Journal articles: 'Neural transmission Effects of drugs on'

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Reardon, Richard, Francis T. Durso, and Donald A. Wilson. "Neural Coding and Synaptic Transmission: Participation Exercises for Introductory Psychology." Teaching of Psychology 21, no. 2 (April 1994): 96–99. http://dx.doi.org/10.1207/s15328023top2102_8.

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We present two simulations of neural transmission for use in an Introductory Psychology class. These simulations illustrate the complex coding properties of a single neuron, especially how excitatory and inhibitory postsynaptic potentials accumulate to produce an action potential. A follow-up exercise, using the framework of the simple children's game Musical Chairs, illustrates synaptic transmission, including the effects of psychoactive drugs at the synapse.

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Hao, Xuechao, Mengchan Ou, Donghang Zhang, Wenling Zhao, Yaoxin Yang, Jin Liu, Hui Yang, Tao Zhu, Yu Li, and Cheng Zhou. "The Effects of General Anesthetics on Synaptic Transmission." Current Neuropharmacology 18, no. 10 (November 4, 2020): 936–65. http://dx.doi.org/10.2174/1570159x18666200227125854.

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General anesthetics are a class of drugs that target the central nervous system and are widely used for various medical procedures. General anesthetics produce many behavioral changes required for clinical intervention, including amnesia, hypnosis, analgesia, and immobility; while they may also induce side effects like respiration and cardiovascular depressions. Understanding the mechanism of general anesthesia is essential for the development of selective general anesthetics which can preserve wanted pharmacological actions and exclude the side effects and underlying neural toxicities. However, the exact mechanism of how general anesthetics work is still elusive. Various molecular targets have been identified as specific targets for general anesthetics. Among these molecular targets, ion channels are the most principal category, including ligand-gated ionotropic receptors like γ-aminobutyric acid, glutamate and acetylcholine receptors, voltage-gated ion channels like voltage-gated sodium channel, calcium channel and potassium channels, and some second massager coupled channels. For neural functions of the central nervous system, synaptic transmission is the main procedure for which information is transmitted between neurons through brain regions, and intact synaptic function is fundamentally important for almost all the nervous functions, including consciousness, memory, and cognition. Therefore, it is important to understand the effects of general anesthetics on synaptic transmission via modulations of specific ion channels and relevant molecular targets, which can lead to the development of safer general anesthetics with selective actions. The present review will summarize the effects of various general anesthetics on synaptic transmissions and plasticity.

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Albalawi, Farraj, Jason C. Lim, Kyle V. DiRenzo, Elliot V. Hersh, and Claire H. Mitchell. "Effects of Lidocaine and Articaine on Neuronal Survival and Recovery." Anesthesia Progress 65, no. 2 (June 1, 2018): 82–88. http://dx.doi.org/10.2344/anpr-65-02-02.

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The local anesthetics lidocaine and articaine are among the most widely used drugs in the dentist's arsenal, relieving pain by blocking voltage-dependent Na+ channels and thus preventing transmission of the pain signal. Given reports of infrequent but prolonged paresthesias with 4% articaine, we compared its neurotoxicity and functional impairment by screening cultured neural SH-SY5Y cells with formulations used in patients (2% lidocaine + 1:100,000 epinephrine or 4% articaine + 1:100,000 epinephrine) and with pure formulations of the drugs. Voltage-dependent sodium channels Na(v)1.2 and Na(v)1.7 were expressed in SH-SY5Y cells. To test the effects on viability, cells were exposed to drugs for 5 minutes, and after washing, cells were treated with the ratiometric Live/Dead assay. Articaine had no effect on the survival of SH-SY5Y cells, while lidocaine produced a significant reduction only when used as pure powder. To determine reversibility of blockage, wells were exposed to drugs for 5 minutes and returned for medium for 30 minutes, and the calcium elevation induced by depolarizing cells with a high-potassium solution was measured using the calcium indicator Fura-2. High potassium raised calcium in control SH-SY5Y cells and those treated with articaine, but lidocaine treatment significantly reduced the response. In conclusion, articaine does not damage neural cells more than lidocaine in this in vitro model. While this does not question the safety of lidocaine used clinically, it does suggest that articaine is no more neurotoxic, at least in the in vitro setting.

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Carr, Kenneth D. "Modulatory Effects of Food Restriction on Brain and Behavioral Effects of Abused Drugs." Current Pharmaceutical Design 26, no. 20 (June 21, 2020): 2363–71. http://dx.doi.org/10.2174/1381612826666200204141057.

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Energy homeostasis is achieved, in part, by metabolic signals that regulate the incentive motivating effects of food and its cues, thereby driving or curtailing procurement and consumption. The neural underpinnings of these regulated incentive effects have been identified as elements within the mesolimbic dopamine pathway. A separate line of research has shown that most drugs with abuse liability increase dopamine transmission in this same pathway and thereby reinforce self-administration. Consequently, one might expect shifts in energy balance and metabolic signaling to impact drug abuse risk. Basic science studies have yielded numerous examples of drug responses altered by diet manipulation. Considering the prevalence of weight loss dieting in Western societies, and the anorexigenic effects of many abused drugs themselves, we have focused on the CNS and behavioral effects of food restriction in rats. Food restriction has been shown to increase the reward magnitude of diverse drugs of abuse, and these effects have been attributed to neuroadaptations in the dopamine-innervated nucleus accumbens. The changes induced by food restriction include synaptic incorporation of calcium-permeable AMPA receptors and increased signaling downstream of D1 dopamine receptor stimulation. Recent studies suggest a mechanistic model in which concurrent stimulation of D1 and GluA2-lacking AMPA receptors enables increased stimulus-induced trafficking of GluA1/GluA2 AMPARs into the postsynaptic density, thereby increasing the incentive effects of food, drugs, and associated cues. In addition, the established role of AMPA receptor trafficking in enduring synaptic plasticity prompts speculation that drug use during food restriction may more strongly ingrain behavior relative to similar use under free-feeding conditions.

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Lüscher, Bernhard, and Hanns Möhler. "Brexanolone, a neurosteroid antidepressant, vindicates the GABAergic deficit hypothesis of depression and may foster resilience." F1000Research 8 (May 29, 2019): 751. http://dx.doi.org/10.12688/f1000research.18758.1.

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The GABAergic deficit hypothesis of depression states that a deficit of GABAergic transmission in defined neural circuits is causal for depression. Conversely, an enhancement of GABA transmission, including that triggered by selective serotonin reuptake inhibitors or ketamine, has antidepressant effects. Brexanolone, an intravenous formulation of the endogenous neurosteroid allopregnanolone, showed clinically significant antidepressant activity in postpartum depression. By allosterically enhancing GABAA receptor function, the antidepressant activity of allopregnanolone is attributed to an increase in GABAergic inhibition. In addition, allopregnanolone may stabilize normal mood by decreasing the activity of stress-responsive dentate granule cells and thereby sustain resilience behavior. Therefore, allopregnanolone may augment and extend its antidepressant activity by fostering resilience. The recent structural resolution of the neurosteroid binding domain of GABAA receptors will expedite the development of more selective ligands as a potential new class of central nervous system drugs.

