scholarly journals Co-regulation of hormone receptors, neuropeptides, and steroidogenic enzymes across the vertebrate social behavior network

2018 ◽  
Author(s):  
Brent M. Horton ◽  
T. Brandt Ryder ◽  
Ignacio T. Moore ◽  
Christopher N. Balakrishnan

AbstractThe vertebrate basal forebrain and midbrain contain a set of interconnected nuclei that control social behavior. Conserved anatomical structures and functions of these nuclei have now been documented among fish, amphibians, reptiles, birds and mammals, and these brain regions have come to be known as the vertebrate social behavior network (SBN). While it is known that nuclei (nodes) of the SBN are rich in steroid and neuropeptide activity linked to behavior, simultaneous variation in the expression of neuroendocrine genes among several SBN nuclei has not yet been described in detail. In this study, we use RNA-seq to profile gene expression across seven brain regions representing five nodes of the vertebrate SBN in a passerine bird, the wire-tailed manakin Pipra filicauda. Using weighted gene co-expression network analysis (WGCNA), we reconstructed sets of coregulated genes, revealing striking patterns of variation in neuroendocrine gene expression across the SBN. We describe regional expression variation networks comprising a broad set of hormone receptors, neuropeptides, steroidogenic enzymes, catecholamines, and other neuroendocrine signaling molecules. Our findings highlight how heterogeneity of brain gene expression across the SBN can provide functional insights into the neuroendocrine and genetic mechanisms that underlie vertebrate social behavior.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Brent M. Horton ◽  
Thomas B. Ryder ◽  
Ignacio T. Moore ◽  
Christopher N. Balakrishnan


2016 ◽  
Vol 3 (8) ◽  
pp. 160033 ◽  
Author(s):  
Johan Bélteky ◽  
Beatrix Agnvall ◽  
Martin Johnsson ◽  
Dominic Wright ◽  
Per Jensen

The domestication of animals has generated a set of phenotypic modifications, affecting behaviour, appearance, physiology and reproduction, which are consistent across a range of species. We hypothesized that some of these phenotypes could have evolved because of genetic correlation to tameness, an essential trait for successful domestication. Starting from an outbred population of red junglefowl, ancestor of all domestic chickens, we selected birds for either high or low fear of humans for five generations. Birds from the fifth selected generation (S 5 ) showed a divergent pattern of growth and reproduction, where low fear chickens grew larger and produced larger offspring. To examine underlying genetic mechanisms, we used microarrays to study gene expression in thalamus/hypothalamus, a brain region involved in fear and stress, in both the parental generation and the S 5 . While parents of the selection lines did not show any differentially expressed genes, there were a total of 33 genes with adjusted p -values below 0.1 in S 5 . These were mainly related to sperm-function, immunological functions, with only a few known to be relevant to behaviour. Hence, five generations of divergent selection for fear of humans produced changes in hypothalamic gene expression profiles related to pathways associated with male reproduction and to immunology. This may be linked to the effects seen on growth and size of offspring. These results support the hypothesis that domesticated phenotypes may evolve because of correlated effects related to reduced fear of humans.



2018 ◽  
Author(s):  
Rafael Romero-Garcia ◽  
Jakob Seidlitz ◽  
Kirstie J Whitaker ◽  
Sarah E Morgan ◽  
Peter Fonagy ◽  
...  

AbstractBackgroundGenetic risk is thought to drive clinical variation on a spectrum of schizophrenia-like traits but the underlying changes in brain structure that mechanistically link genomic variation to schizotypal experience and behaviour are unclear.MethodsWe assessed schizotypy using a self-reported questionnaire, and measured magnetization transfer (MT), as a putative micro-structural MRI marker of intra-cortical myelination, in 68 brain regions, in 248 healthy young people (aged 14-25 years). We used normative adult brain gene expression data, and partial least squares (PLS) analysis, to find the weighted gene expression pattern that was most co-located with the cortical map of schizotypy-related magnetization (SRM).ResultsMagnetization was significantly correlated with schizotypy in bilateral posterior cingulate cortex and precuneus (and for disorganized schizotypy also in medial prefrontal cortex; all FDR-corrected P < 0.05), which are regions of the default mode network specialized for social and memory functions. The genes most positively weighted on the whole genome expression map co-located with SRM were enriched for genes that were significantly down-regulated in two prior case-control histological studies of brain gene expression in schizophrenia. Conversely, the most negatively weighted genes were enriched for genes that were transcriptionally up-regulated in schizophrenia. Positively weighted (down-regulated) genes were enriched for neuronal, specifically inter-neuronal, affiliations and coded a network of proteins comprising a few highly interactive “hubs” such as parvalbumin and calmodulin.ConclusionsMicrostructural MRI maps of intracortical magnetization can be linked to both the behavioural traits of schizotypy and to prior histological data on dysregulated gene expression in schizophrenia.



2021 ◽  
Author(s):  
Z Yan Wang ◽  
Grace C. McKenzie-Smith ◽  
Weijie Liu ◽  
Hyo Jin Cho ◽  
Talmo D Pereira ◽  
...  

