The neurogenomic transition from territory establishment to parenting in a territorial female songbird

Abstract Background The brain plays a critical role in upstream regulation of processes central to mating effort, parental effort, and self-maintenance. For seasonally breeding animals, the brain is likely mediating trade-offs among these processes within a short breeding season, yet research thus far has only explored neurogenomic changes from non-breeding to breeding states or select pathways (e.g., steroids) in male and/or lab-reared animals. Here, we use RNA-seq to explore neural plasticity in three behaviorally relevant neural tissues (ventromedial telencephalon [VmT], hypothalamus [HYPO], and hindbrain [HB]), comparing free-living female tree swallows (Tachycineta bicolor) as they shift from territory establishment to incubation. We additionally highlight changes in aggression-related genes to explore the potential for a neurogenomic shift in the mechanisms regulating aggression, a critical behavior both in establishing and maintaining a territory and in defense of offspring. Results HB had few differentially expressed genes, but VmT and HYPO had hundreds. In particular, VmT had higher expression of genes related to neuroplasticity and processes beneficial for competition during territory establishment, but down-regulated immune processes. HYPO showed signs of high neuroplasticity during incubation, and a decreased potential for glucocorticoid signaling. Expression of aggression-related genes also shifted from steroidal to non-steroidal pathways across the breeding season. Conclusions These patterns suggest trade-offs between enhanced activity and immunity in the VmT and between stress responsiveness and parental care in the HYPO, along with a potential shift in the mechanisms regulating aggression. Collectively, these data highlight important gene regulatory pathways that may underlie behavioral plasticity in females.

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Calpain-1 and Calpain-2 in the Brain: New Evidence for a Critical Role of Calpain-2 in Neuronal Death

Cells ◽

10.3390/cells9122698 ◽

2020 ◽

Vol 9 (12) ◽

pp. 2698

Author(s):

Yubin Wang ◽

Yan Liu ◽

Xiaoning Bi ◽

Michel Baudry

Keyword(s):

Synaptic Plasticity ◽

Critical Role ◽

Protein Targets ◽

Knock Out ◽

Regulatory Pathways ◽

Calcium Dependent ◽

Binding Domains ◽

Calpain 2 ◽

Knock Out Mice ◽

The Brain

Calpains are a family of soluble calcium-dependent proteases that are involved in multiple regulatory pathways. Our laboratory has focused on the understanding of the functions of two ubiquitous calpain isoforms, calpain-1 and calpain-2, in the brain. Results obtained over the last 30 years led to the remarkable conclusion that these two calpain isoforms exhibit opposite functions in the brain. Calpain-1 activation is required for certain forms of synaptic plasticity and corresponding types of learning and memory, while calpain-2 activation limits the extent of plasticity and learning. Calpain-1 is neuroprotective both during postnatal development and in adulthood, while calpain-2 is neurodegenerative. Several key protein targets participating in these opposite functions have been identified and linked to known pathways involved in synaptic plasticity and neuroprotection/neurodegeneration. We have proposed the hypothesis that the existence of different PDZ (PSD-95, DLG and ZO-1) binding domains in the C-terminal of calpain-1 and calpain-2 is responsible for their association with different signaling pathways and thereby their different functions. Results with calpain-2 knock-out mice or with mice treated with a selective calpain-2 inhibitor indicate that calpain-2 is a potential therapeutic target in various forms of neurodegeneration, including traumatic brain injury and repeated concussions.

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Bridging the Gap between Brain-Derived Neurotrophic Factor and Glucocorticoid Effects on Brain Networks

Neuroendocrinology ◽

10.1159/000496392 ◽

2018 ◽

Vol 109 (3) ◽

pp. 277-284 ◽

Cited By ~ 9

Author(s):

Freddy Jeanneteau ◽

Amélie Borie ◽

Moses V. Chao ◽

Michael J. Garabedian

Keyword(s):

Neural Plasticity ◽

Neurotrophic Factor ◽

Glucocorticoid Receptors ◽

Brain Networks ◽

Brain Derived Neurotrophic Factor ◽

Glucocorticoid Signaling ◽

Behavioral Choices ◽

Bdnf Signaling ◽

The Brain ◽

Molecular Framework

Behavioral choices made by the brain during stress depend on glucocorticoid and brain-derived neurotrophic factor (BDNF) signaling pathways acting in synchrony in the mesolimbic (reward) and corticolimbic (emotion) neural networks. Deregulated expression of BDNF and glucocorticoid receptors in brain valuation areas may compromise the integration of signals. Glucocorticoid receptor phosphorylation upon BDNF signaling in neurons represents one mechanism underlying the integration of BDNF and glucocorticoid signals that when off balance may lay the foundation of maladaptations to stress. Here, we propose that BDNF signaling conditions glucocorticoid responses impacting neural plasticity in the mesocorticolimbic system. This provides a novel molecular framework for understanding how brain networks use BDNF and glucocorticoid signaling contingencies to forge receptive neuronal fields in temporal domains defined by behavioral experience, and in mood disorders.