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Fallon, Sean James, Marieke E. van der Schaaf, Niels ter Huurne, and Roshan Cools. "The Neurocognitive Cost of Enhancing Cognition with Methylphenidate: Improved Distractor Resistance but Impaired Updating." Journal of Cognitive Neuroscience 29, no. 4 (April 2017): 652–63. http://dx.doi.org/10.1162/jocn_a_01065.

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A balance has to be struck between supporting distractor-resistant representations in working memory and allowing those representations to be updated. Catecholamine, particularly dopamine, transmission has been proposed to modulate the balance between the stability and flexibility of working memory representations. However, it is unclear whether drugs that increase catecholamine transmission, such as methylphenidate, optimize this balance in a task-dependent manner or bias the system toward stability at the expense of flexibility (or vice versa). Here we demonstrate, using pharmacological fMRI, that methylphenidate improves the ability to resist distraction (cognitive stability) but impairs the ability to flexibly update items currently held in working memory (cognitive flexibility). These behavioral effects were accompanied by task-general effects in the striatum and opposite and task-specific effects on neural signal in the pFC. This suggests that methylphenidate exerts its cognitive enhancing and impairing effects through acting on the pFC, an effect likely associated with methylphenidate's action on the striatum. These findings highlight that methylphenidate acts as a double-edged sword, improving one cognitive function at the expense of another, while also elucidating the neurocognitive mechanisms underlying these paradoxical effects.

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Perlman, Ido, and Richard A. Normann. "The effects of GABA and related drugs on horizontal cells in the isolated turtle retina." Visual Neuroscience 5, no. 5 (November 1990): 469–77. http://dx.doi.org/10.1017/s0952523800000596.

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AbstractThe role of GABA in the outer plexiform layer of the turtle retina has been examined by intracellular recordings from L- and C-type horizontal cells in the isolated retina preparation.GABA (1–5 mM) slightly depolarized the L-type horizontal cells, reduced the amplitude of their photoresponses, and slowed down the rate of hyperpolarization during the ON component of the photoresponse. These effects could not be replicated by either muscimol or baclofen. When synaptic transmission from the photoreceptors had been blocked by either kynurenic acid or cobalt ions, GABA depolarized L-type horizontal cells and augmented the remaining photoresponses. Neither muscimol nor baclofen exerted any effect on L-type horizontal cells under these conditions. Nipecotic acid, a competitive inhibitor of the GABA-uptake system, induced effects on turtle L-type horizontal cells which were similar to those exerted by GABA. Thus, the complex GABA effect on turtle L-type horizontal cells seems to represent the summation of at least two actions; an indirect one mediated by the red cones via GABAa-type receptors and a direct one which probably reflects the activation of an electrogenic GABA-uptake system.GABA (1–5 mM) induced a transient depolarization in C-type horizontal cells but eliminated color opponency in only three cells out of seven studied. This observation is inconsistent with the notion that the only neural mechanism responsible for the chromatic properties of C-type horizontal cells in the turtle retina is a GABAergic negative feedback from the L-type horizontal cells onto the green ones.

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Li, Nuojin, Tian Zhou, and Erkang Fei. "Actions of Metformin in the Brain: A New Perspective of Metformin Treatments in Related Neurological Disorders." International Journal of Molecular Sciences 23, no. 15 (July 27, 2022): 8281. http://dx.doi.org/10.3390/ijms23158281.

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Metformin is a first-line drug for treating type 2 diabetes mellitus (T2DM) and one of the most commonly prescribed drugs in the world. Besides its hypoglycemic effects, metformin also can improve cognitive or mood functions in some T2DM patients; moreover, it has been reported that metformin exerts beneficial effects on many neurological disorders, including major depressive disorder (MDD), Alzheimer’s disease (AD) and Fragile X syndrome (FXS); however, the mechanism underlying metformin in the brain is not fully understood. Neurotransmission between neurons is fundamental for brain functions, and its defects have been implicated in many neurological disorders. Recent studies suggest that metformin appears not only to regulate synaptic transmission or plasticity in pathological conditions but also to regulate the balance of excitation and inhibition (E/I balance) in neural networks. In this review, we focused on and reviewed the roles of metformin in brain functions and related neurological disorders, which would give us a deeper understanding of the actions of metformin in the brain.

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Ma, Dongliang, Su-In Yoon, Chih-Hao Yang, Guillaume Marcy, Na Zhao, Wan-Ying Leong, Vinu Ganapathy, et al. "Rescue of Methyl-CpG Binding Protein 2 Dysfunction-induced Defects in Newborn Neurons by Pentobarbital." Neurotherapeutics 12, no. 2 (March 10, 2015): 477–90. http://dx.doi.org/10.1007/s13311-015-0343-0.

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Abstract Rett syndrome is a neurodevelopmental disorder that usually arises from mutations or deletions in methyl-CpG binding protein 2 (MeCP2), a transcriptional regulator that affects neuronal development and maturation without causing cell loss. Here, we show that silencing of MeCP2 decreased neurite arborization and synaptogenesis in cultured hippocampal neurons from rat fetal brains. These structural defects were associated with alterations in synaptic transmission and neural network activity. Similar retardation of dendritic growth was also observed in MeCP2-deficient newborn granule cells in the dentate gyrus of adult mouse brains in vivo, demonstrating direct and cell-autonomous effects on individual neurons. These defects, caused by MeCP2 deficiency, were reversed by treatment with the US Food and Drug Administration-approved drug, pentobarbital, in vitro and in vivo, possibly caused by modulation of γ-aminobutyric acid signaling. The results indicate that drugs modulating γ-aminobutyric acid signaling are potential therapeutics for Rett syndrome.

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Daniele, Mangano, Durando, Ragni, and Martini. "The Nootropic Drug Α-Glyceryl-Phosphoryl-Ethanolamine Exerts Neuroprotective Effects in Human Hippocampal Cells." International Journal of Molecular Sciences 21, no. 3 (January 31, 2020): 941. http://dx.doi.org/10.3390/ijms21030941.

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Brain aging involves changes in the lipid membrane composition that lead to a decrease in membrane excitability and neurotransmitter release. These membrane modifications have been identified as contributing factors in age-related memory decline. In this sense, precursors of phospholipids (PLs) can restore the physiological composition of cellular membranes and produce valuable therapeutic effects in brain aging. Among promising drugs, alpha-glycerylphosphorylethanolamine (GPE) has demonstrated protective effects in amyloid-injured astrocytes and in an aging model of human neural stem cells. However, the compound properties on mature neuronal cells remain unexplored. Herein, GPE was tested in human hippocampal neurons, which are involved in learning and memory, and characterized by a functional cholinergic transmission, thus representing a valuable cellular model to explore the beneficial properties of GPE. GPE induced the release of the main membrane phospholipids and of the acetylcholine neurotransmitter. Moreover, the compound reduced lipid peroxidation and enhanced membrane fluidity of human brain cells. GPE counteracted the DNA damage and viability decrease observed in in vitro aged neurons. Among GPE treatment effects, the autophagy was found positively upregulated. Overall, these results confirm the beneficial effects of GPE treatment and suggest the compound as a promising drug to preserve hippocampal neurons and virtually memory performances.

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Wang, Fan, Xueheng Xie, Xiaoyan Xing, and Xiaobo Sun. "Excitatory Synaptic Transmission in Ischemic Stroke: A New Outlet for Classical Neuroprotective Strategies." International Journal of Molecular Sciences 23, no. 16 (August 19, 2022): 9381. http://dx.doi.org/10.3390/ijms23169381.