Social isolation, particularly in early life, leads to deleterious physiological and behavioral outcomes. Few studies, if any, have been able to capture the behavioral and neurogenomic consequences of early life social isolation together in a single social animal system. Here, we leverage new high-throughput tools to comprehensively investigate the impact of isolation in the bumblebee (Bombus impatiens) from behavioral, molecular, and neuroanatomical perspectives. We reared newly emerged bumblebees either in complete isolation, small groups, or in their natal colony, and then analyzed their behaviors while alone or paired with another bee. We find that when alone, individuals of each rearing condition show distinct behavioral signatures. When paired with a conspecific, bees reared in small groups or in the natal colony express similar behavioral profiles. Isolated bees, however, showed increased social interactions. To identify the neurobiological correlates of these differences, we quantified brain gene expression and measured the volumes of key brain regions for a subset of individuals from each rearing condition. Overall, we find that isolation increases social interactions and disrupts gene expression and brain development. Limited social experience in small groups is sufficient to preserve typical patterns of brain development and social behavior.



2020 ◽  
Author(s):  
Alex R. DeCasien ◽  
Chet C. Sherwood ◽  
James P. Higham

AbstractSexually dimorphic traits (i.e. phenotypic differences between males and females) are largely produced by sex-biased gene expression (i.e. differential expression of genes present in both sexes). These expression differences may be the result of sexual selection, although other factors (e.g., relaxed purifying selection, pleiotropy, dosage compensation) also contribute. Given that humans and other primates exhibit sex differences in cognition and neuroanatomy, this implicates sex differences in brain gene expression. Here, we compare sex-biased gene expression in humans and rhesus macaques across 16 brain regions using published RNA-Seq datasets. Our results demonstrate that most sex-biased genes are differentially expressed between species, and that overlap across species is limited. Human brains are relatively more sexually dimorphic and exhibit more male-than female-biased genes. Across species, gene expression is biased in opposite directions in some regions and in the same direction in others, suggesting that the latter may be more relevant in nonhuman primate models of neurological disorders. Finally, the brains of both species exhibit positive correlations between sex effects across regions, higher tissue specificity among sex-biased genes, enrichment of extracellular matrix among male-biased genes, and regulation of sex-biased genes by sex hormones. Taken together, our results demonstrate some conserved mechanisms underlying sex-biased brain gene expression, while also suggesting that increased neurodevelopmental plasticity and/or strong sexual selection on cognitive abilities may have played a role in shaping sex-biased brain gene expression in the human lineage.



2017 ◽  
Vol 246 ◽  
pp. 226-232 ◽  
Author(s):  
Alessandra Santillo ◽  
Sara Falvo ◽  
Maria Maddalena Di Fiore ◽  
Gabriella Chieffi Baccari


Endocrinology ◽  
2016 ◽  
Vol 157 (5) ◽  
pp. 1967-1979 ◽  
Author(s):  
Erin P. Harris ◽  
Jean M. Abel ◽  
Lucia D. Tejada ◽  
Emilie F. Rissman

Abstract Calbindin-D(28K) (Calb1), a high-affinity calcium buffer/sensor, shows abundant expression in neurons and has been associated with a number of neurobehavioral diseases, many of which are sexually dimorphic in incidence. Behavioral and physiological end points are affected by experimental manipulations of calbindin levels, including disruption of spatial learning, hippocampal long-term potentiation, and circadian rhythms. In this study, we investigated novel aspects of calbindin function on social behavior, anxiety-like behavior, and fear conditioning in adult mice of both sexes by comparing wild-type to littermate Calb1 KO mice. Because Calb1 mRNA and protein are sexually dimorphic in some areas of the brain, we hypothesized that sex differences in behavioral responses of these behaviors would be eliminated or revealed in Calb1 KO mice. We also examined gene expression in the amygdala and prefrontal cortex, two areas of the brain intimately connected with limbic system control of the behaviors tested, in response to sex and genotype. Our results demonstrate that fear memory and social behavior are altered in male knockout mice, and Calb1 KO mice of both sexes show less anxiety. Moreover, gene expression studies of the amygdala and prefrontal cortex revealed several significant genotype and sex effects in genes related to brain-derived neurotrophic factor signaling, hormone receptors, histone deacetylases, and γ-aminobutyric acid signaling. Our findings are the first to directly link calbindin with affective and social behaviors in rodents; moreover, the results suggest that sex differences in calbindin protein influence behavior.



2016 ◽  
Vol 283 (1843) ◽  
pp. 20161969 ◽  
Author(s):  
Cornelia Voigt

Sex differences in brain structure and behaviour are well documented among vertebrates. An excellent model exploring the neural mechanisms of sex differences in behaviour is represented by sex-role-reversed species. In the majority of bird species, males compete over access to mates and resources more strongly than do females. It is thought that the responsible brain regions are therefore more developed in males than in females. Because these behaviours and brain regions are activated by androgens, males usually have increased testosterone levels during breeding. Therefore, in species with sex-role reversal, certain areas of the female brain should be more developed or steroid hormone profiles should be sexually reversed. Here, I studied circulating hormone levels and gene expression of steroid hormone receptors and aromatase in a captive population of barred buttonquails ( Turnix suscitator ). While females performed courtship and agonistic behaviours, there was no evidence for sexually reversed hormone profiles. However, I found female-biased sex differences in gene expression of androgen receptors in several hypothalamic and limbic brain regions that were already in place at hatching. Such sex differences are not known from non-sex-role-reversed species. These data suggest that increased neural sensitivity to androgens could be involved in the mechanisms mediating sex-role-reversed behaviours.



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