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884 results for “Nicotine”
Data set for "Cell-type-specific nicotinic input disinhibits mouse barrel cortex during active sensing"
<p>Data set for: Gasselin C, Hohl B, Vernet A, Crochet C, Petersen CCH (2021) Cell-type-specific nicotinic input disinhibits mouse barrel cortex during active sensing. Neuron doi: 10.1016/j.neuron.2020.12.018</p> <p>There are 2 files in this upload:</p> <p>1. The file named "2021_Gasselin_Neuron.pdf" is the Open Access pdf of the online publication in Neuron.</p> <p>2. The file named "Gasselin_data_code.zip" (~9 GB) is a zipped version of a folder "Gasselin_data_code" (~13 GB), which contains the data analysed in the study along with the Matlab code used to generate the published figures. To access the data and the code, first unzip the file. Then add the folder with subfolders to the Matlab path and run the different codes. The current folder must be the main folder (‘Gasselin_data_code’). Each code computes and plots the results used in the corresponding figure. Figures and Tables are saved in the subfolder ‘Figures’.</p> <p>The subfolder ‘Functions’ contains functions called by the main codes.</p> <p>The main folder contains the following codes:</p> <p><em>Gasselin_Figure1: computes and plots the results for the panels D, E and F of figure 1.</em></p> <p><em>Gasselin_Figure2: computes and plots the results for the panels B and C of figure 2.</em></p> <p><em>Gasselin_Figure3: computes and plots the results for the panels B, C and D of figure 3.</em></p> <p><em>Gasselin_Figure4: computes and plots the results for the panels A, B and C of figure 4.</em></p> <p><em>Gasselin_FigureS1: computes and plots the results for the panels A, B and C of figure S1.</em></p> <p><em>Gasselin_FigureS2: computes and plots the results for the panels A and B of figure S2.</em></p> <p> </p> <p>The subfolder ‘Data’ contains the data structures used for the different figures:</p> <p><em>data_figure1.mat</em></p> <p><em>data_figure2.mat</em></p> <p><em>data_figure3.mat</em></p> <p><em>data_figure4_MECA.mat</em></p> <p><em>data_figure4_Activation.mat</em></p> <p><em>data_figure4_Inactivation.mat</em></p> <p><em>data_figureS2_Activation.mat</em></p> <p><em>data_figureS2_Inactivation.mat</em></p> <p><em>data_Axon.mat</em></p> <p> </p> <p>The data structures contain the following fields:</p> <p><em>Mouse_Name</em> : name of the mouse.</p> <p><em>Mouse_DateOfBirth</em>: date of birth of the mouse (YMD).</p> <p><em>Mouse_Sex</em>: sex of the mouse (F or M).</p> <p><em>Mouse_Genotype</em>: genotype of the mouse.</p> <p><em>Mouse_Drug</em>: experimental condition of the recording (control = ‘No Drug’; blockade of glutamatergic transmission = ‘CNQX_DAPV’; blockade of glutamatergic transmission and nicotinic receptors = ‘CNQX_DAPV_MECA’; blockade of nicotinic receptors only = ‘MECA’).</p> <p><em>Mouse_Virus</em>: virus injected if any.</p> <p><em>Cell_Counter</em>; cell recorded in a given mouse.</p> <p><em>Cell_Type</em>: type of the recorded cell based on 2P imaging. (EXC, VIP, PV, SST, 5HT3aR_non_VIP).</p> <p><em>Cell_Depth</em>: depth of the recorded cell relative to pia (µm).</p> <p><em>Cell_TargetedBrainArea</em>: cortical area targeted (C2 column of the barrel cortex = C2).</p> <p><em>Cell_Fluorescence</em>: expression of the genetically encoded fluorophore (FALSE or TRUE). A neuron recorded in a VIP_IRES_Cre x LSL_tdTomato (cf <em>Mouse_Genotype</em>) with <em>Cell_Fluorescence</em>=TRUE is considered as a VIP neuron (cf <em>Cell_Type</em>).</p> <p><em>Sweep_Counter</em>: number of the sweep recorded for a given neuron (data were acquired across successive continuous sweeps of 30-60 s).