Recombinant Alphavirus-Mediated Expression of Ion Channels and Receptors in the Brain

2016 ◽  
pp. 77-97 ◽  
Author(s):  
Markus U. Ehrengruber ◽  
Kenneth Lundstrom
Keyword(s):  
Ion Channels ◽  
The Brain

Channeling Force in the Brain: Mechanosensitive Ion Channels Choreograph Mechanics and Malignancies

2021 ◽  
Author(s):  
Ali Momin ◽  
Shahrzad Bahrampour ◽  
Hyun-Kee Min ◽  
Xin Chen ◽  
Xian Wang ◽  
...  
Keyword(s):  
Ion Channels ◽  
Mechanosensitive Ion Channels ◽  
The Brain

scholarly journals Ion Channels as New Attractive Targets to Improve Re-Myelination Processes in the Brain

2021 ◽  
Vol 22 (14) ◽  
pp. 7277
Author(s):  
Federica Cherchi ◽  
Irene Bulli ◽  
Martina Venturini ◽  
Anna Maria Pugliese ◽  
Elisabetta Coppi
Keyword(s):  
Ion Channels ◽  
Demyelinating Disease ◽  
Oligodendrocyte Progenitor Cells ◽  
Target Groups ◽  
Synaptic Inputs ◽  
Drug Actions ◽  
The Central Nervous System ◽  
Therapeutic Mechanisms ◽  
Voltage Gated Channels ◽  
The Brain

Multiple sclerosis (MS) is the most demyelinating disease of the central nervous system (CNS) characterized by neuroinflammation. Oligodendrocyte progenitor cells (OPCs) are cycling cells in the developing and adult CNS that, under demyelinating conditions, migrate to the site of lesions and differentiate into mature oligodendrocytes to remyelinate damaged axons. However, this process fails during disease chronicization due to impaired OPC differentiation. Moreover, OPCs are crucial players in neuro-glial communication as they receive synaptic inputs from neurons and express ion channels and neurotransmitter/neuromodulator receptors that control their maturation. Ion channels are recognized as attractive therapeutic targets, and indeed ligand-gated and voltage-gated channels can both be found among the top five pharmaceutical target groups of FDA-approved agents. Their modulation ameliorates some of the symptoms of MS and improves the outcome of related animal models. However, the exact mechanism of action of ion-channel targeting compounds is often still unclear due to the wide expression of these channels on neurons, glia, and infiltrating immune cells. The present review summarizes recent findings in the field to get further insights into physio-pathophysiological processes and possible therapeutic mechanisms of drug actions.

scholarly journals Mechanismen genetischer Epilepsien

e-Neuroforum ◽  
2013 ◽  
Vol 19 (2) ◽  
Author(s):  
Ulrike Hedrich ◽  
Snezana Maljevic ◽  
Holger Lerche
Keyword(s):  
Ion Channels ◽  
Secondary Effects ◽  
Therapeutic Approaches ◽  
Neuronal Populations ◽  
The Everyday ◽  
The Common ◽  
Genetic Epilepsies ◽  
Idiopathic Epilepsies ◽  
The Brain

AbstractMechanisms of genetic epilepsies. Epilepsy is one of the most common neurological disorders. Already at the time of Hippocrates (460 - 370 BC) it was reported on as the “holy disease” (Fröscher 2004). Today it is known that an epileptic seizure is a consequence of synchronous discharges of neuronal populations in the brain, which abruptly and usually without an observ­able cause evoke involuntary behavioural dysfunction or impaired consciousness. Epilepsies can have various causes and lead to extensive implications for the everyday life of affected patients. Up to 50 % of all epilepsies are caused by genetic defects, in particular the so-called idiopathic epilepsies which occur without easily observable structural alterations of the brain. Genetically caused dysfunctions of neuronal ion channels play a central role in the formation of such epilepsies. The ion channels control the ion flux over the cell membrane of neurons and thus present the basis for the excitability of these neurons. Therefore, medications used for epilepsy treatment affect predominantly ion channels. However, the common anticonvulsants have limited success, not only because one third of epilepsy patients exhibits pharmacoresistance, but also because of the secondary effects which can dramatically affect their quality of life. Furthermore, current therapeutic approaches are mainly symptomatic and do not act on the epileptogenic mechanisms which are still largely unknown. In this review article we will highlight the current main topics of our research on genetically caused epilepsies, their pathomechanisms and therapeutic options.

Calcium-Permeable Ion Channels in Pain Signaling

2014 ◽  
Vol 94 (1) ◽  
pp. 81-140 ◽  
Author(s):  
Emmanuel Bourinet ◽  
Christophe Altier ◽  
Michael E. Hildebrand ◽  
Tuan Trang ◽  
Michael W. Salter ◽  
...  
Keyword(s):  
Ion Channels ◽  
Trp Channels ◽  
Neuronal Firing ◽  
Spinal Cord Neurons ◽  
Wide Range ◽  
Pain Pathway ◽  
Channel Expression ◽  
And Function ◽  
The Brain