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Stroke is one of the leading causes of death and disability in the world, of which ischemia accounts for the majority. There is growing evidence of changes in synaptic connections and neural network functions in the brain of stroke patients. Currently, the studies on these neurobiological alterations mainly focus on the principle of glutamate excitotoxicity, and the corresponding neuroprotective strategies are limited to blocking the overactivation of ionic glutamate receptors. Nevertheless, it is disappointing that these treatments often fail because of the unspecificity and serious side effects of the tested drugs in clinical trials. Thus, in the prevention and treatment of stroke, finding and developing new targets of neuroprotective intervention is still the focus and goal of research in this field. In this review, we focus on the whole processes of glutamatergic synaptic transmission and highlight the pathological changes underlying each link to help develop potential therapeutic strategies for ischemic brain damage. These strategies include: (1) controlling the synaptic or extra-synaptic release of glutamate, (2) selectively blocking the action of the glutamate receptor NMDAR subunit, (3) increasing glutamate metabolism, and reuptake in the brain and blood, and (4) regulating the glutamate system by GABA receptors and the microbiota–gut–brain axis. Based on these latest findings, it is expected to promote a substantial understanding of the complex glutamate signal transduction mechanism, thereby providing excellent neuroprotection research direction for human ischemic stroke (IS).

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Lu, Yi, Hong Wang, Junqing Yang, Wengao Jiang, Hong Xin, Ying Luo, Santiago Loya-López, Huaiyu Gu, and Dongzhi Ran. "Distinct Role of Mono-2-ethylhexyl Phthalate in Neuronal Transmission in Rat CA3 Hippocampal Neurons: Involvement of Ion Channels." Molecules 27, no. 10 (May 11, 2022): 3082. http://dx.doi.org/10.3390/molecules27103082.

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Mono-(2-ethylhexyl) phthalate (MEHP) is one of the main active metabolites of di-(2-ethylhexyl) phthalate (DEHP). In our previous works, by using rat and Drosophila models, we showed a disruption of neural function due to DEHP. However, the exact neural effects of MEHP are still unclear. To explore the effects of MEHP on the central nervous system, the electrophysiological properties of spontaneous action potential (sAP), mini-excitatory postsynaptic currents (mEPSCs), ion channels, including Na+, Ca2+, and K+ channels from rat CA3 hippocampal neurons area were assessed. Our data showed that MEHP (at the concentrations of 100 or 300 μM) decreased the amplitude of sAP and the frequency of mEPSCs. Additionally, MEHP (100 or 300 μM) significantly reduced the peak current density of Ca2+ channels, whereas only the concentration of 300 μM decreased the peak current density of Na+ and K+ channels. Therefore, our results indicate that exposure to MEHP could affect the neuronal excitability and synaptic plasticity of rat CA3 hippocampal neurons by inhibiting ion channels’ activity, implying the distinct role of MEHP in neural transmission.

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Fila, Michal, Anna Sobczuk, Elzbieta Pawlowska, and Janusz Blasiak. "Epigenetic Connection of the Calcitonin Gene-Related Peptide and Its Potential in Migraine." International Journal of Molecular Sciences 23, no. 11 (May 30, 2022): 6151. http://dx.doi.org/10.3390/ijms23116151.

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The calcitonin gene-related peptide (CGRP) is implicated in the pathogenesis of several pain-related syndromes, including migraine. Targeting CGRP and its receptor by their antagonists and antibodies was a breakthrough in migraine therapy, but the need to improve efficacy and limit the side effects of these drugs justify further studies on the regulation of CGRP in migraine. The expression of the CGRP encoding gene, CALCA, is modulated by epigenetic modifications, including the DNA methylation, histone modification, and effects of micro RNAs (miRNAs), circular RNAs, and long-coding RNAs (lncRNAs). On the other hand, CGRP can change the epigenetic profile of neuronal and glial cells. The promoter of the CALCA gene has two CpG islands that may be specifically methylated in migraine patients. DNA methylation and lncRNAs were shown to play a role in the cell-specific alternative splicing of the CALCA primary transcript. CGRP may be involved in changes in neural cytoarchitecture that are controlled by histone deacetylase 6 (HDAC6) and can be related to migraine. Inhibition of HDAC6 results in reduced cortical-spreading depression and a blockade of the CGRP receptor. CGRP levels are associated with the expression of several miRNAs in plasma, making them useful peripheral markers of migraine. The fundamental role of CGRP in inflammatory pain transmission may be epigenetically regulated. In conclusion, epigenetic connections of CGRP should be further explored for efficient and safe antimigraine therapy.

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Hiroi, Noboru, and Takahira Yamauchi. "Modeling and Predicting Developmental Trajectories of Neuropsychiatric Dimensions Associated With Copy Number Variations." International Journal of Neuropsychopharmacology 22, no. 8 (May 28, 2019): 488–500. http://dx.doi.org/10.1093/ijnp/pyz026.

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AbstractCopy number variants, such as duplications and hemizygous deletions at chromosomal loci of up to a few million base pairs, are highly associated with psychiatric disorders. Hemizygous deletions at human chromosome 22q11.2 were found to be associated with elevated instances of schizophrenia and autism spectrum disorder in 1992 and 2002, respectively. Following these discoveries, many mouse models have been developed and tested to analyze the effects of gene dose alterations in small chromosomal segments and single genes of 22q11.2. Despite several limitations to modeling mental illness in mice, mouse models have identified several genes on 22q11.2—Tbx1, Dgcr8, Comt, Sept5, and Prodh—that contribute to dimensions of autism spectrum disorder and schizophrenia, including working memory, social communication and interaction, and sensorimotor gating. Mouse studies have identified that heterozygous deletion of Tbx1 results in defective social communication during the neonatal period and social interaction deficits during adolescence/adulthood. Overexpression of Tbx1 or Comt in adult neural progenitor cells in the hippocampus delays the developmental maturation of working memory capacity. Collectively, mouse models of variants of these 4 genes have revealed several potential neuronal mechanisms underlying various aspects of psychiatric disorders, including adult neurogenesis, microRNA processing, catecholamine metabolism, and synaptic transmission. The validity of the mouse data would be ultimately tested when therapies or drugs based on such potential mechanisms are applied to humans.

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Brunken, William J., and Nigel W. Daw. "Neuropharmacological analysis of the role of indoleamine-accumulating amacrine cells in the rabbit retina." Visual Neuroscience 1, no. 3 (May 1988): 275–85. http://dx.doi.org/10.1017/s0952523800001930.

