Mechanisms of Action of Noradrenaline in the Brain

1985 ◽  
pp. 235-239 ◽  
Author(s):  
M. Segal
Keyword(s):  
Mechanisms Of Action ◽  
The Brain

Acupuncture for Gastrointestinal Disorders

2019 ◽  
pp. 229-254
Author(s):  
Malcolm B. Taw ◽  
Andrew Shubov
Keyword(s):  
Gastric Emptying ◽  
Chinese Medicine ◽  
Vagal Tone ◽  
Evidence Base ◽  
Mechanisms Of Action ◽  
Current Evidence ◽  
Gastrointestinal Disorders ◽  
Current Evidence Base ◽  
The Brain ◽  
East West

This chapter provides an introduction to acupuncture, elucidates known neurobiological mechanisms of action, and summarizes the current evidence base for the use of acupuncture in the treatment of various gastrointestinal (GI) disorders. It reviews how acupuncture can increase esophageal and GI motility, reduce transient lower esophageal sphincter relaxations, stimulate gastric emptying, accelerate antral contractions, regulate neurohormonal mediators, promote autonomic and vagal tone, and modulate different regions of the brain-gut-microbiota axis. The therapeutic rationale for acupuncture as well as basic theories and concepts from a traditional Chinese medicine (TCM) perspective are also described. This chapter concludes with a discussion about the potential therapeutic combination of integrative East-West medicine to treat GI disorders.

scholarly journals Pharmacological Modulators of Tau Aggregation and Spreading

2020 ◽  
Vol 10 (11) ◽  
pp. 858
Author(s):  
Antonio Dominguez-Meijide ◽  
Eftychia Vasili ◽  
Tiago Fleming Outeiro
Keyword(s):  
Tau Protein ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Mechanisms Of Action ◽  
Tau Aggregation ◽  
The Brain ◽  
Pharmacological Modulators

Tauopathies are neurodegenerative disorders characterized by the deposition of aggregates composed of abnormal tau protein in the brain. Additionally, misfolded forms of tau can propagate from cell to cell and throughout the brain. This process is thought to lead to the templated misfolding of the native forms of tau, and thereby, to the formation of newer toxic aggregates, thereby propagating the disease. Therefore, modulation of the processes that lead to tau aggregation and spreading is of utmost importance in the fight against tauopathies. In recent years, several molecules have been developed for the modulation of tau aggregation and spreading. In this review, we discuss the processes of tau aggregation and spreading and highlight selected chemicals developed for the modulation of these processes, their usefulness, and putative mechanisms of action. Ultimately, a stronger understanding of the molecular mechanisms involved, and the properties of the substances developed to modulate them, will lead to the development of safer and better strategies for the treatment of tauopathies.

Mechanisms and the Current State of Deep Brain Stimulation in Neuropsychiatry

CNS Spectrums ◽  
2003 ◽  
Vol 8 (7) ◽  
pp. 522-526 ◽  
Author(s):  
Benjamin D. Greenberg ◽  
Ali R. Rezai
Keyword(s):  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Movement Disorders ◽  
Mechanisms Of Action ◽  
Therapeutic Effects ◽  
Current State ◽  
Investigational Treatment ◽  
Preclinical And Clinical Studies ◽  
The Brain ◽  
Deep Brain

ABSTRACTDeep brain stimulation (DBS) is established as a therapy for movement disorders, and it is an investigational treatment in other neurologic conditions. DBS precisely targets neuroanatomical targets deep within the brain that are proposed to be centrally involved in the pathophysiology of some neuropsychiatric illnesses. DBS is nonablative, offering the advantages of reversibility and adjustability. This might permit therapeutic effectiveness to be enhanced or side effects to be minimized. Preclinical and clinical studies have shown effects of DBS locally, at the stimulation target, and at a distance, via actions on fibers of passage or across synapses. Although its mechanisms of action are not fully elucidated, several effects have been proposed to underlie the therapeutic effects of DBS in movement disorders, and potentially in other conditions as well. The mechanisms of action of DBS are the focus of active investigation in a number of clinical and preclinical laboratories. As in severe movement disorders, DBS may offer a degree of hope for patients with intractable neuropsychiatric illness. It is already clear that research intended to realize this potential will require a very considerable commitment of resources, energy, and time across disciplines including psychiatry, neurosurgery, neurology, neuropsychology, bioengineering, and bioethics. These investigations should proceed cautiously.

scholarly journals Cortical mechanisms of action selection: the affordance competition hypothesis

2007 ◽  
Vol 362 (1485) ◽  
pp. 1585-1599 ◽  
Author(s):  
Paul Cisek
Keyword(s):  
Cerebral Cortex ◽  
Action Plan ◽  
Sensory Information ◽  
Natural World ◽  
Mechanisms Of Action ◽  
Competition Hypothesis ◽  
The World ◽  
Neurophysiological Data ◽  
Single Response ◽  
The Brain

At every moment, the natural world presents animals with two fundamental pragmatic problems: selection between actions that are currently possible and specification of the parameters or metrics of those actions. It is commonly suggested that the brain addresses these by first constructing representations of the world on which to build knowledge and make a decision, and then by computing and executing an action plan. However, neurophysiological data argue against this serial viewpoint. In contrast, it is proposed here that the brain processes sensory information to specify, in parallel, several potential actions that are currently available. These potential actions compete against each other for further processing, while information is collected to bias this competition until a single response is selected. The hypothesis suggests that the dorsal visual system specifies actions which compete against each other within the fronto-parietal cortex, while a variety of biasing influences are provided by prefrontal regions and the basal ganglia. A computational model is described, which illustrates how this competition may take place in the cerebral cortex. Simulations of the model capture qualitative features of neurophysiological data and reproduce various behavioural phenomena.

scholarly journals Does Maternal Arachidonic Acid Influence the Neurodevelopmental Effects of Docosahexaenoic Acid?