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Molecular basis of parental contributions to the behavioural tolerance of elevated pCO 2 in a coral reef fish

Proceedings of The Royal Society B Biological Sciences ◽

10.1098/rspb.2021.1931 ◽

2021 ◽

Vol 288 (1964) ◽

Author(s):

Alison A. Monroe ◽

Celia Schunter ◽

Megan J. Welch ◽

Philip L. Munday ◽

Timothy Ravasi

Keyword(s):

Neural Plasticity ◽

Parental Influence ◽

Expression Patterns ◽

Cellular Mechanisms ◽

Maternal Line ◽

Expression Of Genes ◽

Behavioural Tolerance ◽

Parental Phenotype ◽

Neuron Growth ◽

The Brain

Knowledge of adaptive potential is crucial to predicting the impacts of ocean acidification (OA) on marine organisms. In the spiny damselfish, Acanthochromis polyacanthus , individual variation in behavioural tolerance to elevated pCO 2 has been observed and is associated with offspring gene expression patterns in the brain. However, the maternal and paternal contributions of this variation are unknown. To investigate parental influence of behavioural pCO 2 tolerance, we crossed pCO 2 -tolerant fathers with pCO 2 -sensitive mothers and vice versa, reared their offspring at control and elevated pCO 2 levels, and compared the juveniles' brain transcriptional programme. We identified a large influence of parental phenotype on expression patterns of offspring, irrespective of environmental conditions. Circadian rhythm genes, associated with a tolerant parental phenotype, were uniquely expressed in tolerant mother offspring, while tolerant fathers had a greater role in expression of genes associated with histone binding. Expression changes in genes associated with neural plasticity were identified in both offspring types: the maternal line had a greater effect on genes related to neuron growth while paternal influence impacted the expression of synaptic development genes. Our results confirm cellular mechanisms involved in responses to varying lengths of OA exposure, while highlighting the parental phenotype's influence on offspring molecular phenotype.

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Circular RNAs in the Brain: A Possible Role in Memory?

The Neuroscientist ◽

10.1177/1073858420963028 ◽

2020 ◽

pp. 107385842096302

Author(s):

Esmi L. Zajaczkowski ◽

Timothy W. Bredy

Keyword(s):

Neural Plasticity ◽

Closed Loop ◽

Critical Role ◽

Higher Order ◽

Current Evidence ◽

Circular Rnas ◽

Rna Molecules ◽

Regulatory Rnas ◽

Higher Order Functions ◽

The Brain

Higher-order organisms possess information processing capabilities that are only made possible by their biological complexity. Emerging evidence indicates a critical role for regulatory RNAs in coordinating many aspects of cellular function that are directly involved in experience-dependent neural plasticity. Here, we focus on a structurally distinct class of RNAs known as circular RNAs. These closed loop, single-stranded RNA molecules are highly stable, enriched in the brain, and functionally active in both healthy and disease conditions. Current evidence implicating this ancient class of RNA as a contributor toward higher-order functions such as cognition and memory is discussed.

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Reactive Oxygen Species: Beyond Their Reactive Behavior

Neurochemical Research ◽

10.1007/s11064-020-03208-7 ◽

2021 ◽

Vol 46 (1) ◽

pp. 77-87

Author(s):

Arnaud Tauffenberger ◽

Pierre J. Magistretti

Keyword(s):

Reactive Oxygen Species ◽

Second Messengers ◽

Critical Role ◽

Complex Function ◽

Reactive Oxygen ◽

High Reactivity ◽

Oxygen Species ◽

Health And Disease ◽

Cellular Dysfunction ◽

The Brain

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

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Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Rats

Brain Sciences ◽

10.3390/brainsci11070889 ◽

2021 ◽

Vol 11 (7) ◽

pp. 889

Author(s):

Anton D. Filev ◽

Denis N. Silachev ◽

Ivan A. Ryzhkov ◽

Konstantin N. Lapin ◽

Anastasiya S. Babkina ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Brain Tissue ◽

Target Genes ◽

Neural Function ◽

Stress Genes ◽

Expression Of Genes ◽

Delayed Recovery ◽

The Brain ◽

Lower Expression

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

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Beyond the Reward Pathway: Coding Reward Magnitude and Error in the Rat Subthalamic Nucleus

Journal of Neurophysiology ◽

10.1152/jn.91009.2008 ◽

2009 ◽

Vol 102 (4) ◽

pp. 2526-2537 ◽

Cited By ~ 63

Author(s):