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AbstractIn order to elucidate the role of putative indoleaminergic amacrine cells in visual processing, we have employed pharmacological agents specific for the two classes of serotonin receptor, 5-HT2 and 5-HT1, which have been identified in both the retina and brain. Perfusion of the rabbit retina with 5-HT2 selective antagonists decreases the ON-excitation of all classes of ganglion cell as well as the spontaneous activity of these cells. The effect on OFF-responses depends on the cell type: OFF-excitation of center-surround brisk and sluggish cells is increased or not affected by these drugs, but OFF excitation of ON/OFF direction selective cells is reduced. No disruption of the trigger features of direction selective or orientation selective cells was discovered, suggesting that indoleaminergic amacrine cells do not play a role in the generation of the complex properties of these cells.5-HT1 receptors are heterogeneous and classified as a, b, or c subtypes. Since no selective antagonists are available for these sites, we have employed specific agonists. The most specific of these are for the 5-HT1A receptor. Perfusion with these agonists had physiological effects similar to those with perfusion of 5-HT2 antagonists. Thus, we have suggested that these two classes of serotonin receptors mediate opponent processes in the neural pathway. Since indoleaminergic cells make reciprocal synaptic connections with rod bipolar cell terminals, which are depolarizing in the rabbit retina, we hypothesize that 5-HT2 receptors facilitate the synaptic transmission from the depolarizing rod bipolar cell thus facilitating ON-excitation in the retinal network while 5-HT1A receptors mediate an inhibitory process. Similar self-opponent processing appears to take place in the hypothalamic and hippocampal serotonergic systems as well as in the dopaminergic retinal system. Thus, it is likely that this organization is a general feature of monoamine signal transmission in the central nervous system.

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Morsi, Shereen, Valeria Pittala, Mohammad Alqudah, Mohamed Haider, and Khaled Greish. "In Vivo Evaluation of Anti-Nociceptive Effects of Silver Nanoparticles." Molecules 27, no. 21 (October 26, 2022): 7259. http://dx.doi.org/10.3390/molecules27217259.

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Silver nanoparticles (AgNPs) are widely used commercially due to their antimicrobial effects. Little is known about the effect of AgNPs on neural transmission and pain response. The aim of this study was to assess the anti-nociceptive activity of AgNPs. AgNPs were prepared at 16 ug/mL, white albino rats were injected with various doses of AgNPs, and challenged using a hot-plate test and paw withdrawal latency (PWL) was measured. The chronic constriction injury (CCI) model was utilized to evaluate the pedal withdrawal reflex and tail withdrawal reflex. An electrophysiological study was conducted utilizing colon longitudinal muscle strips. AgNPs increased the latency of PWL in a dose-dependent matter over the duration of 6 h. The paw withdrawal threshold in animals with CCI significantly increased after AgNPs administration. In isolated colon longitudinal muscle strips, AgNPs significantly reduced the colonic migrating motor complexes (MMCs) and contraction. This action was completely reversed after removing the AgNPs and adding acetylcholine to the preparation. In this study, AgNPs showed significant anti-nociception properties. To our knowledge, this is the first report to describe this pharmacological action of AgNPs.

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Bin-Jumah, May N., Monera Al-Abdan, Gadah Al-Basher, and Saud Alarifi. "Molecular Mechanism of Cytotoxicity, Genotoxicity, and Anticancer Potential of Green Gold Nanoparticles on Human Liver Normal and Cancerous Cells." Dose-Response 18, no. 2 (April 1, 2020): 155932582091215. http://dx.doi.org/10.1177/1559325820912154.

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Nanomaterials are extensively applied in various fields such as industry, medicine, and food and drugs due to their unique properties. In this study, gold nanoparticles were biosynthesized using leaf extract of Azadirachta indica and chloroauric acid salt. We have determined the cytotoxicity, genotoxicity, and apoptotic effect of green gold nanoparticles (gGNPs) on human normal (CHANG) and liver cancer (HuH-7) cells. Before exposure to cells, physiochemical characteristic of gGNPs was characterized using a transmission electron microscope and dynamic light scattering. Cytotoxicity of gGNPs was found dose-dependent, as it was confirmed using 2 methods, namely, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide and neutral red uptake. The gGNPs provoked intracellular reactive oxygen species (ROS), lipid peroxide, and reduced total glutathione and mitochondrial membrane potential in CHANG and HuH-7 cells in a dose-dependent manner. We have observed that N-acetyl-l-cysteine inhibits the generation of ROS in both cells after exposure to gGNPs. DNA damaging effects of gGNPs were determined by comet assay, and the maximum DNA damage was observed at 700 µg/mL gGNPs for 24 hours. It was observed that HuH-7 cells are slightly more sensitive to gGNPs exposure than CHANG cells. In conclusion, cytotoxicity and apoptosis in CHANG and HuH-7 cells due to gGNPs were mediated through oxidative stress.

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Leist, Marcel. "Epigenetic effects of drugs on early human neural development." Neurotoxicology and Teratology 49 (May 2015): 144. http://dx.doi.org/10.1016/j.ntt.2015.04.140.

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Domine, D., C. Guillon, J. Devillers, R. Lacroix, J. Lacroix, and J. C. Doré. "Nonlinear Neural Mapping Analysis of the Adverse Effects of Drugs." SAR and QSAR in Environmental Research 8, no. 1-2 (January 1998): 109–20. http://dx.doi.org/10.1080/10629369808033263.

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Xu, Chi, Horace H. Loh, and Ping-Yee Law. "Effects of addictive drugs on adult neural stem/progenitor cells." Cellular and Molecular Life Sciences 73, no. 2 (October 14, 2015): 327–48. http://dx.doi.org/10.1007/s00018-015-2067-z.

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Stewart, Jane. "Psychological and neural mechanisms of relapse." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1507 (July 18, 2008): 3147–58. http://dx.doi.org/10.1098/rstb.2008.0084.

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Relapse, the resumption of drug taking after periods of abstinence, remains the major problem for the treatment of addiction. Even when drugs are unavailable for long periods or when users are successful in curbing their drug use for extended periods, individuals remain vulnerable to events that precipitate relapse. Behavioural studies in humans and laboratory animals show that drug-related stimuli, drugs themselves and stressors are powerful events for the precipitation of relapse. Molecular, neurochemical and anatomical studies have identified lasting neural changes that arise from mere exposure to drugs and other enduring changes that arise from learning about the relationship between drug-related stimuli and drug effects. Chronic drug exposure increases sensitivity of some systems of the brain to the effects of drugs and stressful events. These changes, combined with those underlying conditioning and learning, perpetuate vulnerability to drug-related stimuli. Circuits of the brain involved are those of the mesocorticolimbic dopaminergic system and its glutamatergic connections, and the corticotropin-releasing factor and noradrenergic systems of the limbic brain. This paper reviews advances in our understanding of how these systems mediate the effects of events that precipitate relapse and of how lasting changes in these systems can perpetuate vulnerability to relapse.

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Iovino, Michele, Edoardo Guastamacchia, Vito Angelo Giagulli, Brunella Licchelli, and Vincenzo Triggiani. "Vasopressin Secretion Control: Central Neural Pathways, Neurotransmitters and Effects of Drugs." Current Pharmaceutical Design 18, no. 30 (August 23, 2012): 4714–24. http://dx.doi.org/10.2174/138161212802651607.

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Borodičienė, Jurgita, and Jūratė Gudaitytė. "Haemodynamic effects of central neural blocks." Acta medica Lituanica 19, no. 3 (October 1, 2012): 191–94. http://dx.doi.org/10.6001/actamedica.v19i3.2447.

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Haemodynamic effects are the most important physiological responses to central neural blocks. This article is focused on the etiology of hypotension, bradycardia and asystole understanding of which is essential for the anesthesiologist for successful management in the perioperative period. The main causes of cardiovascular changes are decreased cardiac output, systemic vascular resistance and reflexes related to baroreceptors. Hypotension and / or bradycardia are usually of short duration and easily treatable. However, haemodynamic changes in hypovolaemic, elderly patients with comorbidity, and patients with increased catecholamine production, due to excessive alcohol intake, emergency situation, can be significant with worse outcomes. Therefore it is essential to correct hypovolaemia before surgery. Timely notification, identification and appropriate treatment of haemodynamic changes caused by already performed central neural blockade remain important in the perioperative period as well. Vital functions must be monitored throughout surgery so that adverse cardiovascular reactions could be managed with timely and adequate treatment including elevation of the legs, oxygen and infusion therapy, vasoactive and anticholinergic drugs.

