Relevant bibliographies by topics / Neural transmission Effects of drugs on

Academic literature on the topic 'Neural transmission Effects of drugs on'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "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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Dissertations / Theses on the topic "Neural transmission Effects of drugs on"

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Balaños, Guzman Carlos Alberto. "The effects of the kappa agonist U-50,488 on morphine-induced place preference conditioning and Fos immunoreactivity in the preweanling and periadolescent rat." CSUSB ScholarWorks, 1995. https://scholarworks.lib.csusb.edu/etd-project/1074.

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The effects of the kappa opioid agonist U-50,488 on morphine-induced condtioned place preference (CPP), locomotor activity and Fos immunoreactivity and assessed in 10-, 17- and 35-day old rats. It was predicted that kappa agonist treatment would block the unconditioned and conditioned behaviors produced by morhine (a mu opioid receptor agonist).
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Field, Brent A. "The effects of noradrenaline on cortical signal processing /." view abstract or download file of text, 2000. http://wwwlib.umi.com/cr/uoregon/fullcit?p9978587.

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Thesis (Ph. D.)--University of Oregon, 2000.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 140-159). Also available for download via the World Wide Web; free to University of Oregon users.
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Chan, Ho Ka. "Impact of synaptic properties, background activities and conductance effects on neural computation of correlated inputs." HKBU Institutional Repository, 2015. https://repository.hkbu.edu.hk/etd_oa/176.

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Neurons transmit information through spikes in neural network through synaptic couplings. Given the prevalence of correlation among neural spike trains experimentally observed in different brain areas, it is of interest to study how neurons compute correlated input. Yet how it depends on the synaptic properties and conductance kinetics in neuronal interaction is very little known. Through simulation of leaky integrate-and-fire (LIF) neurons, we have studied the effects of excitatory and inhibitory synaptic decay times, level of background activities and higher-order conductance effects on the output correlation of different time scales for neurons receiving correlated excitatory input, and provided important understanding on the mechanism of how these factors influence neural computation of such correlated input. We showed that when the conductance effects are totally ignored, increasing excitatory synaptic decay time jitters output spike time and shapes the output correlation of short to medium time scale, while the output correlation of very long time scale is determined by the membrane time constant. When conductance effects are considered, this is no longer the case as the effective membrane time constant becomes comparable to the excitatory decay time. We found that the ratio of long-term correlation to short-term correlation (synchrony) increases with excitatory synaptic decay time and decreases with the level of input activities due to the combined effects of jittered spike time, which can be predicted from the time window and magnitude of the effects of a single input spike on membrane potential, and burst firing. In particular, it is possible for neurons with small excitatory synaptic decay time in high conductance state to respond to correlated input by solely giving extra precisely timed synchronous spikes without exhibiting correlation of longer time scale. In addition, we found that inhibitory synaptic decay time shapes correlation by controlling the relative contribution of excitatory and inhibitory input to output firing. As a result, both output correlation and synchrony increase with it. These results are qualitatively true for a wide range of input correlation and synaptic efficacies. Finally, we showed that fluctuations of conductance and membrane potential reduce output correlation, which can be explained by the reduced prevalence of burst firing. These results suggest that spike initiation dynamics of neurons can be well characterized by their synaptic decay times and the level of input activities. These properties are therefore expected to influence neurons’ ability to code temporal information. These results also hint that correlation, in particular that of long time scale, would be lower if more realistic biophysical features like neural adaptations and network circuitry with feed-forward or recurrent inhibition are considered. It suggests that studies using single LIF neurons tend to overestimate output correlation and underestimate the ability of neurons in producing precisely timed output.
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Li, Melissa Wei. "The effects of chronic activation of endothelin ETB receptors on blood pressure, venomotor tone, neurohumoral activity, and oxidative sress." Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph.D.)--Michigan State University. Dept. of Pharmacology and Toxicology, 2008.
Title from PDF t.p. (viewed on July 22, 2009) Includes bibliographical references (p. 175-214). Also issued in print.
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Burton, Susan Frances. "A study of the effects of the pineal hormone, melatonin, on dopaminergic transmission in the central nervous system of rats." Thesis, Rhodes University, 1990. http://hdl.handle.net/10962/d1001463.