</p> <p><em>Sweep_Type</em>: experimental condition during that sweep (Only spontaneous whisking onset = ‘Onset’; Whisking onset and whisker stimulus = ‘Onset_Whisker_Stim’ ; Optogenetic stimulation = ‘Opto_Stim’; Optogenetic activation = ‘Opto_Activation’; Optogenetic inactivation = ‘Opto_Inactivation’; ).</p> <p><em>Sweep_Start_Time</em>: time at the beginning of the sweep recording (YMDHms).</p> <p><em>Sweep_WhiskerAngle</em>: C2 whisker angular position extracted from simultaneous high-speed video filming (deg).</p> <p><em>Sweep_WhiskerAngle_SamplingRate</em>: sampling rate of the whisker angle trace.</p> <p><em>Sweep_WhiskingOnset_Time</em>: time of identified whisking onset - excluding any whisker stimulus shortly before or after (s).</p> <p><em>Sweep_MembranePotential</em>: membrane potential recording (mV) after cutting of the APs.</p> <p><em>Sweep_MembranePotential_SamplingRate</em>: sampling rate of the membrane potential signal (pt.s<sup>-1</sup>).</p> <p><em>Sweep_CurrentInjected</em>: current injected into the cell (pA).</p> <p><em>Sweep_CurrentInjected_SamplingRate</em>: sampling rate of current signal (pt.s<sup>-1</sup>).</p> <p><em>Sweep_WhiskerStim_Name</em>: whisker to which the magnetic stimulus was applied to (C2 or B2&C2).</p> <p><em>Sweep_WhiskerStim_Time</em>: onset times of the whisker stimulus (s).</p> <p><em>Sweep_OptoStim_Power</em>: light power applied for optogenetic manipulations (% of the max power).</p> <p><em>Sweep_OptoStim_Time</em>: onset times of the light pulses for optogenetic manipulations (s).</p> <p><em>Cell_ID</em>: unique cell identifier (= <em>Mouse_Name</em>+<em>Cell_Counter</em>).</p> <p><em>SpikeThreshold</em>: spike threshold used to detect APs (mV).</p> <p><em>Trial_WhiskingOnset</em>: data structure containing the cut signals used to compute averaged responses around whisking onset times.</p> <p><em>Trial_WhiskerStim</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times.</p> <p><em>Trial_WhiskerStim_QuietTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials without whisker movements.</p> <p><em>Trial_WhiskerStim_WhiskingTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials with whisker movements.</p> <p><em>Trial_Opto</em>: data structure containing the cut signals used to compute averaged responses around optogenetic stimulus onset times.</p> <p><em>Trial_OptoAndWhisker_QuietTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials with optogenetic manipulation and no whisker movements.</p> <p><em>Trial_OptoAndWhisker_WhiskingTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials with optogenetic manipulation and with whisker movements.</p> <p><em>Trial_OnlyWhisker_QuietTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials without optogenetic manipulation and without whisker movements.</p> <p><em>Trial_OnlyWhisker_WhiskingTrials</em>: data structure containing the cut signals used to compute averaged responses around whisker stimulus onset times for trials without optogenetic manipulation and with whisker movements.</p> <p><em>Trial_OnlyOpto</em>: data structure containing the cut signals used to compute averaged responses around optogenetic stimulus onset times in trials without whisker stimulus.</p>
Dataset for the QPRTase (Nicotinate-nucleotide pyrophosphorylase [carboxylating]) antibody screening study
<p> This project contains the following underlying data included in a study aimed at characterizing four commercial antibodies against Nicotinate-nucleotide pyrophosphorylase [carboxylating] (QPRTase) protein, encoded by the <em>QPRT</em> gene. The study is available on Zenodo (DOI: 10.5281/zenodo.7459387).</p>
Dataset related to article "On the extension of the use of a standard operating procedure for nicotine, glycerol and propylene glycol analysis in e-liquids using mass spectrometry"
Open the record for dataset details and reuse information.