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Vibert, Jean-François, Fabián Alvarez, and Joël Pham. "Effects of transmission delays and noise in recurrent excitatory neural networks." Biosystems 48, no. 1-3 (November 1998): 255–62. http://dx.doi.org/10.1016/s0303-2647(98)00072-0.

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Vaudin, Pascal, Corinne Augé, Nathalie Just, Sakina Mhaouty-Kodja, Stéphane Mortaud, and Delphine Pillon. "When pharmaceutical drugs become environmental pollutants: Potential neural effects and underlying mechanisms." Environmental Research 205 (April 2022): 112495. http://dx.doi.org/10.1016/j.envres.2021.112495.

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Camporeale, A., D. Agnusdei, D. Gerardi, G. Parisi, C. Cepollaro, and C. Gennari. "Ultrasound transmission velocity in normal and postmenopausal osteoporotic patients: Effects of antiresorptive drugs." Bone and Mineral 17 (April 1992): 172. http://dx.doi.org/10.1016/0169-6009(92)92027-n.

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Szabo, Theresa M., Ted Brookings, Thomas Preuss, and Donald S. Faber. "Effects of Temperature Acclimation on a Central Neural Circuit and Its Behavioral Output." Journal of Neurophysiology 100, no. 6 (December 2008): 2997–3008. http://dx.doi.org/10.1152/jn.91033.2008.

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In this study, we address the impact of temperature acclimation on neuronal properties in the Mauthner (M-) system, a brain stem network that initiates the startle-escape behavior in goldfish. The M-cell can be studied at cellular and behavioral levels, since it is uniquely identifiable physiologically within the intact vertebrate brain, and a single action potential in this neuron determines not only whether a startle response will occur but also the direction of the escape. Using animals acclimated to 15°C as a control, 25°C-acclimated fish showed a significant increase in escape probability and a decrease in the ability to discriminate escape directionality. Intracellular recordings demonstrated that M-cells in this population possessed decreased input resistance and reduced strength and duration of inhibitory inputs. In contrast, fish acclimated to 5°C were behaviorally similar to 15°C fish and had increased input resistance, increased strength of inhibitory transmission, and reduced excitatory transmission. We show here that alterations in the balance between excitatory and inhibitory synaptic transmission in the M-cell circuit underlie differences in behavioral responsiveness in acclimated populations. Specifically, during warm acclimation, synaptic inputs are weighted on the side of excitation and fish demonstrate hyperexcitability and reduced left–right discrimination during rapid escapes. In contrast, cold acclimation results in transmission weighted on the side of inhibition and these fish are less excitable and show improved directional discrimination.

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Bradley, John, Harouna M. Soumaré, Almahamoudou Mahamar, Halimatou Diawara, Michelle Roh, Michael Delves, Chris Drakeley, et al. "Transmission-blocking Effects of Primaquine and Methylene Blue Suggest Plasmodium falciparum Gametocyte Sterilization Rather Than Effects on Sex Ratio." Clinical Infectious Diseases 69, no. 8 (February 12, 2019): 1436–39. http://dx.doi.org/10.1093/cid/ciz134.

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Abstract Gametocyte density and sex ratio can predict the proportion of mosquitoes that will become infected after feeding on blood of patients receiving nongametocytocidal drugs. Because primaquine and methylene blue sterilize gametocytes before affecting their density and sex ratio, mosquito feeding experiments are required to demonstrate their early transmission-blocking effects.

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Takishita, S., H. Muratani, N. Kawazoe, Y. Kimura, M. Tozawa, and K. Fukiyama. "Neural effects on renal blood flow during acute hypotension vary with antihypertensive drugs." Hypertension 23, no. 1_Suppl (January 1, 1994): I97. http://dx.doi.org/10.1161/01.hyp.23.1_suppl.i97.

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McGregor, I. "S.23.05 MDMA and other party drugs: neural and social effects in rodents." European Neuropsychopharmacology 21 (September 2011): S223. http://dx.doi.org/10.1016/s0924-977x(11)70335-2.

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Abramets, Igor I., Yuriy V. Kuznetsov, Dmitriy V. Evdokimov, and Tamara O. Zaika. "Piracetam potentiates neuronal and behavioral effects of ketamine." Research Results in Pharmacology 5, no. 2 (June 27, 2019): 49–55. http://dx.doi.org/10.3897/rrpharmacology.5.35530.

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Introduction: Ketamine has a fast, but short-term antidepressant effect. To support the therapeutic effect, repeated administrations of the drug are needed, which causes cognitive disorders. The drugs with cerebroprotective action can potentially intensify the main and weaken the side effects of drugs. Materials and methods: The impact of ketamine (5 and 20 μM), piracetam (100 μM), and their combinations on the synaptic transmission was studied on hippocampal slices in the CA1 area of rat hippocampus by means of electrophysiological methods. In behavioral experiments were aimed at studying an impact of the used drugs on the predictors which mark depressant behavior of rats: the duration of immobilization in a forced swimming test and preference for the consumption of sucrose solution (comparably with water). The behavioral experiments were performed on intact rats and rats with behavioral depression induced by chronic swimming stress. Results and discussion: Ketamine (5 and 20 μM) potentiates synaptic transmission in the radial layer of the CA1 hippocampal area. At a smaller concentration, ketamine potentiates synaptic transmission only due to the postsynaptic action, and at a greater concentration – with help of post- and presynaptic action. Piracetam (100 µM), like ketamine at a concentration of 5 μM stimulated synaptic transmission, but to a lesser degree. Ketamine at a concentration 5 μM under combined effect with piracetam induced the same effect as that at a concentration of 20 μM without piracetam, only due to a postsynaptic action. Ketamine at doses of 5 and 20 mg/kg one hour after a single systemic administration resulted in the reduced immobilization duration, but not predictors of preference for consuming a sweet solution; piracetam at a dose of 100 mg/kg under these conditions had no impact on the parameters of the rats’ behavior. The studied behavior parameters in cases of behavioral depression also changed after a single administration of ketamine at the doses of 5 and 20 mg/kg. Piracetam significantly stimulated an antidepressant action of ketamine under these circumstances. Conclusion: Piracetam potentiates a ketamine-induced enhancement of the synaptic transmission at the radial layer of the CA1 hippocampal area when investigating at the brain slices. Piracetam stimulates an antidepressant action of a single dose of ketamine in cases of behavioral depression, though it has no antidepressant effect when administered at a single dose.

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van de Borne, Philippe, Mohsen Rahnama, Silvia Mezzetti, Nicola Montano, Alberto Porta, Jean Paul Degaute, and Virend K. Somers. "Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 2 (August 1, 2001): H559—H565. http://dx.doi.org/10.1152/ajpheart.2001.281.2.h559.