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Dopamine mechanisms in the central nervous system are important in the control of both normal and abnormal motor function. The recent observations in both animal and human studies, that melatonin, the principal hormone of the pineal gland, may have a role in the control of movement and the pathophysiology of movement disorders, have given rise to the concept that melatonin may have a modulatory influence on central dopaminergic neurotransmission. This study makes use of three animal behavioural models as well as a biochemical model of central dopaminergic function to further investigate the concept. Results from studies using the biochemical model, which investigated the effect of melatonin on dopamine and apomorphine stimulation of dopamine-sensitive adenylate cylase, suggest that melatonin is neither a competitive antagonist nor agonist at the D₁ receptor level, although the possibility of physiological stimulation or antagonism is not excluded. In behavioural studies, prior melatonin mg/kg administration (1 and 10 (8M) ip) inhibited apomorphine induced stereotypy and locomotor activity in normal rats, and apomorphine-induced rotational behaviour in 6-hydroxydopamine and quinolinic acid lesioned rats. The possibility that these results may have physiological significance is borne out by the observation that, under enviromental lighting conditions that are associated with raised endogeous melatonin levels, apomorphine- induced stereotypy and locomotor activity is attenuated. The general conclusion is that melatonin has an inhibitory influence on central nervous system dopaminergic function, suggesting therefore, that the pineal gland and melatonin may have a role in the pathophysiology and treatment of movement and behavioural disorders associated with dopaminergic dysfunction
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Harmon, Amanda L. "Preventing Mother-to-Child Transmission of Human Immunodeficiency Virus-1 (HIV-1): Effects of Intrapartum and Neonatal Single-Dose Nevirapine Prophylaxis and Subsequent HIV-1 Drug Resistance at Antiretroviral Treatment Initiation." Scholarship @ Claremont, 2011. http://scholarship.claremont.edu/cmc_theses/305.

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The prevention of mother-to-child transmission is one of the most powerful tools in human immunodeficiency virus type 1 (HIV-1) prevention and has huge potential to improve both maternal and child health. In the absence of any preventative measures, infants born to and breastfed by their HIV-positive mothers have roughly a one-in-three chance of acquiring the infection themselves. HIV can be passed on from mother-to-child during pregnancy, during labor and delivery, and even after during breastfeeding. Intrapartum and neonatal single-dose nevirapine (sd-NVP) is the foundation of preventing mother-to-child transmission in lower resource settings where it has been used alone or as part of combination regimens. Both its simplicity and its long plasma half-life contribute to the success of sd-NVP based therapy. However, sd-NVP frequently results in HIV-1 viral resistance in mothers and children who become HIV infected despite prophylaxis. Sd-NVP leads to the development of non-nucleoside reverse transcriptase inhibitors (NNRTI) drug resistance, compromising the success of treatment of mother and child with subsequent antiretroviral combinations. Resistance to NNRTIs is particularly worrisome in lower resource settings since many subsequent regimens for maternal and infant antiretroviral therapy include a NNRTI drug.
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Huang, Kuan-Chang, and 黃冠章. "Studies of the effects of carboxamide derivatives on the neural transmission." Thesis, 2014. http://ndltd.ncl.edu.tw/handle/5tfmsa.

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碩士
中山醫學大學
生物醫學科學學系碩士班
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Recent studies have shown that KCNQ openers have potential for the treatment of several central nervous system disorders, eg., epilepsy, migraine. The purpose of this study was to find new compounds of KCNQ opener. We used the structure of KCNQ (potassium channel, voltage-gated, KQT-like Subfamily) openers ML213 and retigabine as the template to search the possible KCNQ openers. Dr. Min-Jon Lin used the website Hit2lead.com to compare the structure of KCNQ openers and found that 21 derivatives of KCNQ opener. In these experiments the nerve-evoked muscle tension is inhibited by the treatment 2-amantyl-N~1~mesitylglycinamide hydrochloride (#0342；50μM). Treatment with #0342, 1 -cyclohexyl -N- mesitylprolinamide hydrochloride (#0335), 2 - (1-azepanyl) -N- mesitylbutanamide (#0331) and mesityl -2-peridinecarbox amide hydrochloride (#0321) produced the significant effect of titanic failure (50 Hz stimulation). In terminal spike recordings, the treatment of #0342, #0321 and #0335 produced the significant inhibition effect of sodium spikes. Therefore, the effects of the #0342, #0335 and #0321 are not similar to the KCNQ openers. These data suggested that #0342, #0335 and #0321 are more likely to be the sodium channel blockers than KCNQ modulators. Our initial research planning is to screen of new KCNQ openers from the predicted compounds. However these unexpected results indicate that the effects of #0342, #0321, and #0335 on the blocked of nerve – muscle conduction are more likely through the inhibition of sodium channels.
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Blaak, John B. "Effects of volume and exercise complexity on neural adaptations, strength gains and lean body mass in untrained adults." 2002. http://www.oregonpdf.org.

