scholarly journals Gene Expression and Synaptic Plasticity in the Auditory Forebrain of Songbirds

2000 ◽  
Vol 7 (5) ◽  
pp. 235-243 ◽  
Author(s):  
S. Ribeiro
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Auditory Forebrain

The Neuromolecular Brain

Neuro ◽  
2013 ◽  
Author(s):  
Nikolas Rose ◽  
Joelle M. Abi-Rached
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Time Scales ◽  
Molecular Level ◽  
Human Life ◽  
Neuronal Circuits ◽  
Molecular Processes ◽  
Nerve Development ◽  
The Brain

This chapter examines the neuromolecular and plastic brain. Ideas about plasticity and the openness of brains to environment influences, from initial evidence about nerve development, through the recognition that synaptic plasticity was the very basis of learning and memory, to evidence about the influence of environment on gene expression and the persistence throughout life of the capacity to make new neurons—all this made the neuromolecular brain seem exquisitely open to its milieu, with changes at the molecular level occurring throughout the course of a human life and thus shaping the growth, organization, and regeneration of neurons and neuronal circuits at time scales from the millisecond to the decade. This was an opportunity to explore the myriad ways in which the milieu got “under the skin,” implying an openness of these molecular processes of the brain to biography, sociality, and culture, and hence perhaps even to history and politics.

scholarly journals Acute social isolation alters neurogenomic state in songbird forebrain

2019 ◽  
Vol 117 (38) ◽  
pp. 23311-23316 ◽  
Author(s):  
Julia M. George ◽  
Zachary W. Bell ◽  
Daniel Condliffe ◽  
Kirstin Dohrer ◽  
Teresa Abaurrea ◽  
...  
Keyword(s):  
Gene Expression ◽  
Social Isolation ◽  
Axonal Guidance ◽  
Sequencing Analysis ◽  
Negative Effects ◽  
Auditory Forebrain ◽  
Gene Sets ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Brain

Prolonged social isolation has negative effects on brain and behavior in humans and other social organisms, but neural mechanisms leading to these effects are not understood. Here we tested the hypothesis that even brief periods of social isolation can alter gene expression and DNA methylation in higher cognitive centers of the brain, focusing on the auditory/associative forebrain of the highly social zebra finch. Using RNA sequencing, we first identified genes that individually increase or decrease expression after isolation and observed general repression of gene sets annotated for neurotrophin pathways and axonal guidance functions. We then pursued 4 genes of large effect size: EGR1 and BDNF (decreased by isolation) and FKBP5 and UTS2B (increased). By in situ hybridization, each gene responded in different cell subsets, arguing against a single cellular mechanism. To test whether effects were specific to the social component of the isolation experience, we compared gene expression in birds isolated either alone or with a single familiar partner. Partner inclusion ameliorated the effect of solo isolation on EGR1 and BDNF, but not on FKBP5 and UTS2B nor on circulating corticosterone. By bisulfite sequencing analysis of auditory forebrain DNA, isolation caused changes in methylation of a subset of differentially expressed genes, including BDNF. Thus, social isolation has rapid consequences on gene activity in a higher integrative center of the brain, triggering epigenetic mechanisms that may influence processing of ongoing experience.

scholarly journals S205. A TRANSLATIONAL HOMER 1A-BASED NETWORK APPROACH: IMAGING HOW HALOPERIDOL MODULATES GLUTAMATE SYSTEM FUNCTIONAL CONNECTIVITY

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S116-S117
Author(s):  
Licia Vellucci ◽  
Felice Iasevoli ◽  
Elisabetta Filomena Buonaguro ◽  
Gianmarco Latte ◽  
Carmine Tomasetti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Nucleus Accumbens ◽  
Side Effects ◽  
Functional Connectivity ◽  
Acute Administration ◽  
Functional Interaction ◽  
Treatment Groups ◽  
Student’S T ◽  
Glutamate System

