Supplementary data for "Design and development of a robotic predator as a stimulus in conditioned place aversion for the study of the effect of ethanol and citalopram in zebrafish" by Clement et al.
Contributors:Verity J. Brown, Jiachao Wang, David Tait, Eric Bowman
An excel spreadsheet of trial by trial behavioural data from 68 rats performing an ID/ED attentional set-shifting task. The file contains columns to specify rat ID; stage of task; which stimuli (i.e., a pair of bowls containing scented digging media) were presented in which location; which location/stimulus the rat chose; whether it sampled both bowls before digging in one.
The likelihoods associated with each of the potential 'hypotheses' are shown: If the rat sampled only one of the bowls, spatial hypotheses are given higher weight than if it sampled both.
Posterior probabilities are calculated by multiplying the prior (which is the posterior probability from the previous trial) by the likelihood. The posterior probabilities are then normalised (i.e., divided by the sum of all posterior probabilities) to give a 'b-value'.
The final columns gives an example of how the b-values can be calculated in Excel, although they were actually calculated using Matlab.
Contributors:luxian lv, Luwen Zhang, Minglong Shao, Zhaoxi Zhong, Yongfeng Yang, Xi Su, Yaqi Cai, Wenqiang Li, Qing Liu, Keke Hao, Binbin Luo, Meng Song
I promise that all datas are authentic and reliable.
Contributors:Ben Greenwood, Isabella Fallon, Michael Baratta, Margaret Tanner
Data set for Tanner et al. Behavioral Brain Research
Contributors:Zhaohui Wang, Kun Liu, Jinsong Liu, Jin Bu
Fig1:Flow chart for the systematic literature search.
Fig2. Forest plot demonstrating the association between gut α-synuclein and PD(CI, conﬁdence interval; PD, Parkinson’s disease; OR, odds ratio).
Fig3. Forest plot in subgroup analysis demonstrating the association between gut α-synuclein and PD(a: subgroup analyzes by IHC sites; b: subgroup analyzes by antibody species).
Fig4. SROC curve(a: sites:colon and stomach; b:antibody: α-synuclein and phosphorylated α-synuclein).
Abstract: While animal research has consistently reported preventive effectiveness of exercise against drug abuse vulnerability, little is known about the influence of the developmental stage during which exercise is displayed on addictive drugs responsiveness. The aim of this study was to determine whether prenatal exercise could attenuate cocaine acute reactivity and psychomotor sensitization in youth offspring. We used a split-plot factorial design where C57BL/6J females were randomly assigned into sedentary or exercised (wheel-running) conditions before and during gestation, the wheels being removed on gestational day 18. Offspring were weaned, gendered and individually housed on 24-28 days old. At 38-42 days old, they were tested for their acute psychomotor responsiveness to 8 mg/kg cocaine and their initiation of sensitization over 8 additional once-daily administrations, the long-term expression of sensitization occurring 30 days later. Adolescent females born from exercised mothers were much less responsive to the acute psychomotor-stimulating effect of cocaine than those born from sedentary mothers (d = 0.75, p = .02), whereas there was no evidence for such a difference in males (d = 0.34, p = .17). However, we did not find sizeable attenuating effects of prenatal exercise on the initiation and the long-term expression of the psychomotor-activating effect of cocaine, in either sex (Cohen’s ds varying from -0.13 to 0.39). These results suggest that prenatal exercise may induce initial protection against cocaine responsiveness in youth females, a finding that warrants further research.