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Hayes, Bradley T. "The neuromuscular effects of a long-term static stretching program on the human soleus." 2006. http://www.oregonpdf.org.

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Thesis (Ph. D.)--Oregon State University, 2006.
Blank pages 143 and 159 not microfilmed. Includes bibliographical references. Also available online (PDF file) by a subscription to the set or by purchasing the individual file.
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Servonnet, Alice. "Neural substrates mediating the behavioural effects of antipsychotic medications and pavlovian cues : importance for maladaptive processes in psychiatric disorders." Thesis, 2020. http://hdl.handle.net/1866/25546.

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Les antipsychotiques sont administrés chroniquement pour prévenir de nouveaux épisodes psychotiques dans la schizophrénie. Ces médicaments diminuent l’activité des récepteurs dopaminergiques de type 2. Diminuer chroniquement la transmission dopaminergique induit des compensations pouvant mener à une sensibilisation du système dopaminergique. Cette sensibilisation pourrait diminuer l’efficacité des antipsychotiques et exacerber la psychose. Chez le rat, la sensibilisation dopaminergique induite par les antipsychotiques augmente les effets psychomoteurs et motivationnels des agonistes dopaminergiques. Le premier objectif de la présente thèse était de caractériser les substrats neuronaux régulant l’expression de la sensibilisation dopaminergique évoquée par les antipsychotiques. Ceci est important afin d’améliorer le traitement à long terme de la schizophrénie. Pour ce faire, des rats ont reçu un traitement cliniquement pertinent à l’antipsychotique halopéridol. Ce traitement sensibilise aux effets psychomoteurs de l’agoniste dopaminergique d-amphétamine. Cet indice comportemental de sensibilisation dopaminergique a été utilisé pour déterminer les contributions spécifiques du système dopaminergique et l’implication des effets centraux de la d-amphétamine. Puisqu’il y a une relation étroite entre le stress et l’activité dopaminergique, les réponses liées au stress ont également été mesurées. Ceci est important, puisque le stress exacerbe la psychose. La présente thèse démontre que les récepteurs dopaminergiques régulent de manière distincte la sensibilisation dopaminergique. En effet, la transmission via les récepteurs de type 2 exacerbe cette sensibilisation, alors que la transmission via les récepteurs de type 1 la tempère. Également, la présente thèse suggère que des processus périphériques sont nécessaires à l’expression de la sensibilisation dopaminergique. De plus, la sensibilisation pourrait augmenter les réponses au stress. En effet, cette sensibilisation est renversée lorsque la synthèse de l’hormone de stress corticostérone est inhibée, en plus d’être associée à certains comportements suggérant un stress augmenté. Chez le rat, la sensibilisation dopaminergique évoquée par les antipsychotiques potentialise également les effets motivationnels des stimuli conditionnés prédisant des récompenses. Lorsque ces stimuli acquièrent trop de valeur motivationnelle, ils peuvent motiver des comportements pathologiques. Ainsi, une potentialisation de la valeur motivationnelle des stimuli conditionnés provoquée par les antipsychotiques pourrait avoir des implications importantes dans des processus motivationnels anormaux dans la schizophrénie, tels que la psychose et la forte prévalence de toxicomanie. Ainsi, le deuxième objectif de la présente thèse était d’étudier les mécanismes neurobiologiques régulant les effets comportementaux des stimuli conditionnés, particulièrement le rôle du noyau basolatéral de l’amygdale. Ici, le rôle de ce noyau a été étudié chez des animaux non traités aux antipsychotiques, puisque sa contribution reste incomprise. Ce travail pourrait révéler des mécanismes neurobiologiques potentiellement impliqués dans la sensibilisation dopaminergique évoquée par les antipsychotiques. La présente thèse démontre que l’activation optogénétique de l’amygdale basolatérale potentialise les effets comportementaux des stimuli conditionnés, en augmentant leur valeur motivationnelle et leur capacité à guider le comportement vers des récompenses imminentes. Ainsi, une activité excessive de l’amygdale basolatérale pourrait attribuer trop de pouvoir aux stimuli conditionnés, et ceci pourrait jouer un rôle dans l’état motivationnel anormal provoqué par les antipsychotiques. La présente thèse identifie de nouveaux mécanismes par lesquels les antipsychotiques et les stimuli conditionnés favorisent des réponses pathologiques.