Abstract Background Schizophrenia has been conceptualized both as synaptic plasticity and a functional connectivity disorder. Data on brain connectivity can be rendered in the form of network models. In our study we want to evaluate a particular kind of the structural and functional interaction between region of interest (ROI) relevant to schizophrenia pathophysiology: we evaluated the expression of Immediate Early Gene (IEG), Homer1a (H1a), in the different ROI and its functional interaction after Haloperidol (antipsychotic drug) acute administration. H1a is an IEG expressed in an activity-dependent manner, coding for a protein involved in the activity-induced reorganization of glutamatergic synapses. Methods Sprague-Dawley rats were randomly assigned to two treatment groups (n=23), receiving vehicle (NaCl 0.9%; VEH) or haloperidol 0.8 mg/kg (HAL) i.p. injection. H1a induction was evaluated using in situ hybridization. Signal intensity analysis was performed in 34 ROIs in the cortex, in the caudate-putamen and the nucleus accumbens. Student’s t-test was used to detect treatment effects. A signal correlation analysis was performed, computing all possible pairwise Pearson correlations among ROIs separately in the two groups. Using significant correlations, two networks were created for HAL and VEH groups, and their network, node, and edge properties were assessed. Results Bonferroni-corrected Student’s t-tests revealed statistically significant differences between the two treatment groups. Haloperidol significantly induced Homer1a gene expression compared to vehicle in all ROIs of the striatum (dmCP: p<.0001, t=9.089, df=44; dlCP: p<.0001, t=10.684, df=44; vlCP: p<.0001, t=10.870, df=44; vmCP: p<.0001, t=9.760, df=44; AcCo: p<.0001, t=8,573, df= 44; AcSh: p<.0001, t=6.615, df=44), a result that is consistent with our previous observations. No significant statistical differences were detected among cortical ROIs explored. Correlations between dmCP-AcSh, dlCP-AcSh, vlCP-AcCo, vlCP-AcSh and vmCP-AcSh were significantly different between the VEH and the HAL group (p<.01); correlations between I-vlCP and dlCP-AcCo were also significantly different between the two treatment groups (p<.05); the I-dlCP and I-vmCP showed a trend towards significance. Discussion Haloperidol acute administration led to a modification of the gene expression pattern in the brain regions considered herein, and consequently to differential functional connectivity. The observed disruption in the functional correlations of the nucleus accumbens may play a role in the affective, motivational and emotional consequences of haloperidol administration, with the loss of functional correlations with the lateral subregions of the caudate-putamen being potentially more relevant to the motor side-effects of haloperidol. These functional connectivity changes are potentially related to neural activity and synaptic plasticity within the glutamate system and may play a role in antipsychotic therapeutic and side effects. As far as we know, this is the first network analysis study on after haloperidol acute treatment of a gene deeply correlated to dendritic spine architecture.

scholarly journals Integration of Long-Term-Memory-Related Synaptic Plasticity Involves Bidirectional Regulation of Gene Expression and Chromatin Structure

Cell ◽  
2002 ◽  
Vol 111 (4) ◽  
pp. 483-493 ◽  
Author(s):  
Zhonghui Guan ◽  
Maurizio Giustetto ◽  
Stavros Lomvardas ◽  
Joung-Hun Kim ◽  
Maria Concetta Miniaci ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Chromatin Structure ◽  
Regulation Of Gene Expression ◽  
Long Term Memory ◽  
Term Memory ◽  
Bidirectional Regulation

scholarly journals Microarray analysis reveals distinctive signaling between the bed nucleus of the stria terminalis, nucleus accumbens, and dorsal striatum

2008 ◽  
Vol 32 (3) ◽  
pp. 283-298 ◽  
Author(s):  
Christopher M. Olsen ◽  
Yong Huang ◽  
Shirlean Goodwin ◽  
Daniel C. Ciobanu ◽  
Lu Lu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Nucleus Accumbens ◽  
Signaling Pathways ◽  
Microarray Analysis ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Insight Into