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The relative contributions of a central neural oscillator and of the delay in α-adrenergic transmission within the baroreflex loop in the predominance of low-frequency (LF) cardiovascular variability during sympathetic activation in humans are unclear. We measured R-R interval (RR), muscle sympathetic nerve activity (MSNA), blood pressure (BP), and their variability in 10 normal subjects during sympathetic activation achieved by BP lowering with sodium nitroprusside (SNP) and α-adrenergic blockade using phentolamine. SNP and phentolamine induced comparable reductions in BP ( P > 0.25). Despite tachycardia and sympathetic activation with both SNP and phentolamine, LF variability in RR, MSNA, and BP increased during SNP and decreased during phentolamine (SNP: RR +20 ± 6%, MSNA +3 ± 5%, systolic BP +9 ± 6%, diastolic BP +7 ± 5%; phentolamine: RR −2 ± 7%, MSNA −34 ± 6%, systolic BP −16 ± 8%, diastolic BP −13 ± 4%, P< 0.05 except systolic BP, where P = 0.09). Thus LF variability is reduced when sympathetic activation is induced by α-adrenergic blockade. This suggests that α-adrenergic transmission within the baroreflex loop may contribute importantly to the predominance of LF cardiovascular variability associated with sympathetic excitation in humans.

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SUTHERLAND, COLIN J., HAMZA BABIKER, MARGARET J. MACKINNON, LISA RANFORD-CARTWRIGHT, and BADRIA BABIKER EL SAYED. "Rational deployment of antimalarial drugs in Africa: should first-line combination drugs be reserved for paediatric malaria cases?" Parasitology 138, no. 12 (August 3, 2011): 1459–68. http://dx.doi.org/10.1017/s0031182011001144.

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SUMMARYArtemisinin-based combination therapy is exerting novel selective pressure upon populations of Plasmodium falciparum across Africa. Levels of resistance to non-artemisinin partner drugs differ among parasite populations, and so the artemisinins are not uniformly protected from developing resistance, already present in South East Asia. Here, we consider strategies for prolonging the period of high level efficacy of combination therapy for two particular endemicities common in Africa. Under high intensity transmission, two alternating first-line combinations, ideally with antagonistic selective effects on the parasite genome, are advocated for paediatric malaria cases. This leaves second-line and other therapies for adult cases, and for intermittent preventive therapy. The drug portfolio would be selected to protect the ‘premier’ combination regimen from selection for resistance, while maximising impact on severe disease and mortality in children. In endemic areas subject to low, seasonal transmission of Plasmodium falciparum, such a strategy may deliver little benefit, as children represent a minority of cases. Nevertheless, the deployment of other drug-based interventions in low transmission and highly seasonal areas, such as mass drug administration aimed to interrupt malaria transmission, or intermittent preventive therapy, does provide an opportunity to diversify drug pressure. We thus propose an integrated approach to drug deployment, which minimises direct selective pressure on parasite populations from any one drug component. This approach is suitable for qualitatively and quantitatively different burdens of malaria, and should be supported by a programme of routine surveillance for emerging resistance.

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Werner, Felix-Martin, and Rafael Coveñas. "Neural Networks in Generalized Epilepsy and Novel Antiepileptic Drugs." Current Pharmaceutical Design 25, no. 4 (June 3, 2019): 396–400. http://dx.doi.org/10.2174/1381612825666190319121505.

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Background:In previous works, alterations of neurotransmitters and neuropeptides in the brain areas involved in generalized epilepsy have been reported.Objective:We reviewed the alterations of these neurotransmitters and neuropeptides in the following brain areas involved in generalized epilepsy: hippocampus, hypothalamus, thalamus and cerebral cortex. In these brain areas, the neural networks are also actualized. The mechanisms of action of newer antiepileptic drugs in the treatment of generalized epilepsy are also discussed.Results:Up-dating the neurotransmitter and neuropeptide alterations, we found that hippocampal GABAergic neurons presynaptically inhibit epileptogenic neurons via GABAB receptors. Epilepsy modulating neuropeptides (galanin, neuropeptide Y, dynorphin) are also involved. GABA deficiency, serotonin hyperactivity, dopamine hyperactivity and glutamate excitotoxicity can enhance ictogenesis: neurons containing these neurotransmitters form the main neural circuit. An increased excitability occurs when the alteration of these neurotransmitters is permanent.Conclusion:In preclinical studies, the GABAB receptor agonist GS 39,783 exerted a good antiepileptic effect. Perampanel, an AMPA receptor antagonist, showed good clinical effects in the treatment of partial-onset seizures and primary generalized tonic-clonic seizures. In this treatment, perampanel can be combined with other antiepileptic drugs. Brivaracetam, which shows a high affinity for the synaptic vesicle 2A, exerted a good efficacy in the treatment of adult focal seizures and secondarily generalized tonic-clonic seizures.

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Cortes, J. M., J. J. Torres, J. Marro, P. L. Garrido, and H. J. Kappen. "Effects of Fast Presynaptic Noise in Attractor Neural Networks." Neural Computation 18, no. 3 (March 1, 2006): 614–33. http://dx.doi.org/10.1162/neco.2006.18.3.614.

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We study both analytically and numerically the effect of presynaptic noise on the transmission of information in attractor neural networks. The noise occurs on a very short timescale compared to that for the neuron dynamics and it produces short-time synaptic depression. This is inspired in recent neurobiological findings that show that synaptic strength may either increase or decrease on a short timescale depending on presynaptic activity. We thus describe a mechanism by which fast presynaptic noise enhances the neural network sensitivity to an external stimulus. The reason is that, in general, presynaptic noise induces nonequilibrium behavior and, consequently, the space of fixed points is qualitatively modified in such a way that the system can easily escape from the attractor. As a result, the model shows, in addition to pattern recognition, class identification and categorization, which may be relevant to the understanding of some of the brain complex tasks.

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Villa, M., M. Buysse, A. Berthomieu, and A. Rivero. "The transmission-blocking effects of antimalarial drugs revisited: fitness costs and sporontocidal effects of artesunate and sulfadoxine-pyrimethamine." International Journal for Parasitology 51, no. 4 (March 2021): 279–89. http://dx.doi.org/10.1016/j.ijpara.2020.09.012.

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Castro, José A., María Montalto deMecca, and Laura C. Bartel. "Toxic Side Effects of Drugs Used to Treat Chagas’ Disease (American Trypanosomiasis)." Human & Experimental Toxicology 25, no. 8 (August 2006): 471–79. http://dx.doi.org/10.1191/0960327106het653oa.