Varenicline for Nicotine Vaping Cessation in Adolescents
ClinicalTrials.gov study NCT05367492. IPD Sharing: YES. Countries: 1. Publications: 3.
Impact of Nicotine Messaging on Nicotine Beliefs and Tobacco Use Behavior
ClinicalTrials.gov study NCT04805515. IPD Sharing: YES. Countries: 1. Publications: 1.
Data for: Possible synergistic effects of thymol and nicotine against Crithidia bombi parasitism in bumble bees
<p>Data and R scripts for analysis of nicotine-thymol synergy experiment and thymol dose experiment evaluating effects of nectar secondary metabolite treatments on <em>Crithidia bombi </em>parasite load and mortality in the bumble bee <em>Bombus impatiens.</em></p>
Data from: Hepatic steatosis induced by nicotine plus Coca-Cola™ is prevented by nicotinamide riboside (NR)
<p><strong>Introduction.</strong> Cigarettes containing nicotine (Nic) are a risk factor for the development of cardiovascular and metabolic diseases. We reported that Nic delivered via injections or e-cigarette vapor led to hepatic steatosis in mice fed with a high-fat diet. High-fructose corn syrup (HFCS) is the main sweetener in sugar-sweetened beverages (SSBs) in the US. Increased consumption of SSBs with HFCS is associated with increased risks of non-alcoholic fatty liver disease (NAFLD). Nicotinamide riboside (NR) increases mitochondrial nicotinamide adenine dinucleotide (NAD<sup>+</sup>) and protects mice against hepatic steatosis. This study evaluated if Nic plus Coca-Cola™ (Coke) with HFCS can cause hepatic steatosis and that can be protected by NR.</p> <p><strong>Methods.</strong> C57BL6 mice received twice daily intraperitoneal (IP) injections of Nic or saline and were given Coke (HFCS), or Coke with sugar, and NR supplementation for 10 weeks.</p> <p><strong>Results.</strong> Our results show that Nic+Coke caused increased caloric intake and induced hepatic steatosis, and the addition of NR prevented these changes. Western blot analysis showed lipogenesis markers were activated (increased cleavage of the sterol regulatory element-binding protein 1 [SREBP1c] and reduction of phospho-Acetyl-CoA Carboxylase [p-ACC]) in the Nic+Coke compared to the Sal+Water group. The hepatic detrimental effects of Nic+Coke were mediated by decreased NAD<sup>+</sup> signaling, increased oxidative stress, and mitochondrial damage. NR reduced oxidative stress and prevented mitochondrial damage by restoring protein levels of Sirtuin1 (Sirt1) and peroxisome proliferator-activated receptor coactivator 1-alpha (PGC1a) signaling.</p> <p><strong>Discussion.</strong> We conclude that Nic+Coke has an additive effect on producing hepatic steatosis, and NR is protective. This study suggests concern for the development of NAFLD in subjects who consume nicotine and drink SSBs with HFCS.</p>
Individualistic reward-seeking strategies that predict response to nicotine emerge among isogenic male mice living in a micro-society
<p>This repository contains data and basic code for analysis and modeling used in the following paper: Fayad et al. ""Individualistic reward-seeking strategies that predict response to nicotine emerge among isogenic male mice living in a micro-society", published on BioRxiv (https://www.biorxiv.org/content/10.1101/2023.10.28.564522v1)</p> <p> </p>
Data for "Transient nicotine exposure in early adolescent male mice freezes their dopamine circuits in an immature state"
<p>This repository contains data for the analysis used in the following paper: Reynolds et al. "Transient nicotine exposure in early adolescent male mice freezes their dopamine circuits in an immature state", published on BioRxiv (https://www.biorxiv.org/content/10.1101/2023.10.28.564518v1). Information about using the data files is in the "readme.rtf" file. </p>
Data from: Positive allosteric modulation of the α7 nicotinic acetylcholine receptor as a treatment for cognitive deficits after traumatic brain injury