Schizophrenia requires long-term antipsychotic treatment to prevent psychosis relapse. Antipsychotic drugs temper psychotic symptoms by reducing dopamine D2 receptor-mediated signalling. Chronically decreasing dopamine transmission produces neuronal compensation leading to supersensitivity to dopamine stimulation. In patients, this dopamine supersensitivity would compromise antipsychotic efficacy and exacerbate psychotic symptoms. In laboratory animals, antipsychotic-evoked dopamine supersensitivity enhances the psychomotor and reward-enhancing effects of dopamine agonists. The first objective of the present thesis was to characterize the biological substrates mediating the expression of antipsychotic-evoked dopamine supersensitivity, a necessary work for developing better long-term treatment strategies. To do so, rats were chronically exposed to a clinically relevant antipsychotic treatment regimen, using the drug haloperidol. Haloperidol produces dopamine supersensitivity, as indicated by an exaggerated psychomotor response to the dopamine agonist d-amphetamine. This behavioural index of supersensitivity was used to examine the specific contributions of the dopamine system and the central effects of d-amphetamine. Given that there is a close relationship between stress and dopamine activity, it was also determined whether antipsychotic-evoked dopamine supersensitivity alters stress-like responses. This is important to consider because stress is a contributing factor to psychosis relapse. The present thesis first reveals that D1- and D2-mediated transmissions contribute distinctively to the expression of antipsychotic-evoked dopamine supersensitivity, with D2 transmission promoting this supersensitivity and D1 transmission tempering it. The present thesis also provides evidence that peripheral processes play a necessary role in dopamine supersensitivity. Additionally, antipsychotic-evoked dopamine supersensitivity could potentiate stress-like responses. Indeed, the expression of supersensitivity is reversed by inhibition of the synthesis of the stress hormone corticosterone and is linked with some signs of heightened stress-related behaviours. In rats, antipsychotic-evoked dopamine supersensitivity potentiates the incentive motivational effects of reward-predictive conditioned stimuli. When these stimuli acquire too much motivational value, they motivate maladaptive responses. Hence, the increased motivational value of conditioned stimuli elicited by antipsychotic exposure could be involved in impaired motivational processes found in schizophrenia, such as psychosis and the greater vulnerability to drug addiction. Thereby, the last goal of the present thesis was to investigate the neurobiological substrates mediating the behavioural effects of reward-predictive stimuli, with a special focus on the role of the basolateral nucleus of the amygdala. This was investigated in antipsychotic-naïve rats because there are important caveats in our current understanding of the functional role of the basolateral amygdala. Such investigation could give novel insights on the neurobiological effects of antipsychotic-evoked dopamine supersensitivity. Here it is shown that optogenetic stimulation of basolateral amygdala neurons potentiates the behavioural effects of conditioned stimuli, by increasing their motivational value and their ability to guide behaviour toward impending rewards. The implication for this is that excessive activity in the basolateral amygdala could attribute too much motivational power to conditioned stimuli, and this could be involved in the abnormal motivational state produced by antipsychotic drugs. Taken together, the present thesis provides novel mechanisms by which antipsychotic drugs and reward-predictive stimuli promote maladaptive responses.
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Books on the topic "Neural transmission Effects of drugs on"

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J, Pycock Christopher, ed. Neurotransmitters and drugs. 3rd ed. London: Chapman & Hall, 1991.