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Chagas’ disease (American trypanosomiasis) is an endemic parasitic disease in some areas of Latin America. About 16-18 million persons are infected with the aetiological agent of the disease, Trypanosoma cruzi, and more than 100 million are living at risk of infection. There are different modes of infection: 1) via blood sucking vector insects infected with T. cruzi, accounting for 80-90% of transmission of the disease; 2) via blood transfusion or congenital transmission, accounting for0.5-8% of transmission; 3) other less common forms of infection, eg, from infected food or drinks or via infected organs used in transplants. The acute phase of the disease can last from weeks to months and typically is asymptomatic or associated with fever and other mild non-specific manifestations. However, life-threatening myocarditis or meningoencephalitis can occur during the acute phase. The death rate for persons in this phase is about 10%. Approximately 10-50% of the survivors develop chronic Chagas’ disease, which is characterized by potentially lethal cardiopathy and megacolon or megaoesophagus. There are two drugs available for the aetiological treatment of Chagas’ disease: nifurtimox (Nfx) and benznidazole (Bz). Nfx is a nitrofurane and Bz is a nitroimidazole compound. The use of these drugs to treat the acute phase of the disease is widely accepted. However, their use in the treatment of the chronic phase is controversial. The undesirable side effects of both drugs are a major drawback in their use, frequently forcing the physician to stop treatment. The most frequent adverse effects observed in the use of Nfx are: anorexia, loss of weight, psychic alterations, excitability, sleepiness, digestive manifestations such as nausea or vomiting, and occasionally intestinal colic and diarrhoea. In the case of Bz, skin manifestations are the most notorious (eg, hypersensitivity, dermatitis with cutaneous eruptions, generalized oedema, fever, lymphoadenopathy, articular and muscular pain), with depression of bone marrow, thrombocytopenic purpura and agranulocytosis being the more severe manifestations. Experimental toxicity studies with Nfx evidenced neurotoxicity, testicular damage, ovarian toxicity, and deleterious effects in adrenal, colon, oesophageal and mammary tissue. In the case of Bz, deleterious effects were observed in adrenals, colon and oesophagus. Bz also inhibits the metabolism of several xenobiotics biotransformed by the cytochrome P450 system and its reactive metabolites react with fetal components in vivo. Both drugs exhibited significant mutagenic effects and were shown to be tumorigenic or carcinogenic in some studies. The toxic side effects of both nitroheterocyclic derivatives require enzymatic reduction of their nitro group. Those processes are fundamentally mediated by cytochrome P450 reductase and cytochrome P450. Other enzymes such as xanthine oxidoreductase or aldehyde oxidase may also be involved.

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Yu, Dong, Guowei Wang, Qianming Ding, Tianyu Li, and Ya Jia. "Effects of bounded noise and time delay on signal transmission in excitable neural networks." Chaos, Solitons & Fractals 157 (April 2022): 111929. http://dx.doi.org/10.1016/j.chaos.2022.111929.

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Becker, Daniel E. "Basic and Clinical Pharmacology of Autonomic Drugs." Anesthesia Progress 59, no. 4 (December 1, 2012): 159–69. http://dx.doi.org/10.2344/0003-3006-59.4.159.

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Abstract Autonomic drugs are used clinically to either imitate or inhibit the normal functions of the sympathetic and parasympathetic nervous systems. A large number of additional drug classes also interact with these systems to produce a stunning number of possible side effects. This article reviews the basic function of the autonomic nervous system and the various drug classes that act within these neural synapses.

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Houben, Akke Mats. "Frequency Selectivity of Neural Circuits With Heterogeneous Discrete Transmission Delays." Neural Computation 33, no. 8 (July 26, 2021): 2068–86. http://dx.doi.org/10.1162/neco_a_01404.

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Neurons are connected to other neurons by axons and dendrites that conduct signals with finite velocities, resulting in delays between the firing of a neuron and the arrival of the resultant impulse at other neurons. Since delays greatly complicate the analytical treatment and interpretation of models, they are usually neglected or taken to be uniform, leading to a lack in the comprehension of the effects of delays in neural systems. This letter shows that heterogeneous transmission delays make small groups of neurons respond selectively to inputs with differing frequency spectra. By studying a single integrate-and-fire neuron receiving correlated time-shifted inputs, it is shown how the frequency response is linked to both the strengths and delay times of the afferent connections. The results show that incorporating delays alters the functioning of neural networks, and changes the effect that neural connections and synaptic strengths have.

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MONTEIRO, J. F. G., D. J. ESCUDERO, C. WEINREB, T. FLANIGAN, S. GALEA, S. R. FRIEDMAN, and B. D. L. MARSHALL. "Understanding the effects of different HIV transmission models in individual-based microsimulation of HIV epidemic dynamics in people who inject drugs." Epidemiology and Infection 144, no. 8 (January 12, 2016): 1683–700. http://dx.doi.org/10.1017/s0950268815003180.

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SUMMARYWe investigated how different models of HIV transmission, and assumptions regarding the distribution of unprotected sex and syringe-sharing events (‘risk acts’), affect quantitative understanding of HIV transmission process in people who inject drugs (PWID). The individual-based model simulated HIV transmission in a dynamic sexual and injecting network representing New York City. We constructed four HIV transmission models: model 1, constant probabilities; model 2, random number of sexual and parenteral acts; model 3, viral load individual assigned; and model 4, two groups of partnerships (low and high risk). Overall, models with less heterogeneity were more sensitive to changes in numbers risk acts, producing HIV incidence up to four times higher than that empirically observed. Although all models overestimated HIV incidence, micro-simulations with greater heterogeneity in the HIV transmission modelling process produced more robust results and better reproduced empirical epidemic dynamics.

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Johnston, Geoffrey L., Peter W. Gething, Simon I. Hay, David L. Smith, and David A. Fidock. "Modeling Within-Host Effects of Drugs on Plasmodium falciparum Transmission and Prospects for Malaria Elimination." PLoS Computational Biology 10, no. 1 (January 23, 2014): e1003434. http://dx.doi.org/10.1371/journal.pcbi.1003434.

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O'Neill, Robert D. "Uric acid levels and dopamine transmission in rat striatum: diurnal changes and effects of drugs." Brain Research 507, no. 2 (January 1990): 267–72. http://dx.doi.org/10.1016/0006-8993(90)90281-f.

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Piazza, P. V., M. Barrot, F. Rouge-Pont, M. Marinelli, S. Maccari, D. N. Abrous, H. Simon, and M. Le Moal. "Suppression of glucocorticoid secretion and antipsychotic drugs have similar effects on the mesolimbic dopaminergic transmission." Proceedings of the National Academy of Sciences 93, no. 26 (December 24, 1996): 15445–50. http://dx.doi.org/10.1073/pnas.93.26.15445.

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Iqbal, Naveed, Abdulmajid Lawal, and Azzedine Zerguine. "MitigatingWireless Channel Impairments in Seismic Data Transmission Using Deep Neural Networks." Sensors 21, no. 18 (September 12, 2021): 6105. http://dx.doi.org/10.3390/s21186105.

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The traditional cable-based geophone network is an inefficient way of seismic data transmission owing to the related cost and weight. The future of oil and gas exploration technology demands large-scale seismic acquisition, versatility, flexibility, scalability, and automation. On the one hand, a typical seismic survey can pile up a massive amount of raw seismic data per day. On the other hand, the need for wireless seismic data transmission remains immense. Moving from pre-wired to wireless geophones faces major challenges given the enormous amount of data that needs to be transmitted from geophones to the on-site data collection center. The most important factor that has been ignored in the previous studies for the realization of wireless seismic data transmission is wireless channel effects. While transmitting the seismic data wirelessly, impairments like interference, multi-path fading, and channel noise need to be considered. Therefore, in this work, a novel amalgamation of blind channel identification and deep neural networks is proposed. As a geophone already is responsible for transmitting a tremendous amount of data under tight timing constraints, the proposed setup eschews sending any additional training signals for the purpose of mitigating the channel effects. Note that the deep neural network is trained only on synthetic seismic data without the need to use real data in the training process. Experiments show that the proposed method gives promising results when applied to the real/field data set.

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Kirmse, Knut, Christian A. Hübner, Dirk Isbrandt, Otto W. Witte, and Knut Holthoff. "GABAergic Transmission during Brain Development: Multiple Effects at Multiple Stages." Neuroscientist 24, no. 1 (April 5, 2017): 36–53. http://dx.doi.org/10.1177/1073858417701382.

