiroyuki Umegaki ◽  
Takashi Sakurai ◽  
Hidenori Arai
Keyword(s):  
Physical Activity ◽  
Brain Volume ◽  
Clear Understanding ◽  
Protective Effects ◽  
Brain Health ◽  
Beneficial Effects ◽  
Active Life ◽  
Two Factors ◽  
Underlying Mechanisms ◽  
The Brain

A growing body of evidence clearly indicates the beneficial effects of physical activity (PA) on cognition. The importance of PA is now being reevaluated due to the increase in sedentary behavior in older adults during the COVID-19 pandemic. Although many studies in humans have revealed that PA helps to preserve brain health, the underlying mechanisms have not yet been fully elucidated. In this review, which mainly focuses on studies in humans, we comprehensively summarize the mechanisms underlying the beneficial effects of PA or exercise on brain health, particularly cognition. The most intensively studied mechanisms of the beneficial effects of PA involve an increase in brain-derived neurotrophic factor (BDNF) and preservation of brain volume, especially that of the hippocampus. Nonetheless, the mutual associations between these two factors remain unclear. For example, although BDNF presumably affects brain volume by inhibiting neuronal death and/or increasing neurogenesis, human data on this issue are scarce. It also remains to be determined whether PA modulates amyloid and tau metabolism. However, recent advances in blood-based biomarkers are expected to help elucidate the beneficial effects of PA on the brain. Clinical data suggest that PA functionally modulates cognition independently of neurodegeneration, and the mechanisms involved include modulation of functional connectivity, neuronal compensation, neuronal resource allocation, and neuronal efficiency. However, these mechanisms are as yet not fully understood. A clear understanding of the mechanisms involved could help motivate inactive persons to change their behavior. More accumulation of evidence in this field is awaited.

The Acute Effect of Alcohol on Various Memory Processes

2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál
Keyword(s):  
Low Dose ◽  
Short Term Memory ◽  
Acute Effect ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Processes ◽  
Different Types ◽  
The Brain ◽  
Legal Consequences

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.

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