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Pharmacology of neuromuscular function. 2nd ed. London: Wright, 1990.

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Behavioral neurobiology of the endocannabinoid system. Berlin: Springer-Verlag, 2009.

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Geoffrey, Burnstock, and Hoyle, Charles H. V., 1955-, eds. Autonomic neuroeffector mechanisms. Chur, Switzerland: Harwood Academic Publishers, 1992.

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Oliver von Bohlen und Halbach. Neurotransmitters and neuromodulators: Handbook of receptors and biological effects. Weinheim: Wiley-VCH, 2002.

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Rolf, Dermietzel, ed. Neurotransmitters and neuromodulators: Handbook of receptors and biological effects. Weinheim: Wiley-VCH, 2002.

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The benzodiazepine receptor: Drug acceptor only or a physiologically relevant part of our central nervous system? Cambridge: Cambridge University Press, 1987.

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Richard, Pates, McBride Andrew 1957-, and Arnold Karin, eds. Injecting illicit drugs. Oxford: Blackwell Publishing/Addiction Press, 2005.

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Nobel Symposium (76th 1989 Lidingö, Sweden). Cholinergic neurotransmission: Functional and clinical aspects : proceedings of Nobel Symposium 76. Amsterdam: Elsevier, 1990.

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B, Dunnett S., and Björklund Anders 1945-, eds. Functional neural transplantation II: Novel cell therapies for CNS disorders. Amsterdam: Elsevier, 2000.

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Book chapters on the topic "Neural transmission Effects of drugs on"

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Thotahewa, Kasun M. S., Ahmed I. Al-Kalbani, Jean-Michel Redouté, and Mehmet Rasit Yuce. "Electromagnetic Effects of Wireless Transmission for Neural Implants." In Neural Computation, Neural Devices, and Neural Prosthesis, 1–22. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8151-5_1.

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dos Passos, Hudelson, and Ian Carlos Hübner. "Effects of Substance Use on Neural Development." In Drugs and Human Behavior, 141–49. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62855-0_10.

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Grundman, M., J. Corey-Bloom, and L. J. Thal. "Perspectives in clinical Alzheimer’s disease research and the development of antidementia drugs." In Journal of Neural Transmission. Supplementa, 255–75. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6467-9_23.

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Mielke, R., J. Kessler, B. Szelies, K. Herholz, K. Wienhard, and W. D. Heiss. "Vascular dementia: perfusional and metabolic disturbances and effects of therapy." In Journal of Neural Transmission Supplement, 183–91. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-6892-9_12.

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Schwab, M., I. Antonow-Schlorke, U. Dürer, and R. Bauer. "Effects of Cerebrolysin® on cytoskeletal proteins after focal ischemia in rats." In Journal of Neural Transmission Supplement, 279. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-6892-9_24.

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Funke, M., J. Fiehler, I. Mewes, M. Eiselt, I. Rother, and M. Windisch. "Dose-dependent effects of Cerebrolysin® on EEG and short term memory of healthy volunteers during control and hyperventilation induced cerebral ischemia." In Journal of Neural Transmission. Supplementa, 385–98. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6467-9_34.

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Eckert, Michael J., and Wickliffe C. Abraham. "Effects of Environmental Enrichment Exposure on Synaptic Transmission and Plasticity in the Hippocampus." In Neurogenesis and Neural Plasticity, 165–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/7854_2012_215.

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Vanier, Michael C., and James M. Bower. "Differential Effects of Norepinephrine on Synaptic Transmission in Layers 1A and 1B of Rat Olfactory Cortex." In Computation and Neural Systems, 267–71. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3254-5_41.

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See, Ronald E., and Peter W. Kalivas. "Tolerance and Sensitization to the Effects of Antipsychotic Drugs on Dopamine Transmission." In Antipsychotics, 203–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61007-3_7.

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Rousseau, Jean-Philippe, and Gaspard Montandon. "Neural Mechanisms Regulating Opioid-Induced Respiratory Depression and Therapeutic Strategies to Alleviate the Respiratory Side-Effects of Opioid Drugs." In Control of Breathing during Sleep, 233–45. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003000631-23.

