Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA110653 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Here we tested a hypothesis that epileptogenesis influences expression pattern of genes in the basolateral amygdala that are critical for fear conditioning. Whole genome molecular profiling of basolateral rat amygdala was performed to compare the transcriptome changes underlying fear learning in epileptogenic and control animals. Our analysis revealed that after acquisition of fear conditioning 26 genes were regulated differently in the basolateral amygdala of both groups. Thus, our study provides the first evidence that not only the damage to the neuronal pathways but also altered composition or activity level of molecular machinery responsible for formation of emotional memories within surviving pathways can contribute to impairment in emotional learning in epileptogenic animals. Understanding the function of those genes in emotional learning provides an attractive avenue for identification of novel drug targets for treatment of emotional disorders after epileptogenesis-inducing insult.
2009-02-13 | GSE13624 | GEO
Project description:Here we tested a hypothesis that epileptogenesis influences expression pattern of genes in the basolateral amygdala that are critical for fear conditioning. Whole genome molecular profiling of basolateral rat amygdala was performed to compare the transcriptome changes underlying fear learning in epileptogenic and control animals. Our analysis revealed that after acquisition of fear conditioning 26 genes were regulated differently in the basolateral amygdala of both groups. Thus, our study provides the first evidence that not only the damage to the neuronal pathways but also altered composition or activity level of molecular machinery responsible for formation of emotional memories within surviving pathways can contribute to impairment in emotional learning in epileptogenic animals. Understanding the function of those genes in emotional learning provides an attractive avenue for identification of novel drug targets for treatment of emotional disorders after epileptogenesis-inducing insult. Experiment Overall Design: Experiment description: Experiment Overall Design: Array: Rat Genome 230-2.0 (Affymetrix). Experiment Overall Design: Samples: 2 biological replicates from 4 experimental groups (control unpaired = CU, CU1, control paired = CP, CP1, epileptogenic unpaired = EU, EU1, epileptogenic paired = EP, EP1). Experiment Overall Design: Animals&model: Amygdala stimulation model (Nissinen et al., 2000): Experiment Overall Design: control (C) animals = operated, not stimulated; Experiment Overall Design: epileptogenic (E) animals = stimulated, responded with "good" status epilepticus (at least 40HAFDs within first 3h of SE), not expressing spontaneous seizures through the whole study. Experiment Overall Design: All animals received 5 habituation session to the fear conditioning apparatus lasting 10 min, starting on day 5 (2 sessions on day 5 and 6 and 1 session on day 7) after stimulation (induction of SE). Experiment Overall Design: On 8th day after stimulation: Experiment Overall Design: unpaired (U) = twice received: 2min in apparatus â footshock (1.5mA, 1s)â tone (75dB for 20 sec) Experiment Overall Design: paired (P) = twice received: 2min in apparatus â tone (75dB for 20 sec) co-terminated by footshock (1.5mA, 1s). Experiment Overall Design: RNA isolation: decapitation â ipsilateral temporal lobe isolated, embed in OCT and frozen in -70C. Cut into 10µm sections, thionin stained (Ambion protocol), basal and lateral nuclei of the amygdala laser-microdissected; total cellular RNA isolated with PicoPure RNA isolation kit (Arcturus). Experiment Overall Design: RNA amplification: 30ng of of total cellular RNA from each rat underwent of 2 rounds of amplification using MessageAmp II aRNA kit (Ambion), according to manufacturer protocol (in vitro transcription time 14h in both rounds). Experiment Overall Design: Sample pooling: aRNA from 2 animals was pooled (10µg in total = 2x5µg) and 8 samples were labeled and hybridized: CP, CP1, CU, CU1, EP, EP1, EU, EU1; (altogether aRNA from 16 rats was used).
2009-02-26 | E-GEOD-13624 | biostudies-arrayexpress
Project description:Transitions in infant learning are modulated by dopamine within the amygdala
| PRJNA118603 | ENA
Project description:Syracuse High/Low Avoidance Learning in Rats
| PRJNA87963 | ENA
Project description:Amygdala transcriptome in rats prenatally exposed to valproic acid
| PRJNA386180 | ENA
Project description:Male Sprague-Dawley rats were used to establish exhausted-exercise model by motorized rodent treadmill. Yu-Ping-Feng-San at doses of 2.18 g/kg was administrated by gavage before exercise training for 10 consecutive days. Quantitative proteomics was performed for assessing the related mechanism of Yu-Ping-Feng-San.
2022-08-12 | PXD032737 | Pride
Project description:Circular RNA profiles in the amygdala of rats after restraint stress
| PRJNA1071307 | ENA
Project description:Comparisons of hippocampi of Syracuse High Avoidance (SHA) and Syracuse Low Avoidance (SLA) learning rats
2007-10-12 | E-GEOD-932 | biostudies-arrayexpress
Project description:Right ventricular heart failure (RVF) associated with pulmonary hypertension (PH) is characterized by a distinct gene expression pattern when compared with functional compensatory hypertrophy. Carvedilol treatment after RVF has been established reduces right ventricle (RV) hypertrophy and improves the RV function. In addition, carvedilol treatment has been shown to alter the gene expression of select genes. We sought to identify, on a genome-wide basis, the effect of carvedilol on gene expression. RVF was induced in male Sprague-Dawley rats by the combination of VEGF-receptor blockade and chronic hypoxia; thereafter, one group was treated with carvedilol. RNA was isolated from the RV and subjected to microarray analysis. A prediction analysis of the carvedilol-treated RVs showed that carvedilol treated RVs most resembled in their expression pattern the RVF pattern. However, an analysis beyond the boundaries of the prediction set revealed a small set of genes associated with carvedilol reversal of RVF. Pathway analysis of this set of genes revealed expression changes of genes involved in cardiac hypertrophy, mitochondrial dysfunction, protein ubiquitination, and sphingolipid metabolism. Genes encoding proteins in the cardiac hypertrophy and protein ubiquitination pathways were downregulated in the RV by carvedilol, while genes encoding proteins in the mitochondrial dysfunction and sphingolipid metabolism pathways were upregulated by carvedilol.
2013-05-06 | GSE42579 | GEO