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Neurotransmitters and receptors

In view of the universal role of the area postrema (AP) in emesis among animal species, including man [54], an analysis of this structure in terms of receptors, neurotransmitters and neurophysiological responses is indicated. The AP has also been implicated in several other functions (cardiovascular, caloric intake, osmotic water balance) unrelated to emesis [55], The reader is referred to general and comprehensive references on this neuronal structure [36, 37, 56],... [Pg.308]

See also Biochemistry of Neurotransmission, Neurotransmitters and Receptors, Neurotransmitters and Biological Regulators... [Pg.1710]

The G-proteins are heterotrimers made of three families of subunits, a, P, and y, which can interact specifically with discrete regions on G-protein-coupled receptors. This includes most receptors for neurotransmitters and polypeptide hormones (see Neuroregulators). G-protein-coupled receptors also embrace the odorant receptor family and the rhodopsin-linked visual cascade. [Pg.278]

Signal-transducing receptors are plasma membrane proteins that bind specific molecules, such as growth factors, hormones, or neurotransmitters, and then transmit a signal to the cell s interior, causing the cell to respond in a... [Pg.278]

Synaptic vesicles mediate the release of small molecules other than classical neurotransmitters and neuropeptides. Of these, zinc and ATP are the best characterized. NMDA and GABA receptors contain binding sites for zinc, and zinc exerts a direct effect on... [Pg.1281]

Traditionally receptors have been classified according to their pharmacology. Each neurotransmitter acts on its own family of receptors and these receptors show a high degree of specificity for their transmitter. Thus, the receptors on which acetylcholine (ACh) works do not respond to glutamate (or any other neurotransmitter) and vice versa. Diversity of neurotransmitter action is provided by the presence of multiple receptor subtypes for each neurotransmitter, all of which still remain specific to that neurotransmitter. This principle is illustrated by the simple observations outlined in... [Pg.57]

These approaches to receptor identification and classification were, of course, pioneered by studies with peripheral systems and isolated tissues. They are more difficult to apply to the CNS, especially in in vivo experiments, where responses depend on a complex set of interacting systems and the actual drug concentration at the receptors of interest is rarely known. However, the development of in vitro preparations (acute brain slices, organotypic brain slice cultures, tissue-cultured neurons and acutely dissociated neuronal and glial cell preparations) has allowed more quantitative pharmacological techniques to be applied to the action of drugs at neurotransmitter receptors while the development of new recording methods such as patch-clamp... [Pg.58]

The following sections of this chapter will consider some general and comparative aspects of receptor structure and function. More detailed material on these topics may be found in the relevant chapters on individual neurotransmitters. [Pg.62]

Figure 20.1 Schematic diagram illustrating how antidepressants increase the concentration of extraneuronal neurotransmitter (noradrenaline and/or 5-HT). In the absence of drug (b), monoamine oxidase on the outer membrane of mitochondria metabolises cytoplasmic neurotransmitter and limits its concentration. Also, transmitter released by exocytosis is sequestered from the extracellular space by the membrane-bound transporters which limit the concentration of extraneuronal transmitter. In the presence of a MAO inhibitor (a), the concentration of cytoplasmic transmitter increases, causing a secondary increase in the vesicular pool of transmitter (illustrated by the increase in the size of the vesicle core). As a consequence, exocytotic release of transmitter is increased. Blocking the inhibitory presynaptic autoreceptors would also increase transmitter release, as shown by the absence of this receptor in the figure. In the presence of a neuronal reuptake inhibitor (c), the membrane-bound transporter is inactivated and the clearance of transmitter from the synapse is diminished... Figure 20.1 Schematic diagram illustrating how antidepressants increase the concentration of extraneuronal neurotransmitter (noradrenaline and/or 5-HT). In the absence of drug (b), monoamine oxidase on the outer membrane of mitochondria metabolises cytoplasmic neurotransmitter and limits its concentration. Also, transmitter released by exocytosis is sequestered from the extracellular space by the membrane-bound transporters which limit the concentration of extraneuronal transmitter. In the presence of a MAO inhibitor (a), the concentration of cytoplasmic transmitter increases, causing a secondary increase in the vesicular pool of transmitter (illustrated by the increase in the size of the vesicle core). As a consequence, exocytotic release of transmitter is increased. Blocking the inhibitory presynaptic autoreceptors would also increase transmitter release, as shown by the absence of this receptor in the figure. In the presence of a neuronal reuptake inhibitor (c), the membrane-bound transporter is inactivated and the clearance of transmitter from the synapse is diminished...

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See also in sourсe #XX -- [ Pg.3 , Pg.135 , Pg.138 ]

See also in sourсe #XX -- [ Pg.3 , Pg.135 , Pg.138 ]




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Neurotransmitters and their receptor subtypes

Neurotransmitters and their receptors

Neurotransmitters receptors

Pharmacologically important neurotransmitters and their receptors

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