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Conference papers on the topic "Neural transmission Effects of drugs on"

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Bradburn. "Reducing transmission error effects using a self-organizing network." In International Joint Conference on Neural Networks. IEEE, 1989. http://dx.doi.org/10.1109/ijcnn.1989.118294.

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Chen, Huiyuan, and Jing Li. "Learning Data-Driven Drug-Target-Disease Interaction via Neural Tensor Network." In Twenty-Ninth International Joint Conference on Artificial Intelligence and Seventeenth Pacific Rim International Conference on Artificial Intelligence {IJCAI-PRICAI-20}. California: International Joint Conferences on Artificial Intelligence Organization, 2020. http://dx.doi.org/10.24963/ijcai.2020/477.

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Precise medicine recommendations provide more effective treatments and cause fewer drug side effects. A key step is to understand the mechanistic relationships among drugs, targets, and diseases. Tensor-based models have the ability to explore relationships of drug-target-disease based on large amount of labeled data. However, existing tensor models fail to capture complex nonlinear dependencies among tensor data. In addition, rich medical knowledge are far less studied, which may lead to unsatisfied results. Here we propose a Neural Tensor Network (NeurTN) to assist personalized medicine treatments. NeurTN seamlessly combines tensor algebra and deep neural networks, which offers a more powerful way to capture the nonlinear relationships among drugs, targets, and diseases. To leverage medical knowledge, we augment NeurTN with geometric neural networks to capture the structural information of both drugs’ chemical structures and targets’ sequences. Extensive experiments on real-world datasets demonstrate the effectiveness of the NeurTN model.
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Shi, Rongye, Thomas C. Jackson, Brian Swenson, Soummya Kar, and Lawrence Pileggi. "On the design of phase locked loop oscillatory neural networks: Mitigation of transmission delay effects." In 2016 International Joint Conference on Neural Networks (IJCNN). IEEE, 2016. http://dx.doi.org/10.1109/ijcnn.2016.7727450.

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Hao, Man-Zhao, Xin He, Daryl R. Kipke, and Ning Lan. "Effects of electrical stimulation of cutaneous afferents on corticospinal transmission of tremor signals in patients with Parkinson's disease." In 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2013. http://dx.doi.org/10.1109/ner.2013.6695945.

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Catanese, Clara, Reda Ayassi, Erwan Pincemin, and Yves Jaouen. "A Fully Connected Neural Network Approach to Mitigate Fiber Nonlinear Effects in 200G DP-16-QAM Transmission System." In 2020 22nd International Conference on Transparent Optical Networks (ICTON). IEEE, 2020. http://dx.doi.org/10.1109/icton51198.2020.9203197.

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Jaipradidtham, C. "Probability parameter estimation of outage rate effects for lightning overvoltage analysis on 500 kV EHV double circuit transmission lines using neural networks." In 2005 International Power Engineering Conference. IEEE, 2005. http://dx.doi.org/10.1109/ipec.2005.207018.

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Yalcin, Huseyin, Hissa Al-Thani, and Samar Shurbaji. "Development and In Vivo Testing of Smart Nanoparticles for Enhanced Anti-Cancer Activity and Reduced Cardiotoxicity Associated with Tyrosine Kinase Inhibitors." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0088.

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Tyrosine kinase inhibitors (TKIs) are new generation of anti-cancer drugs with very high efficiency against cancer cells. However, TKIs are associated with severe cardiotoxicity limiting their clinical benefits. One TKI that has been developed recently but not explored much is Ponatinib. The use of nanoparticles as a better therapeutic agent to deliver anti-cancer drugs and reduce their cardiotoxicity has been recently considered. In this study, PLGA-PEG-PLGA nanoparticles were synthesized to deliver Ponatinib while reducing its cardiotoxicity for treatment of chronic myeloid leukemia. Shape, size, surface charge and drug uptake ability of these nanoparticles were assessed using transmission electron microscopy (TEM), ZetaSIZER NANO and high-performance liquid chromatography (HPLC). Cardiotoxicity of Ponatinib, unloaded and loaded PLGA-PEG-PLGA nanoparticles were studied on zebrafish model through measuring the survival rate and cardiac function parameters, to optimize efficient drug concentrations in an in vivo setting. These particles were tested on zebrafish cancer xenograft model in which, K562 cell line, was transplanted into zebrafish embryos. We showed that, at an optimal concentration (0.0025mg/ml), Ponatinib loaded PLGA-PEG-PLGA particles are non-toxic/non-cardio-toxic and are very efficient against cancer growth and metastasis. Zebrafish is a good animal model for investigating the cardiotoxicity associated with the anti-cancer drugs such as TKIs, to determine the optimum concentration of smart nanoparticles with the least side effects and to generate xenograft model of several cancer types. Also, PLGA-PEG-PLGA NPs could be good candidate for CML treatment, but their cellular internalization should be enhanced. This could be achieved by coating and labeling the surface of PLGA-PEG-PLGA NPs with specific ligands that are unique to CML cells.
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Soares, Mariana, Ana Clara Mota Gonçalo, Kaline dos Santos Kishishita Castro, and Victoria de Menezes Sá Lazera. "Use of cannabidiol as a therapeutic method in epilepsy." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.388.

