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Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Having discussed the neuromuscular junction (NMJ) in the previous chapter, the main focus in the present chapter is on synapses in the central nervous system. The chapter begins with a general overview of the various types of synapses, including an equivalent electric circuit and a careful definition of the criteria for considering a synapse to be excitatory or inhibitory. Neurotransmitter types are discussed in some detail. Fast chemical synapses, both excitatory and inhibitory, are considered next, including the highly important NMDA and non-NMDA types of receptors. The basic principles underlying the operation of second-messenger systems are explained. These systems are slower in speed than the fast chemical synapses but are more varied and have a profound effect on many aspects of cell function. The main neuromodulatory systems, which act mostly through second-messenger systems are presented, followed by presynaptic inhibition and facilitation as a means for selectively affecting certain inputs to a neuron. Synaptic plasticity, manifested as short-term and long-term modification of synaptic efficacy, is then discussed in terms of its operational effects and basic molecular mechanisms. Synaptic plasticity is of great importance, as it affects neuronal responses to stimulation and underlies learning and memory. The Chapter ends with a discussion of the less common electrical synapses, which have some important properties that distinguish them from chemical synapses.
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
ATP is required to fuel: Energy production itself. It is necessary to initiate glycolysis and fatty acid oxidation.Active transport of electrolytes across the plasma membrane, e.g., the Na+/K+ pump that restores the resting potential of the heart’s pacemaker cells.The amplification of the second messenger systems in cells. This process involves small amounts of signalling molecules (for example, water soluble hormones and neurotransmitters) attaching to the surface of the cell and initiating a process involving a number of membrane and intracellular proteins, that amplify the message to ensure that there is a sufficient response within the cell. This means that a relatively weak signal can produce a significant cellular action. The amino acid endocrines, such as antidiuretic hormone, function in this way.Contraction of skeletal, cardiac and smooth muscle cells.Phosphorylation of molecules to enable and enhance reactions in the cell.
Endothelin and Cardiac Hypertrophy
Published in Malcolm J. Lewis, Ajay M. Shah, Endothelial Modulation of Cardiac Function, 2020
Biochemical mechanisms which link ET-1 receptors to the increase in transcriptional activity still remain to be elucidated. Recent studies have suggested that the putative second messenger system of α1-adrenergic stimulation, which is a classical hypertrophic factor for cardiomyocytes, is phospholipase C-mediated hydrolysis of phosphoinositide-4,5-biphosphate (PIP2), thereby leading to formation of inositol-1,4,5 triphosphate (IP3) and diacylglycerol (DG) (Ohtani et al., 1988). Endogenous DG as well as phorbol esters, such as 12-O-tetradecanoylphorbol-13-acetate (TPA), increase synthesis of DNA and protein by activating protein kinase C (PKC) in adult rat cardiocytes (Claycomb et al., 1988), suggesting that their growth is mediated by PKC. It has been also reported that ET-1 stimulates mitogen-activated protein kinase (MAPK) and MAPK kinase activity in cultured cardiomyocytes (Bogoyevitch et al., 1993; Bogoyevitch et al., 1994). This signaling cascade may also be relevant to the hypertrophic response of the heart following PKC activation.
Gastroparesis syndromes: emerging drug targets and potential therapeutic opportunities
Published in Expert Opinion on Investigational Drugs, 2023
Le Yu Naing, Matthew Heckroth, Prateek Mathur, Thomas L Abell
Substance P is a neuropeptide in the tachykinin peptide family that plays a role in various processes throughout the body, including pain perception and inflammation. Substance P’s receptor, neurokinin type 1 (NK-1 R), is a transmembrane bound receptor located on many cell types including GI vagal afferents and CNS areas involved in the vomiting reflex. It is a G-protein linked receptor that acts through both the inositol trisphosphate/diacylglycerol (IP3/DAG) and cAMP second messenger systems, depending on cell type. The binding of Substance P to NK-1 R in the area postrema and nucleus tractus solitarius triggers emesis. Additionally, in the GI tract, enteric motor neurons release both acetylcholine and substance P onto smooth muscle. Recent animal studies suggest that Substance P, via the NK-1 R, also acts as a co-neurotransmitter important for maintaining muscular responsiveness to acetylcholine and regulating gastric motility[34].
Sialylated milk oligosaccharides alter neurotransmitters and brain metabolites in piglets: an In vivo magnetic resonance spectroscopic (MRS) study
Published in Nutritional Neuroscience, 2021
Hong Xin Wang, Yue Chen, Ziaul Haque, Michael de Veer, Gary Egan, Bing Wang
The absolute concentrations of 33 brain metabolites including alanine (Ala), aspartate (Asp), Cr, Cho, γ-aminobutyric acid (GABA), glycerophosphorylcholine (GPC), d-Glucose (Glc), glutamine (Gln), glutathione (Glth), glutamate (Glu), lipid (Lip) (09, 13a, 13b, 20), macromolecular (MM) (09, 12, 14, 17, 20), NAA, N-acetylaspartylglutamate (NAAG), myo-inositol (mIns), lactate (Lac), phosphorylcholine (PCh), phosphocreatine (PCr), scyllo-inositol (SI) taurine (Tau), total NAA (TNAA), total choline (TCho), total creatine (TCr), total lipid and macromolecular (TLM) were detected and automatically analysed at TE 270 ms between the three piglet groups using TARQUIN software. The mean absolute concentration of 33 metabolites in 3 different groups of 38 d-old piglet is shown in Figure 4. An astrocyte marker [19] and essential part of the inositol triphosphate intracellular second messenger system [20] of mIns was higher in both SL/SLN (22.11 ± 1.12 mM) and SL (19.02 ± 1.13 mM) compared with the control (17.75 ± 1.13 mM). The overall difference between the three groups was statistically significant (P = .031, Figure 4). These differences were even more significant when the data was analysed after adjustment for volume of whole brain, white matter, grey matter, brain weight or body weight gain as covariates (P = .029), or when comparing the relative concentration for mIns using the ratios of mIns/NAA, mIns/Cho and mIns/Cr with or without adjustment for volume of whole brain, white matter, grey matter, brain weight or body weight as covariates (Supplemental Table 2).
Proton pump inhibitors: use and misuse in the clinical setting
Published in Expert Review of Clinical Pharmacology, 2018
Vincenzo Savarino, Elisa Marabotto, Patrizia Zentilin, Manuele Furnari, Giorgia Bodini, Costanza De Maria, Gaia Pellegatta, Claudia Coppo, Edoardo Savarino
The study of gastric acid secretion has attracted the interest of both physiologists and physicians for many years, because a great number of diseases of the upper gastrointestinal (GI) tract are related to dysfunctions in acid production. Many investigations have documented that gastric acid is produced by both resting and meal-stimulated parietal cells in the stomach, following neurocrine, paracrine, and endocrine stimulation by various substances, such as acetylcholine, histamine, or gastrin, which bind to their specific receptors placed on the basolateral membrane of the above cells [1]. Thereafter, intracellular second messenger systems are activated leading to protein kinase formation and activation of H+/K+ ATPase enzyme (proton pump), which fuse with the secretory canaliculus of the parietal cell resulting in acid production, whereby intracellular hydrogen ions are exchanged for extracellular potassium ions [2]. Once acid is produced, the lower luminal intragastric pH stimulates a feedback mechanism to maintain appropriate homeostatic control of acid secretion. This response is mediated primarily by the paracrine release of somatostatin from gastric antral D cells, which inhibit G cell production of gastrin and enterochromaffin-like (ECL) formation of histamine in order to reverse the stimulus for acid secretion [3].