Neuroplasticity Induced by Exercise
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Targeting Neuroplasticity for Balance Or Gait Deficit
August 2021 Volume 1 Issue 8 CADTH Horizon Scan The Portable Neuromodulation Stimulator: Targeting Neuroplasticity for Balance or Gait Deficit Health Technology Update Authors: Sara D. Khangura ISSN: 2563-6596 Disclaimer: The information in this document is intended to help Canadian health care decision-makers, health care professionals, health systems leaders, and policy-makers make well-informed decisions and thereby improve the quality of health care services. While patients and others may access this document, the document is made available for informational purposes only and no representations or warranties are made with respect to its fitness for any particular purpose. The information in this document should not be used as a substitute for professional medical advice or as a substitute for the application of clinical judgment in respect of the care of a particular patient or other professional judgment in any decision-making process. The Canadian Agency for Drugs and Technologies in Health (CADTH) does not endorse any information, drugs, therapies, treatments, products, processes, or services. While care has been taken to ensure that the information prepared by CADTH in this document is accurate, complete, and up to date as at the applicable date the material was first published by CADTH, CADTH does not make any guarantees to that effect. CADTH does not guarantee and is not responsible for the quality, currency, propriety, accuracy, or reasonableness of any statements, information, or conclusions contained in any third-party materials used in preparing this document. The views and opinions of third parties published in this document do not necessarily state or reflect those of CADTH. -
The Creation of Neuroscience
The Creation of Neuroscience The Society for Neuroscience and the Quest for Disciplinary Unity 1969-1995 Introduction rom the molecular biology of a single neuron to the breathtakingly complex circuitry of the entire human nervous system, our understanding of the brain and how it works has undergone radical F changes over the past century. These advances have brought us tantalizingly closer to genu- inely mechanistic and scientifically rigorous explanations of how the brain’s roughly 100 billion neurons, interacting through trillions of synaptic connections, function both as single units and as larger ensem- bles. The professional field of neuroscience, in keeping pace with these important scientific develop- ments, has dramatically reshaped the organization of biological sciences across the globe over the last 50 years. Much like physics during its dominant era in the 1950s and 1960s, neuroscience has become the leading scientific discipline with regard to funding, numbers of scientists, and numbers of trainees. Furthermore, neuroscience as fact, explanation, and myth has just as dramatically redrawn our cultural landscape and redefined how Western popular culture understands who we are as individuals. In the 1950s, especially in the United States, Freud and his successors stood at the center of all cultural expla- nations for psychological suffering. In the new millennium, we perceive such suffering as erupting no longer from a repressed unconscious but, instead, from a pathophysiology rooted in and caused by brain abnormalities and dysfunctions. Indeed, the normal as well as the pathological have become thoroughly neurobiological in the last several decades. In the process, entirely new vistas have opened up in fields ranging from neuroeconomics and neurophilosophy to consumer products, as exemplified by an entire line of soft drinks advertised as offering “neuro” benefits. -
Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: a Steered-Glutamatergic Perspective