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Introduction: Cannabis sativa has several therapeutic properties and has been used for millennials for healing purposes. Among its benefits are analgesic, antiemetic and tranquilizing effects, acting strongly on the nervous system. Objective: This study aims to emphasize the importance of Cannabidiol as a therapeutic purpose for epilepsy, especially in Brazil, where its use is still controlled. Method: A systematic literature review, using bibliographic searches carried out in the electronic databases LILACS, PubMed and SciELO with the descriptors “cannabidiol” and “epilepsy”. Of 1645 searches found, 06 were used in the study. Results: Epileptic seizures can be generalized or partial and are determined by the affected area. The treatment for epilepsy are drugs that decrease the arousal capacity of neural tissue and a significant percentage of individuals cannot control them with traditional drugs alone. Endocannabinoids work in response to epileptiform activity, to activate CB1 receptors for excitatory neurons, to contain excess neuronal activity, which occurs during seizures. It is proven that patients who use it do not have toxic adverse effects. Conclusions: In Brazil, Cannabis is a controlled drug and the fact that it is imported, interfere in the treatment, who is interrupted while patient waits the new dosage. The importance of cannabidiol as a target for research and studies is verified, as it has ample potential in the treatment of epilepsy and reduces brain damage caused by it. In order that patients with epilepsy, have improvements in their quality of life.
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Pearson, W. N., A. F. Armitage, and D. S. Henderson. "A Novel Method for the Performance Control of a Gas Transmission Compressor." In ASME Turbo Expo 2002: Power for Land, Sea, and Air. ASMEDC, 2002. http://dx.doi.org/10.1115/gt2002-30539.

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This paper presents the application of feed forward neural networks to the performance control of a gas transmission compressor. It is estimated that a global saving in compressor fuel gas of 1% could prevent the production of 6 million tonnes of CO2 per year, [1]. Results of compressor model testing suggest that compressor speed can be estimated to within ± 2.5%. The neural network property of function approximation is used to predict compressor speed for given process constraints and instrument input sets. The effects of training set size, instrument noise, reduced input sets and extrapolation from the training domain, are quantified. Various neural network architectures and training schema were examined. The embedding of a neural network into an expert system is also discussed.
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Souza, Marco Aurelio Bastos, Edson Eduardo Borges da Silva, João Pedro Mantovani Tarrega, Renato Tinós, and Ariadne de Andrade Costa. "Simulation of Rat Behavior in a Light-Dark Box via Neuroevolution." In Encontro Nacional de Inteligência Artificial e Computacional. Sociedade Brasileira de Computação - SBC, 2022. http://dx.doi.org/10.5753/eniac.2022.227630.

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The light-dark box is a widely used test for the investigation of animal behavior commonly used to identify and study anxious-like behavioral patterns in rodents. We propose a neuroevolution model for virtual rats in a simulated light-dark box. The virtual rat is controlled by an artificial neural network (ANN) optimized by a genetic algorithm (GA). The fitness function is given by a weighed sum of two terms (punishment and reward). By changing the weight of the punishment term, we are able to simulate the effects of anxiolytic/anxiogenic drugs on rats. We also propose using GAs to optimize the number of the ANN hidden neurons and sensors for the virtual rat. According to the experiments, the best results are obtained by ANNs combining both luminosity and wall sensors.
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