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In recent years, considerable progress has been achieved in deciphering the cellular and network functions of GABAergic transmission in the intact developing brain. First, in vivo studies in non-mammalian and mammalian species confirmed the long-held assumption that GABA acts as a mainly depolarizing neurotransmitter at early developmental stages. At the same time, GABAergic transmission was shown to spatiotemporally constrain spontaneous cortical activity, whereas firm evidence for GABAergic excitation in vivo is currently missing. Second, there is a growing body of evidence indicating that depolarizing GABA may contribute to the activity-dependent refinement of neural circuits. Third, alterations in GABA actions have been causally linked to developmental brain disorders and identified as potential targets of timed prophylactic interventions. In this article, we review these major recent findings and argue that both depolarizing and inhibitory GABA actions may be crucial for physiological brain maturation.

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Yanagisawa, Kiminori, Masayasu Toratani, Ayumu Asai, Masamitsu Konno, Hirohiko Niioka, Tsunekazu Mizushima, Taroh Satoh, et al. "Convolutional Neural Network Can Recognize Drug Resistance of Single Cancer Cells." International Journal of Molecular Sciences 21, no. 9 (April 30, 2020): 3166. http://dx.doi.org/10.3390/ijms21093166.

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It is known that single or isolated tumor cells enter cancer patients’ circulatory systems. These circulating tumor cells (CTCs) are thought to be an effective tool for diagnosing cancer malignancy. However, handling CTC samples and evaluating CTC sequence analysis results are challenging. Recently, the convolutional neural network (CNN) model, a type of deep learning model, has been increasingly adopted for medical image analyses. However, it is controversial whether cell characteristics can be identified at the single-cell level by using machine learning methods. This study intends to verify whether an AI system could classify the sensitivity of anticancer drugs, based on cell morphology during culture. We constructed a CNN based on the VGG16 model that could predict the efficiency of antitumor drugs at the single-cell level. The machine learning revealed that our model could identify the effects of antitumor drugs with ~0.80 accuracies. Our results show that, in the future, realizing precision medicine to identify effective antitumor drugs for individual patients may be possible by extracting CTCs from blood and performing classification by using an AI system.

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Satoh, Ryusei, Kiyoharu Kawakami, and Kazuhiko Nakadate. "Effects of Smart Drugs on Cholinergic System and Non-Neuronal Acetylcholine in the Mouse Hippocampus: Histopathological Approach." Journal of Clinical Medicine 11, no. 12 (June 9, 2022): 3310. http://dx.doi.org/10.3390/jcm11123310.

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In recent years, people in the United States and other countries have been using smart drugs, called nootropic or cognitive enhancers, to improve concentration and memory learning skills. However, these drugs were originally prescribed for attention-deficit hyperactivity disorder and dementia, and their efficacy in healthy people has not yet been established. We focused on acetylcholine in the hippocampus, which is responsible for memory learning, and elucidate the long-term effects of smart drugs on the neural circuits. Smart drugs were administered orally in normal young mice for seven weeks. The hippocampus was sectioned and compared histologically by hematoxylin and eosin (HE) staining, immunohistochemistry for acetylcholine, and immunoelectron microscopy. There were no significant changes in acetylcholinesterase staining. However, in HE, we found perivascular edema, and choline acetyltransferase staining showed increased staining throughout the hippocampus and new signal induction in the perivascular area in the CA3, especially in the aniracetam and α-glyceryl phosphoryl choline group. Additionally, new muscarinic acetylcholine receptor signals were observed in the CA1 due to smart drug intake, suggesting that vasodilation might cause neuronal activation by increasing the influx of nutrients and oxygen. Moreover, these results suggest a possible new mechanism of acetylcholine-mediated neural circuit activation by smart drug intake.

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Elmorsy, E., SM Attalla, E. Fikry, A. Kocon, R. Turner, D. Christie, A. Warren, LL Nwidu, and WG Carter. "Adverse effects of anti-tuberculosis drugs on HepG2 cell bioenergetics." Human & Experimental Toxicology 36, no. 6 (July 26, 2016): 616–25. http://dx.doi.org/10.1177/0960327116660751.

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Tuberculosis (TB) is an intractable chronic infection. Disease treatment with anti-TB drugs remains challenging due to drug-induced hepatotoxicity. The toxicity of the anti-TB drugs rifampicin (RIF), isoniazid (INH) and pyrazinamide (PZA) either alone or in combination was investigated in HepG2 cells. Assays of intracellular adenosine triphosphate (ATP) levels at 4-, 24- and 48-h post-exposure to gradient concentrations of RIF, INH and PZA were conducted. Drug-induced effects on mitochondrial membrane potential (MMP), mitochondrial complex I and complex III activity, nicotinamide adenine dinucleotide (NAD+) levels and cellular lactate production were assessed. Decreased ATP levels were dose-dependent and correlated with drug exposure duration. Approximate 24-h IC50s were 0.5 mM, 70 mM and 84 mM for RIF, INH and PZA, respectively. Twenty-four hours post-drug treatment, reductions of MMP ( p = 0.0005), mitochondrial complex I and III activities ( p = 0.0001 and p = 0.0003, respectively), NAD+ levels ( p = 0.0057) and increased lactate production ( p < 0.0001) were observed. Drug combinations used to mimic cumulative drug treatments induced a synergistic inhibition of mitochondrial complex I activity. An assessment of cellular ultrastructure using transmission electron microscopy indicated drug-induced mitophagy. Collectively, our study suggests that hepatotoxicity of commonly employed anti-TB drugs is mediated by their curtailment of mitochondrial function.

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Schneider, Petra, Andrew S. Bell, Derek G. Sim, Aidan J. O'Donnell, Simon Blanford, Krijn P. Paaijmans, Andrew F. Read, and Sarah E. Reece. "Virulence, drug sensitivity and transmission success in the rodent malaria, Plasmodium chabaudi." Proceedings of the Royal Society B: Biological Sciences 279, no. 1747 (September 26, 2012): 4677–85. http://dx.doi.org/10.1098/rspb.2012.1792.

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Here, we test the hypothesis that virulent malaria parasites are less susceptible to drug treatment than less virulent parasites. If true, drug treatment might promote the evolution of more virulent parasites (defined here as those doing more harm to hosts). Drug-resistance mechanisms that protect parasites through interactions with drug molecules at the sub-cellular level are well known. However, parasite phenotypes associated with virulence might also help parasites survive in the presence of drugs. For example, rapidly replicating parasites might be better able to recover in the host if drug treatment fails to eliminate parasites. We quantified the effects of drug treatment on the in-host survival and between-host transmission of rodent malaria ( Plasmodium chabaudi ) parasites which differed in virulence and had never been previously exposed to drugs. In all our treatment regimens and in single- and mixed-genotype infections, virulent parasites were less sensitive to pyrimethamine and artemisinin, the two antimalarial drugs we tested. Virulent parasites also achieved disproportionately greater transmission when exposed to pyrimethamine. Overall, our data suggest that drug treatment can select for more virulent parasites. Drugs targeting transmission stages (such as artemisinin) may minimize the evolutionary advantage of virulence in drug-treated infections.

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Journal articles on the topic 'Neural transmission Effects of drugs on'

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