brain sciences Review Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective Amjad H. Bazzari * and H. Rheinallt Parri School of Life and Health Sciences, Aston University, Birmingham B4 7ET, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-(0)1212044186 Received: 7 October 2019; Accepted: 29 October 2019; Published: 31 October 2019 Abstract: The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights into neuronal encoding processes as molecular substrates of not only learning and memory but potentially other sensory, motor and behavioural functions that reflect previous experience. However, one key element receiving little attention in the study of synaptic plasticity is the role of neuromodulators, which are known to orchestrate neuronal activity on brain-wide, network and synaptic scales. We aim to review current evidence on the mechanisms by which certain modulators, namely dopamine, acetylcholine, noradrenaline and serotonin, control synaptic plasticity induction through corresponding metabotropic receptors in a pathway-specific manner. Lastly, we propose that neuromodulators control plasticity outcomes through steering glutamatergic transmission, thereby gating its induction and maintenance. Keywords: neuromodulators; synaptic plasticity; learning; memory; LTP; LTD; GPCR; astrocytes 1. Introduction A huge emphasis has been put into discovering the molecular pathways that govern synaptic plasticity induction since it was first discovered [1], which markedly improved our understanding of the functional aspects of plasticity while introducing a surprisingly tremendous complexity due to numerous mechanisms involved despite sharing common “glutamatergic” mediators [2]. -
Brain Stimulation and Neuroplasticity
brain sciences Editorial Brain Stimulation and Neuroplasticity Ulrich Palm 1,2,* , Moussa A. Chalah 3,4 and Samar S. Ayache 3,4 1 Department of Psychiatry and Psychotherapy, Klinikum der Universität München, 80336 Munich, Germany 2 Medical Park Chiemseeblick, Rasthausstr. 25, 83233 Bernau-Felden, Germany 3 EA4391 Excitabilité Nerveuse & Thérapeutique, Université Paris Est Créteil, 94010 Créteil, France; [email protected] (M.A.C.); [email protected] (S.S.A.) 4 Service de Physiologie—Explorations Fonctionnelles, Hôpital Henri Mondor, Assistance Publique—Hôpitaux de Paris, 94010 Créteil, France * Correspondence: [email protected] Electrical or magnetic stimulation methods for brain or nerve modulation have been widely known for centuries, beginning with the Atlantic torpedo fish for the treatment of headaches in ancient Greece, followed by Luigi Galvani’s experiments with frog legs in baroque Italy, and leading to the interventional use of brain stimulation methods across Europe in the 19th century. However, actual research focusing on the development of tran- scranial magnetic stimulation (TMS) is beginning in the 1980s and transcranial electrical brain stimulation methods, such as transcranial direct current stimulation (tDCS), tran- scranial alternating current stimulation (tACS), and transcranial random noise stimulation (tRNS), are investigated from around the year 2000. Today, electrical, or magnetic stimulation methods are used for either the diagnosis or exploration of neurophysiology and neuroplasticity functions, or as a therapeutic interven- tion in neurologic or psychiatric disorders (i.e., structural damage or functional impairment of central or peripheral nerve function). This Special Issue ‘Brain Stimulation and Neuroplasticity’ gathers ten research articles Citation: Palm, U.; Chalah, M.A.; and two review articles on various magnetic and electrical brain stimulation methods in Ayache, S.S. -
Review Article Mechanisms of Cerebrovascular Autoregulation and Spreading Depolarization-Induced Autoregulatory Failure: a Literature Review
Int J Clin Exp Med 2016;9(8):15058-15065 www.ijcem.com /ISSN:1940-5901/IJCEM0026645 Review Article Mechanisms of cerebrovascular autoregulation and spreading depolarization-induced autoregulatory failure: a literature review Gang Yuan1*, Bingxue Qi2*, Qi Luo1 1Department of Neurosurgery, The First Hospital of Jilin University, Changchun, China; 2Department of Endocrinology, Jilin Province People’s Hospital, Changchun, China. *Equal contributors. Received February 25, 2016; Accepted June 4, 2016; Epub August 15, 2016; Published August 30, 2016 Abstract: Cerebrovascular autoregulation maintains brain hemostasis via regulating cerebral flow when blood pres- sure fluctuation occurs. Monitoring autoregulation can be achieved by transcranial Doppler ultrasonography, the pressure reactivity index (PRx) can serve as a secondary index of vascular deterioration, and outcome and prognosis are assessed