To identify distinct transcriptional patterns between the major subcortical dopamine targets commonly studied in addiction we studied differences in gene expression between the bed nucleus of the stria terminalis (BNST), nucleus accumbens (NAc), and dorsal striatum (dStr) using microarray analysis. We first tested for differences in expression of genes encoding transcripts for common neurotransmitter systems as well as calcium binding proteins routinely used in neuroanatomical delineation of brain regions. This a priori method revealed differential expression of corticotropin releasing hormone ( Crh), the GABA transporter ( Slc6a1), and prodynorphin ( Pdyn) mRNAs as well as several others. Using a gene ontology tool, functional scoring analysis, and Ingenuity Pathway Analysis, we further identified several physiological pathways that were distinct among these brain regions. These two different analyses both identified calcium signaling, G-coupled protein receptor signaling, and adenylate cyclase-related signaling as significantly different among the BNST, NAc, and dStr. These types of signaling pathways play important roles in, amongst other things, synaptic plasticity. Investigation of differential gene expression revealed several instances that may provide insight into reported differences in synaptic plasticity between these brain regions. The results support other studies suggesting that crucial pathways involved in neurotransmission are distinct among the BNST, NAc, and dStr and provide insight into the potential use of pharmacological agents that may target region-specific signaling pathways. Furthermore, these studies provide a framework for future mouse-mouse comparisons of transcriptional profiles after behavioral/pharmacological manipulation.

Hippocampal chromatin-modifying enzymes are pivotal for scopolamine-induced synaptic plasticity gene expression changes and memory impairment

2015 ◽  
Vol 134 (4) ◽  
pp. 642-651 ◽  
Author(s):  
Padmanabh Singh ◽  
Arpita Konar ◽  
Ashish Kumar ◽  
Sweta Srivas ◽  
Mahendra K. Thakur
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Memory Impairment

scholarly journals Brain-Derived Neurotrophic Factor-Induced Gene Expression Reveals Novel Actions of VGF in Hippocampal Synaptic Plasticity

2003 ◽  
Vol 23 (34) ◽  
pp. 10800-10808 ◽  
Author(s):  
Janet Alder ◽  
Smita Thakker-Varia ◽  
Debra A. Bangasser ◽  
May Kuroiwa ◽  
Mark R. Plummer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Hippocampal Synaptic Plasticity

scholarly journals Comparative chromatin accessibility upon BDNF-induced neuronal activity delineates neuronal regulatory elements

2021 ◽  
Author(s):  
Ignacio L. Ibarra ◽  
Vikram S. Ratnu ◽  
Lucia Gordillo ◽  
In-Young Hwang ◽  
Luca Mariani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Synaptic Plasticity ◽  
Neuronal Activity ◽  
Cortical Neurons ◽  
Complex Traits ◽  
Regulatory Elements ◽  
Chromatin Accessibility ◽  
Regulatory Control ◽  
Comparative Genomic ◽  
Regulatory Sequences

Neuronal activity induced by brain-derived neurotrophic factor (BDNF) triggers gene expression, which is crucial for neuronal survival, differentiation, synaptic plasticity, memory formation, and neurocognitive health. However, its role in chromatin regulation is unclear. Here, using temporal profiling of chromatin accessibility and transcription in mouse primary cortical neurons upon either BDNF stimulation or depolarization (KCl), we identify features that define BDNF-specific chromatin-to-gene expression programs. Enhancer activation is an early event in the regulatory control of BDNF-treated neurons, where the bZIP motif-binding Fos protein pioneered chromatin opening and cooperated with co-regulatory transcription factors (Homeobox, EGRs, and CTCF) to induce transcription. Deleting cis-regulatory sequences decreased BDNF-mediated Arc expression, a regulator of synaptic plasticity. BDNF-induced accessible regions are linked to preferential exon usage by neurodevelopmental disorder-related genes and heritability of neuronal complex traits, which were validated in human iPSC-derived neurons. Thus, we provide a comprehensive view of BDNF-mediated genome regulatory features using comparative genomic approaches to dissect mammalian neuronal activity.

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