<p><span>Cognitive impairments are a common consequence of traumatic brain injury (TBI). The hippocampus is a subcortical structure that plays a key role in the formation of declarative memories and is highly vulnerable to TBI. The α7 nicotinic acetylcholine receptor (nAChR) is highly expressed in the hippocampus and reduced expression and function of this receptor are linked with cognitive impairments in Alzheimer's disease and schizophrenia. Positive allosteric modulation of α7 nAChRs with AVL-3288 enhances receptor currents and improves cognitive functioning in naïve animals and healthy human subjects. Therefore, we hypothesized that targeting the α7 nAChR with the positive allosteric modulator AVL-3288 would enhance cognitive functioning in the chronic recovery period of TBI. To test this hypothesis, adult male Sprague Dawley rats received moderate parasagittal fluid-percussion brain injury or sham surgery. At 3 months after recovery, animals were treated with vehicle or AVL-3288 at 30 min prior to cue and contextual fear conditioning and the water maze task. Treatment of TBI animals with AVL-3288 rescued learning and memory deficits in water maze retention and working memory. AVL-3288 treatment also improved cue and contextual fear memory when tested at 24 hr and 1 month after training, when TBI animals were treated acutely just during fear conditioning at 3 months post-TBI. Hippocampal atrophy but not cortical atrophy was reduced with AVL-3288 treatment in the chronic recovery phase of TBI. AVL-3288 application to acute hippocampal slices from animals at 3 months after TBI rescued basal synaptic transmission deficits and long-term potentiation (LTP) in area CA1. Our results demonstrate that AVL-3288 improves hippocampal synaptic plasticity, and learning and memory performance after TBI in the chronic recovery period. Enhancing cholinergic transmission through positive allosteric modulation of the α7 nAChR may be a novel therapeutic to improve cognition after TBI.</span></p>
Functional impact of subunit composition and compensation on Drosophila melanogaster nicotinic receptors: Targets of neonicotinoids
<p>Neonicotinoid insecticides target insect nicotinic acetylcholine receptors (nAChRs) and their adverse effects on non-target insects are of serious concern. We recently found that cofactor TMX3 enables robust functional expression of insect nAChRs in Xenopus laevis oocytes and showed that neonicotinoids (imidacloprid, thiacloprid, and clothianidin) exhibited agonist actions on some nAChRs of the fruit fly (<em>Drosophila melanogaster</em>), honeybee (<em>Apis mellifera</em>) and bumblebee (<em>Bombus terrestris</em>) nAChRs with more potent actions on the pollinator nAChRs. However, other subunits from the nAChR family remain to be explored. We show that the Dα3 subunit co-exists with Dα1, Dα2, Dβ1, and Dβ2 subunits in the same neurons of adult <em>D. melanogaster</em>, thereby expanding the possible nAChR subtypes in these cells alone from 4 to 12. The presence of Dα1 and Dα2 subunits reduced the affinity of imidacloprid, thiacloprid, and clothianidin for nAChRs expressed in <em>Xenopus laevis</em> oocytes, whereas the Dα3 subunit enhanced it. RNAi targeting <em>Dα1</em>, <em>Dα2,</em> or <em>Dα3</em> in adults reduced expression of targeted subunits but commonly enhanced <em>Dβ3</em> expression. Also, <em>Dα1</em> RNAi enhanced <em>Dα7</em> expression, <em>Dα2</em> RNAi reduced <em>Dα1</em>, <em>Dα6</em>, and <em>Dα7</em> expression and <em>Dα3</em> RNAi reduced <em>Dα1</em> expression while enhancing <em>Dα2</em> expression, respectively. In most cases, RNAi treatment of either <em>Dα1</em> or <em>Dα2</em> reduced neonicotinoid toxicity in larvae, but <em>Dα2</em> RNAi enhanced neonicotinoid sensitivity in adults reflecting the affinity-reducing effect of <em>Dα2</em>. Substituting each of <em>Dα1</em>, <em>Dα2</em>, and <em>Dα3</em> subunits by <em>Dα4</em> or <em>Dβ3</em> subunit mostly increased neonicotinoid affinity and reduced efficacy. Therefore, <span>functional expression studies and RNAi targeting of subunits show that neonicotinoid action and toxicity involve the integrated actions of multiple nAChR subunit combinations, counseling caution in interpreting toxicity to insects by subunit gene modification alone.</span></p>