2021 ◽  
Author(s):  
Sanjay Basak ◽  
Rahul Mallick ◽  
Antara Banerjee ◽  
Surajit Pathak ◽  
Asim K. Duttaroy
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Cerebral Cortex ◽  
Docosahexaenoic Acid ◽  
Mechanisms Of Action ◽  
Structural Function ◽  
Rapid Rate ◽  
Functional Roles ◽  
The Brain ◽  
Neurodevelopmental Effects

During the last trimester of gestation and for the first 18 months after birth, docosahexaenoic acid,22:6n-3 (DHA) and arachidonic acid,20:4n-6 (ARA) deposited within the cerebral cortex at a rapid rate. The mode of action of these two fatty acids and their derivatives at different structural-function and signaling pathways levels in the brain have been continuously emanating. These fatty acids are also involved in various brain developmental processes; however, their mechanisms of action are not yet well known. Recent data suggest that there may be a need for a balanced proportion of ARA and DHA in infant formula due to their complementary benefits. This review describes the importance of maternal preferential transfer of ARA and DHA to support the infant's optimal brain development and growth and functional roles in the brain.

NITRIC OXIDE IN BLOOD VESSELS AND BRAIN IN NORMAL AND IN HYPOXIA / ISCHEMIA

2021 ◽  
Author(s):  
Valentin Reutov ◽  
◽  
Elena Sorokina ◽  
Keyword(s):  
Nitric Oxide ◽  
Blood Vessels ◽  
Mechanisms Of Action ◽  
Physiological Conditions ◽  
Hypoxia Ischemia ◽  
The Brain

The review presents an analysis and generalization of literature data and the results of our own studies on the mechanisms of action of nitric oxide on blood vessels and the brain under normal physiological conditions, as well as during hypoxia / ischemia.

Fundamental Psychotropic Drug Structures and Mechanisms

2018 ◽  
pp. 29-52
Author(s):  
S. Nassir Ghaemi
Keyword(s):  
Psychotropic Drug ◽  
Chemical Structure ◽  
A Priori ◽  
Mechanisms Of Action ◽  
Clinical Effects ◽  
Clinical Judgments ◽  
Drug Classes ◽  
Similarities And Differences ◽  
Basic Ideas ◽  
The Brain

A few basic ideas about fundamental psychotropic drug structures and mechanisms can be stated: Two drugs that are very similar in pharmacological structure can differ wildly in clinical effect. Two drugs that differ markedly in pharmacological structure can exert similar clinical effects. Understanding pharmacological structure is most useful for appreciating classification with similar agents structurally. Clinical conclusions should be based, however, on clinical confirmation or refutation of similarity of effect to other drugs in the same class. No a priori clinical judgments should be made based primarily on pharmacological structure. Structure is a beginning point to understand what drugs do, not the end. This chapter details the pharmacological structure of the main drug classes and specific agents within those drug classes. Similarities and differences of chemical structure are examined. Pharmacodynamic mechanisms of action in the brain, at the synapse and postsynaptically, are discussed.

scholarly journals Bacterial Extracellular DNA Promotes β-amyloid Aggregation

2021 ◽  
Author(s):  
George Tetz ◽  
Victor Tetz
Keyword(s):  
Protein Misfolding ◽  
Mechanisms Of Action ◽  
Extracellular Dna ◽  
Pathogenic Role ◽  
Bacterial Dna ◽  
Beta Peptide ◽  
Β Amyloid ◽  
The Brain

Alzheimer’s disease is associated with prion-like aggregation of the amyloid β (Aβ) peptide and the subsequent accumulation of misfolded neurotoxic aggregates in the brain. Therefore, it is critical to clearly identify the factors that trigger the cascade of Aβ misfolding and aggregation. Numerous studies have pointed out the association between microorganisms and their virulence factors and Alzheimer’s disease; however, their exact mechanisms of action remain unclear. Recently, we discovered a new pathogenic role of bacterial extracellular DNA, triggering the formation of misfolded Tau aggregates. In this study, we investigated the possible role of DNA extracted from different bacterial and eukaryotic cells in triggering Aβ aggregation in vitro. Interestingly, we found that the extracellular DNA of some, but not all, bacteria is an effective trigger of Aβ aggregation. Furthermore, the acceleration of Aβ nucleation and elongation can vary based on the concentration of the bacterial DNA and the bacterial strain from which this DNA had originated. Our findings suggest that bacterial extracellular DNA might play a previously overlooked role in the Aβ protein misfolding associated with Alzheimer’s disease pathogenesis. Moreover, it highlights a new mechanism of how distantly localized bacteria can remotely contribute to protein misfolding and diseases associated with this process. These findings might lead to the use of bacterial DNA as a novel therapeutic target for the prevention and treatment of Alzheimer’s disease.

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