by the low-frequency PRx. Although great changes in arterial blood pressure (ABP) occur, complex neu- rogenic, myogenic, endothelial, and metabolic mechanisms are involved to maintain the flow within its narrow limits. The steady association between ABP and cerebral blood flow (CBF) reflects static cerebral autoregulation (CA). Spreading depolarization (SD) is a sustained depolarization of neurons with concomitant pronounced breakdown of ion gradients, which originates in patients with brain ischemia, hemorrhage, trauma, and migraine. It is character- ized by the propagation of an extracellular negative potential, followed by an increase in O2 and glucose consump- tion. Immediately after SD, CA is transiently impaired but is restored after 35 min. This process initiates a cascade of pathophysiological mechanisms, leading to neuronal damage and loss if consecutive events are evoked. The clini- cal application of CA in regulating CBF is to dilate the cerebral arteries as a compensatory mechanism during low blood pressure, thus protecting the brain from ischemia. -
How Drugs Affect the Brain and Medication‐Assisted Treatment
How Drugs Affect the Brain And Medication‐Assisted Treatment Presented by Carl M. Dawson, M.S., MAC, LPC, Q‐SAP Learning Objectives After completing this section, participants will be able to: • Understand the scientific modalities neuroscientists use when studying addictions (Bio‐Psycho‐Social model of addictions, genetics and neuroplasticity) • Explore basic facts regarding the development and function of the human brain • Identify three “Feel Good” chemicals released by the brain (dopamine, serotonin, norepinephrine) • Discuss how addictive behaviors and drugs routinely “hijack” the human brain How Neuroscientists Study Addiction • All addictions (alcohol, drugs, gambling, porn, video games, food) activate the same neurological pleasure (reward) routes (pathways) in the brain • Addictionology uses the “Bio‐Psycho‐Social” model when studying addictions • Research has identified a strong genetic basis for all addiction behaviors (There is no single “addiction” gene, there are approx. 90 genes associated with addictions) How Neuroscientists Study Addiction • Remember: “Our genetics load the gun, but the environment pulls the trigger” • Addictions aren't only hijacking the brain’s activities but they have the ability to modify the neurological structures and activities of the brain (neuroplasticity) Neuroplasticity: is a term used in the field of neuroscience that defines the brain's ability to adapt, adjust and change based upon the strength and reward of the experience ‐ “Neurons that Fire Together, Wire Together” Donald O. Hebb (1904‐1985) Basic Facts and Regions of the Human Brain The average human brain weighs approximately three (3 lbs.) pounds, consisting of 60% protein (fat), possessing approximately 85 to 110 billion neurons and produces 15 watts of electricity, traveling at a speed of one‐half to 250 miles per hour Approximate Ages of the Human Brain 7,000 7,000 480,000 6 to 10 mil. -
The Brain That Changes Itself
The Brain That Changes Itself Stories of Personal Triumph from the Frontiers of Brain Science NORMAN DOIDGE, M.D. For Eugene L. Goldberg, M.D., because you said you might like to read it Contents 1 A Woman Perpetually Falling . Rescued by the Man Who Discovered the Plasticity of Our Senses 2 Building Herself a Better Brain A Woman Labeled "Retarded" Discovers How to Heal Herself 3 Redesigning the Brain A Scientist Changes Brains to Sharpen Perception and Memory, Increase Speed of Thought, and Heal Learning Problems 4 Acquiring Tastes and Loves What Neuroplasticity Teaches Us About Sexual Attraction and Love 5 Midnight Resurrections Stroke Victims Learn to Move and Speak Again 6 Brain Lock Unlocked Using Plasticity to Stop Worries, OPsessions, Compulsions, and Bad Habits 7 Pain The Dark Side of Plasticity 8 Imagination How Thinking Makes It So 9 Turning Our Ghosts into Ancestors Psychoanalysis as a Neuroplastic Therapy 10 Rejuvenation The Discovery of the Neuronal Stem Cell and Lessons for Preserving Our Brains 11 More than the Sum of Her Parts A Woman Shows Us How Radically Plastic the Brain Can Be Appendix 1 The Culturally Modified Brain Appendix 2 Plasticity and the Idea of Progress Note to the Reader All the names of people who have undergone neuroplastic transformations are real, except in the few places indicated, and in the cases of children and their families. The Notes and References section at the end of the book includes comments on both the chapters and the appendices. Preface This book is about the revolutionary discovery that the human brain can change itself, as told through the stories of the scientists, doctors, and patients who have together brought about these astonishing transformations. -