Interactive computational and experimental approaches improve the sensitivity of periplasmic binding protein-based nicotine biosensors for measurements in biofluids
<p>Here are the raw simulation trajectories (water removed).</p>
Deidentified public survey data for: Patterns and perceptions of nicotine use among U.S. adolescents and young adults receiving medication treatment for opioid use disorder
<p>Nicotine use among U.S. youth is cause for concern, as previous studies have shown that nicotine use in adolescence increases the risk of developing substance use disorders later in life. This exploratory study aimed to understand patterns of nicotine use and perceptions of various nicotine products among adolescents and young adults (AYA) receiving medication treatment for opioid use disorder (MOUD). We administered an adapted version of the National Youth Tobacco Survey via REDCap to AYA (n=32) receiving outpatient care in the Medication-Assisted Treatment of Addiction at Nationwide Children's Hospital in Columbus, Ohio, U.S.A. Thirty (97%) participants had tried a combustible cigarette and 27 (90%) had tried an electronic cigarette. By age 13, nineteen (61%) participants had tried combustible cigarettes and eight (25%) had tried opioids. Twenty-two (71%) participants reported smoking combustible cigarettes every day for the past 30 days, and 15 (48%) reported smoking more than 10 cigarettes per day on average. Only ten (32%) participants reported e-cigarette use in the last 30 days. Participants universally agreed that tobacco products are dangerous, and twenty (67%) current tobacco users reported that they planned to quit in the next year. Nicotine use patterns among AYA receiving MOUD differ from that previously shown in the general population, primarily by high prevalence of nicotine use in early adolescence and high current combustible cigarette use. Interventions such as universal screening for nicotine use before age 13 and tailored smoking cessation programs for AYA with OUD may help optimize care for these individuals.</p>
Effects of Transdermal Nicotine on Response Inhibition to Emotional Cues in Schizophrenia
ClinicalTrials.gov study NCT03838484. IPD Sharing: NO. Countries: 1. Publications: 3.
N-Acetyl Cysteine Plus Behavioral Therapy for Nicotine Dependent Pathological Gamblers
ClinicalTrials.gov study NCT00967005. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Project 2 Cigarette and E-cigarette Nicotine Content and E-liquid Flavors
ClinicalTrials.gov study NCT03185546. IPD Sharing: YES. Countries: 1. Publications: 25.
Phase 2 Trial of a Nicotinic Agonist in Schizophrenia
ClinicalTrials.gov study NCT00100165. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Comparison of Standard Versus Extended Nicotine Patch Therapy for Smoking Cessation
ClinicalTrials.gov study NCT00364156. IPD Sharing: Not stated. Countries: 1. Publications: 6.
Highdose Nicotine Patch Therapy for Smokeless Tobacco Use
ClinicalTrials.gov study NCT00939029. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Varenicline for Nicotine Dependence Among Those With HIV/AIDS
ClinicalTrials.gov study NCT01710137. IPD Sharing: Not stated. Countries: 1. Publications: 1.
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Allen Brain Atlas
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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