The detection and processing of painful stimuli in afferent sensory neurons is critically dependent on a wide range of different types of voltage- and ligand-gated ion channels, including sodium, calcium, and TRP channels, to name a few. The functions of these channels include the detection of mechanical and chemical insults, the generation of action potentials and regulation of neuronal firing patterns, the initiation of neurotransmitter release at dorsal horn synapses, and the ensuing activation of spinal cord neurons that project to pain centers in the brain. Long-term changes in ion channel expression and function are thought to contribute to chronic pain states. Many of the channels involved in the afferent pain pathway are permeable to calcium ions, suggesting a role in cell signaling beyond the mere generation of electrical activity. In this article, we provide a broad overview of different calcium-permeable ion channels in the afferent pain pathway and their role in pain pathophysiology.

scholarly journals Computational approaches to understand cardiac electrophysiology and arrhythmias

2012 ◽  
Vol 303 (7) ◽  
pp. H766-H783 ◽  
Author(s):  
Byron N. Roberts ◽  
Pei-Chi Yang ◽  
Steven B. Behrens ◽  
Jonathan D. Moreno ◽  
Colleen E. Clancy
Keyword(s):  
Ion Channels ◽  
Electrical Activity ◽  
Cardiac Electrophysiology ◽  
Cardiac Activity ◽  
Computational Approaches ◽  
Cardiac Electrical Activity ◽  
Whole Heart ◽  
Arrhythmia Therapy ◽  
Emergent Behaviors ◽  
The Brain

Cardiac rhythms arise from electrical activity generated by precisely timed opening and closing of ion channels in individual cardiac myocytes. These impulses spread throughout the cardiac muscle to manifest as electrical waves in the whole heart. Regularity of electrical waves is critically important since they signal the heart muscle to contract, driving the primary function of the heart to act as a pump and deliver blood to the brain and vital organs. When electrical activity goes awry during a cardiac arrhythmia, the pump does not function, the brain does not receive oxygenated blood, and death ensues. For more than 50 years, mathematically based models of cardiac electrical activity have been used to improve understanding of basic mechanisms of normal and abnormal cardiac electrical function. Computer-based modeling approaches to understand cardiac activity are uniquely helpful because they allow for distillation of complex emergent behaviors into the key contributing components underlying them. Here we review the latest advances and novel concepts in the field as they relate to understanding the complex interplay between electrical, mechanical, structural, and genetic mechanisms during arrhythmia development at the level of ion channels, cells, and tissues. We also discuss the latest computational approaches to guiding arrhythmia therapy.

Norbornane-induced changes in the density of chloride-ion channels in the brain of rodents

1996 ◽  
Vol 122 (1) ◽  
pp. 660-662
Author(s):  
A. I. Golovko ◽  
G. A. Sofronov ◽  
T. V. Klyuntina ◽  
S. G. Suftin ◽  
L. A. Garbuz
Keyword(s):  
Ion Channels ◽  
Chloride Ion ◽  
Induced Changes ◽  
Chloride Ion Channels ◽  
The Brain

scholarly journals Resting easy with a sleep regulator

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
William J Giardino ◽  
Luis de Lecea
Keyword(s):  
Ion Channels ◽  
Potassium Ion ◽  
Potassium Ion Channels ◽  
The Brain

Potassium ion channels in a subset of neurons in the brain of zebrafish may have a role in promoting sleep.

Nicotinic Acetylcholine Receptors

2018 ◽  
Author(s):  
Roger L. Papke
Keyword(s):  
Ion Channels ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Neuromuscular Junctions ◽  
Cognitive Disorders ◽  
The Body ◽  
Nicotinic Acetylcholine ◽  
Synaptic Receptors ◽  
The Central Nervous System ◽  
The Brain

Acetylcholine, exquisitely evolved as a neurotransmitter, is made and released by the neurons that take the integrated output of the central nervous system throughout the body. At both neuromuscular junctions and autonomic ganglia, acetylcholine activates synaptic ion channels that take their name from the plant alkaloid nicotine, which is a mimic of the natural neurotransmitter. This chapter begins with the scientific discoveries related to the nicotinic acetylcholine receptors (nAChR) of the neuromuscular junction and how resulting insights led to an understanding of the fundamentals of synaptic transmission. The nAChR are one member of a superfamily of ligand-gated ion channels, and although in the brain excitatory neurotransmission is mediated by another family of synaptic receptors that are gated by glutamate, nicotinic receptors are important modulators of brain function and significant targets for drug development. In the brain, nAChR are targets for cognitive disorders and, tragically, responsible for tobacco addiction.

Transient Receptor Potential (TRP) Channels in the Brain: the Good and the Ugly

2012 ◽  
Vol 20 (3) ◽  
pp. 343-355 ◽  
Author(s):  
Bernd Nilius
Keyword(s):  
Ion Channels ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Sensory Function ◽  
Short Paper ◽  
The Novel ◽  
Cellular Functions ◽  
Transient Receptor ◽  
The Brain

The ‘transient receptor potential’ (TRP) multigene family encodes sixspan membrane proteins that function as ion channels in mostly tetrameric structures. Members of this family are conserved from yeast, worm, fly to invertebrate, vertebrate and man. These channels have been stigmatized to function only as cell sensors occupied by sensory function. It turns out that TRP channels fulfil a plethora of cellular functions, including non-sensory functions in our brain. This short paper will highlight the advent of novel ion channels in the brain serving different functions and being significantly involved in the genesis of multiple diseases. We will certainly witness a plethora of the novel roles of this protein family in physiological and pathophysiological functions in our central nervous system.

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