Michael M. Merzenich
Michael M. Merzenich BORN: Lebanon, Oregon May 15, 1942 EDUCATION: Public Schools, Lebanon, Oregon (1924–1935) University of Portland (Oregon), B.S. (1965) Johns Hopkins University, Ph.D. (1968) University of Wisconsin Postdoctoral Fellow (1968–1971) APPOINTMENTS: Assistant and Associate Professor, University of California at San Francisco (1971–1980) Francis A. Sooy Professor, University of California at San Francisco (1981–2008) President and CEO, Scientifi c Learning Corporation (1995–1996) Chief Scientifi c Offi cer, Scientifi c Learning Corporation (1996–2003) Chief Scientifi c Offi cer, Posit Science Corporation (2004–present) President and CEO, Brain Plasticity Institute (2008–present) HONORS AND AWARDS (SELECTED): Cortical Discoverer Prize, Cajal Club (1994) IPSEN Prize (Paris, 1997) Zotterman Prize (Stockholm, 1998) Craik Prize (Cambridge, 1998) National Academy of Sciences, U.S.A. (1999) Lashley Award, American Philosophical Society (1999) Thomas Edison Prize (Menlo Park, NJ, 2000) American Psychological Society Distinguished Scientifi c Contribution Award (2001) Zülch Prize, Max-Planck Society (2002) Genius Award, Cure Autism Now (2002) Purkinje Medal, Czech Academy (2003) Neurotechnologist of the Year (2006) Institute of Medicine (2008) Michael M. Merzenich has conducted studies defi ning the functional organization of the auditory and somatosensory nervous systems. Initial models of a commercially successful cochlear implant (now distributed by Boston Scientifi c) were developed in his laboratory. Seminal research on cortical plasticity conducted in his laboratory contributed to our current understanding of the phenomenology of brain plasticity across the human lifetime. Merzenich extended this research into the commercial world by co-founding three brain plasticity-based therapeutic software companies (Scientifi c Learning, Posit Science, and Brain Plasticity Institute). -
Protocol Title: Cracking Addiction
Protocol Title: Cracking addiction: does BRAIN Stimulation-induced neuroplasticity reverse prefrontal cortex hypoactivity in cocaine and neW stImulanTs addiCtion in Humans (BRAIN SWITCH)? Abbreviated title: Transcranial Magnetic Stimulation for Cocaine Addiction Protocol Number: 1496 Date of Approval: June 29, 2017 Principal Investigator Name, Degree Branch/Institute Phone E-mail Massimo di Dept. of +39 0871358928 [email protected] Giannantonio, Neuroscience, MD Imaging and Clinical Sciences (ITAB) – University of Chieti Co- Principal Investigator Name, Degree Branch/Institute Phone E-mail Giovanni Dept. of +39 08713556914 [email protected] Martinotti, M.D., Neuroscience, Ph.D. Imaging and Clinical Sciences (ITAB) – University of Chieti Villa Maria Pia Clinic - Rome Associate Investigators Name, Degree Branch/Institute Phone E-mail Chiara MNB/NINDS +39 3281264713 [email protected] Montemitro, M.D. Mauro MNB/NINDS +39 3391979487 [email protected] Pettorruso, M.D. Lamberto Office of +39 3474727282 [email protected] Manzoli, Ph.D. Biostatistics/ University of Ferrara Referral Contact Name, Degree Branch/Institute Phone E-mail Mauro Pettorruso, MNB/NINDS +39 3391979487 [email protected] M.D. 1 Accountable Investigator Name, Degree Branch/Institute Phone E-mail Giovanni Dept. of +39 08713556914 [email protected] Martinotti, M.D., Neuroscience, Ph.D. Imaging and Clinical Sciences (ITAB) – University of Chieti Villa Maria Pia Clinic - Rome 2 A. Précis Background: Cocaine use disorder (CUD) are a major public health concern, associated with high relapse rates, significant disability and substantial mortality. In Italy, it has been recently estimated that up to 4.8% of subjects between the ages of 15-64 have assumed cocaine at least once, whereas 1.3% subjects currently have a diagnosis of CUD. -