Sylvie Lardeux ◽

Remy Pernaud ◽

Dany Paleressompoulle ◽

Christelle Baunez

Keyword(s):

Subthalamic Nucleus ◽

Firing Pattern ◽

Sucrose Solution ◽

Critical Role ◽

The Other ◽

Reward Circuitry ◽

Reward Delivery ◽

Reward Pathway ◽

Subthalamic Neurons ◽

The Brain

It was recently shown that subthalamic nucleus (STN) lesions affect motivation for food, cocaine, and alcohol, differentially, according to either the nature of the reward or the preference for it. The STN may thus code a reward according to its value. Here, we investigated how the firing of subthalamic neurons is modulated during expectation of a predicted reward between two possibilities (4 or 32% sucrose solution). The firing pattern of neurons responding to predictive cues and to reward delivery indicates that STN neurons can be divided into subpopulations responding specifically to one reward and less or giving no response to the other. In addition, some neurons (“oops” neurons) specifically encode errors as they respond only during error trials. These results reveal that the STN plays a critical role in ascertaining the value of the reward and seems to encode that value differently depending on the magnitude of the reward. These data highlight the importance of the STN in the reward circuitry of the brain.

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Aggressive interactions rapidly increase androgen synthesis in the brain during the non-breeding season

Hormones and Behavior ◽

10.1016/j.yhbeh.2010.01.008 ◽

2010 ◽

Vol 57 (4-5) ◽

pp. 381-389 ◽

Cited By ~ 98

Author(s):

Devaleena S. Pradhan ◽

Amy E.M. Newman ◽

Douglas W. Wacker ◽

John C. Wingfield ◽

Barney A. Schlinger ◽

...

Keyword(s):

Breeding Season ◽

Aggressive Interactions ◽

Androgen Synthesis ◽

The Brain

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Thyroid hormones and seasonal reproductive neuroendocrine interactions

Reproduction ◽

10.1530/rep-08-0041 ◽

2008 ◽

Vol 136 (1) ◽

pp. 1-8 ◽

Cited By ~ 67

Author(s):

Nobuhiro Nakao ◽

Hiroko Ono ◽

Takashi Yoshimura

Keyword(s):

Thyroid Hormone ◽

Thyroid Hormones ◽

Biological Process ◽

Critical Role ◽

Day Length ◽

Seasonal Reproduction ◽

Seasonal Breeding ◽

Length Changes ◽

Neuroendocrine Axis ◽

The Brain

Many animals that breed seasonally measure the day length (photoperiod) and use these measurements as predictive information to prepare themselves for annual breeding. For several decades, thyroid hormones have been known to be involved in this biological process; however, their precise roles remain unknown. Recent molecular analyses have revealed that local thyroid hormone activation in the hypothalamus plays a critical role in the regulation of the neuroendocrine axis involved in seasonal reproduction in both birds and mammals. Furthermore, functional genomics analyses have revealed a novel function of the hormone thyrotropin. This hormone plays a key role in signaling day-length changes to the brain and thus triggers seasonal breeding. This review aims to summarize the currently available knowledge on the interactions between elements of the thyroid hormone axis and the neuroendocrine system involved in seasonal reproduction.

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The Potential Roles of Blood–Brain Barrier and Blood–Cerebrospinal Fluid Barrier in Maintaining Brain Manganese Homeostasis

Nutrients ◽

10.3390/nu13061833 ◽

2021 ◽

Vol 13 (6) ◽

pp. 1833

Author(s):

Shannon Morgan McCabe ◽

Ningning Zhao

Keyword(s):

Cerebrospinal Fluid ◽

Blood Brain Barrier ◽

Blood Circulation ◽

Critical Role ◽

Systemic Circulation ◽

Brain Parenchyma ◽

Brain Barrier ◽

Blood Brain ◽

The Brain

Manganese (Mn) is a trace nutrient necessary for life but becomes neurotoxic at high concentrations in the brain. The brain is a “privileged” organ that is separated from systemic blood circulation mainly by two barriers. Endothelial cells within the brain form tight junctions and act as the blood–brain barrier (BBB), which physically separates circulating blood from the brain parenchyma. Between the blood and the cerebrospinal fluid (CSF) is the choroid plexus (CP), which is a tissue that acts as the blood–CSF barrier (BCB). Pharmaceuticals, proteins, and metals in the systemic circulation are unable to reach the brain and spinal cord unless transported through either of the two brain barriers. The BBB and the BCB consist of tightly connected cells that fulfill the critical role of neuroprotection and control the exchange of materials between the brain environment and blood circulation. Many recent publications provide insights into Mn transport in vivo or in cell models. In this review, we will focus on the current research regarding Mn metabolism in the brain and discuss the potential roles of the BBB and BCB in maintaining brain Mn homeostasis.

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