China 
Africa 
Explore chapters and articles related to this topic
The Neuromuscular Junction
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The neurotransmitter thus binds to the receptor, and the neurotransmitter-receptor complex dissociates by the unbinding of the neurotransmitter from the receptor due to random thermal motion of the neurotransmitter and the receptor atoms at the binding site. A higher concentration of neurotransmitter in the medium surrounding the receptor increases the number of neurotransmitter-receptor complexes, that is, drives the process described by Reaction 5.1 more to the right, whereas a lower concentration of neurotransmitter drives the reaction to the left, decreasing the number of neurotransmitter-receptor complexes.
Different Methods of Measuring Binding to the Effector Ligand Binding Sites of Neurotransmitter Receptors: A Note of Caution
Published in W. R. Wayne Martin, Functional Imaging in Movement Disorders, 2019
Finally, with the newly emerging knowledge of the amino acid sequences, tertiary structure, and cellular location of neurotransmitter receptors it is apparent that there are numerous potential sites for regulation of sensitivity to drugs and neurotransmitters other than via changes in receptor number or density.10 Given the currently available data, it is far from clear that the changes in sensitivity of the striatum to dopamine and dopamine agonists after loss of dopamine afferents, as in PD, are a result of changes in dopamine receptor density or number.
Identification Of Receptors In Vitro
Published in William C. Eckelman, Lelio G. Colombetti, Receptor-Binding Radiotracers, 2019
This criterion for the identification of a binding site as a receptor is discussed in the chapter by Kuhar. Briefly, binding activity must be located in the places where the physiological response is found, and nowhere else. This criterion can be used at different levels. An extremely crude application is that a neurotransmitter receptor should be located in the nervous system (or some target organ). If the receptor is known to be present in certain areas of the nervous system (e.g., in certain brain nuclei), it should be present in higher levels there than in the rest of the nervous system. More sophisticated localization of binding, particularly demonstration that the binding activity is located at the synapse, where neurotransmitter receptors should be concentrated, requires histochemical or autoradiographic techniques, rather than the biochemical binding methods that are the focus of this chapter.
Innovative screening models for the discovery of new schizophrenia drug therapies: an integrated approach
Published in Expert Opinion on Drug Discovery, 2021
Marinos G. Sotiropoulos, Eleni Poulogiannopoulou, Foteini Delis, Christina Dalla, Katerina Antoniou, Nikolaos Kokras
Moreover, the challenge is to replace symptom-based with mechanistic-based animal equivalents, and turn from face to construct (etiologic) validity, even if the animal phenotype developed is not exactly homologous with the human one [110,111]. Focusing drug development solely on one neurotransmitter receptor seems obsolete and inadequate. Building on numerous new data concerning pathophysiology and genetics, candidate drugs should be diversified, with more target- than ligand-based structures [7]. Moreover, schizophrenia-related neurodevelopmental impairment and cognitive deficits involve many different neurobiological domains, indicating the need of developing drug combination strategies to thoroughly address the disease [2]. The identification of additional, more specific endophenotypes or further aspects of currently known endophenotypes will indicate new therapeutic candidates. In reverse, the identification of novel efficient drug categories will give investigators the opportunity to evaluate the predictive validity of current animal models and develop new ones, more specific to schizophrenia [15].
CBF regulation in hypertension and Alzheimer’s disease
Published in Clinical and Experimental Hypertension, 2020
Noushin Yazdani, Mark S. Kindy, Saeid Taheri
NE preferentially binds α1-adrenoreceptors to cause VSMCs contraction which increases vessel tone and resistance (80). In normotensive human α1-adrenoreceptor blocker does not influence CBF (81). Even in mild hypertensive humans, vascular α-receptor sensitivity to NE remains unchanged (82). However, in both patients with primary hypertension (83) as well as in AD patients (84) autoantibody of α1-adrenoreceptor was found. Of note is that there is heterogeneity in the expression of neurotransmitter receptors across the cerebrovascular tree that causes different actions with the same neurotransmitter. For example, there is a shift in receptor population from α- to β-adrenoreceptors in penetrating arterioles. NE activation of α1-adrenoreceptors causes major cranial arteries such as middle cerebral artery contraction (85), but NE activation of β-adrenoreceptors causes penetrating arterioles dilation (86). Moreover, Aβ accumulation has been shown in animal models that activate α1-adrenoreceptors (87). Therefore, we cannot assume that parenchymal and pial arteries will behave similarly when challenged with an increase in blood pressures and Aβ accumulation. It has become evident that the depletion of central and peripheral catecholamine stores could prevent or attenuate the development of hypertension (88).
Molecular spectroscopic studies examining the interactions between phenobarbital and human serum albumin in alcohol consumption
Published in The American Journal of Drug and Alcohol Abuse, 2018
Sheng-Feng Cui, Wei Li, Cheng-He Zhou
Alcohol dependence is one of the most highly prevalent chronic disorders worldwide and is caused by the accumulation and deposition of complex interactions among environmental, genetic, and biological risk factors. This chronic disorder can lead to many serious health and social consequences, such as type 2 diabetes mellitus, gout, drunk driving, violence, attempted suicide, and illicit drug use (1). Alcohol policies in many countries have been formulated to reduce the harmful use of alcohol and alcohol-attributable burdens on health and society. Meanwhile, in recent years, studies have focused on alcohol dependence in the field of medicine, which have become an extremely attractive area. Many valuable studies (2) on the development of alcohol dependence have suggested that the major inhibitory neurotransmitter receptors, including GABAA, in the human brain are involved in acute and chronic alcohol effects, including dependence, withdrawal, sedation, ethanol preference, and lack of motor coordination. Based on evidence from clinical studies (3), the most difficult part of alcohol dependence treatment is that alcohol withdrawal syndrome occurs frequently when alcohol consumption is suddenly stopped or reduced after a period of high regular dinking. The consequences resulting from alcohol withdrawal syndrome are potentially life-threatening and are usually characterized by tachycardia, agitation and tremor and, in severe cases, memory and attention lapses, loss of coordination, and seizures (4).