Gut Microbiota and Neuroplasticity
cells Review Gut Microbiota and Neuroplasticity Julia Murciano-Brea 1,2, Martin Garcia-Montes 1,2, Stefano Geuna 3 and Celia Herrera-Rincon 1,2,* 1 Department of Biodiversity, Ecology & Evolution, Biomathematics Unit, Complutense University of Madrid, 28040 Madrid, Spain; [email protected] (J.M.-B.); [email protected] (M.G.-M.) 2 Modeling, Data Analysis and Computational Tools for Biology Research Group, Complutense University of Madrid, 28040 Madrid, Spain 3 Department of Clinical and Biological Sciences, School of Medicine, University of Torino, 10124 Torino, Italy; [email protected] * Correspondence: [email protected]; Tel.: +34-91394-4888 Abstract: The accumulating evidence linking bacteria in the gut and neurons in the brain (the microbiota–gut–brain axis) has led to a paradigm shift in the neurosciences. Understanding the neurobiological mechanisms supporting the relevance of actions mediated by the gut microbiota for brain physiology and neuronal functioning is a key research area. In this review, we discuss the literature showing how the microbiota is emerging as a key regulator of the brain’s function and behavior, as increasing amounts of evidence on the importance of the bidirectional communication between the intestinal bacteria and the brain have accumulated. Based on recent discoveries, we suggest that the interaction between diet and the gut microbiota, which might ultimately affect the brain, represents an unprecedented stimulus for conducting new research that links food and mood. We also review the limited work in the clinical arena to date, and we propose novel approaches for deciphering the gut microbiota–brain axis and, eventually, for manipulating this relationship to boost mental wellness. -
Long-Term Potentiation and Long-Term Depression of Primary Afferent Neurotransmission in the Rat Spinal Cord
The Journal of Neuroscience, December 1993. 13(12): 52286241 Long-term Potentiation and Long-term Depression of Primary Afferent Neurotransmission in the Rat Spinal Cord M. RandiC, M. C. Jiang, and R. Cerne Department of Veterinary Physiology and Pharmacology, Iowa State University, Ames, Iowa 50011 Synaptic transmission between dorsal root afferents and ably mediated by L-glutamate, or a related amino acid (Jahr and neurons in the superficial laminae of the spinal dorsal horn Jessell, 1985; Gerber and RandiC, 1989; Kangrga and Randic, (laminae I-III) was examined by intracellular recording in a 1990, 1991; Yoshimura and Jessell, 1990; Ceme et al., 1991). transverse slice preparation of rat spinal cord. Brief high- Neuronal excitatory amino acids (EAAs), including gluta- frequency electrical stimulation (300 pulses at 100 Hz) of mate, produce their effects through two broad categoriesof re- primary afferent fibers produced a long-term potentiation ceptors called ionotropic and metabotropic (Honor6 et al., 1988; (LTP) or a long-term depression (LTD) of fast (monosynaptic Schoepp et al., 1991; Watkins et al., 1990). The ionotropic and polysynaptic) EPSPs in a high proportion of dorsal horn NMDA, a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic neurons. Both the AMPA and the NMDA receptor-mediated acid (AMPA)/quisqualate (QA), and kainate receptors directly components of synaptic transmission at the primary afferent regulate the opening of ion channelsto Na, K+, and, in the case synapses with neurons in the dorsal horn can exhibit LTP of NMDA receptors, CaZ+as well (Mayer and Westbrook, 1987; and LTD of the synaptic responses. In normal and neonatally Ascher and Nowak, 1987). -
Neural Plasticity in the Brain During Neuropathic Pain
biomedicines Review Neural Plasticity in the Brain during Neuropathic Pain Myeong Seong Bak 1, Haney Park 1 and Sun Kwang Kim 1,2,* 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] (M.S.B.); [email protected] (H.P.) 2 Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea * Correspondence: [email protected]; Tel.: +82-2-961-0491 Abstract: Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and mainte- nance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas. Keywords: neuropathic pain; neural plasticity; primary somatosensory cortex; anterior cingulate cortex; periaqueductal grey; basal ganglia Citation: Bak, M.S.; Park, H.; Kim, S.K.