Differential and temporal expression of corticotropin releasing hormone and its receptors in the nucleus of the hippocampal commissure and paraventricular nucleus during the stress response in chickens (Gallus gallus)

Kadhim, Hakeem J.; Kang, Seong Wook; Kuenzel, Wayne J.

doi:10.1016/j.brainres.2019.02.018

Cited by 23 publications

(25 citation statements)

References 42 publications

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“…It is worth noting that there was no difference between the BPTES-injected control and BPTES-injected EHC group body temperatures ( P = 0.93) during the heat challenge, indicating that glutamatergic transmission affecting thermal regulation was not damaged by the in-ovo injection of BPTES in the embryonic period. In addition to body temperature, we measured mRNA expression, in the hypothalamus 6 h into the heat challenge, of heat and stress related genes including: HSP70 which is an indicator of the chick’s heat sensitivity ( Kisliouk et al, 2017 ); brain derived neurotrophic factor ( BDNF) which is epigenetically regulated during heat conditioning ( Katz and Meiri, 2006 ; Kisliouk and Meiri, 2009 ); glucocorticoid-induced leucine zipper ( GILZ ), involved in glucocorticoids anti-inflammatory effect ( Riccardi, 2015 ); eukaryotic initiation factor 2b5 ( EIF2B5 ) involved in the epigenetic regulation of thermal control establishment ( Kisliouk et al, 2009 ); and corticotrophin release hormone receptors ( CRHR ) 1 and 2 which are increased in the hypothalamus of chicks during food deprivation ( Kadhim et al, 2019 ). The expression of each group was normalized to the expression in a parallel t 0 group which was not subjected to heat challenge.…”

Section: Resultsmentioning

confidence: 99%

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

et al. 2020

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Early life encounters with stress can lead to long-lasting beneficial alterations in the response to various stressors, known as cross-tolerance. Embryonic heat conditioning (EHC) of chicks was previously shown to mediate resilience to heat stress later in life. Here we demonstrate that EHC can induce cross-tolerance with the immune system, attenuating hypothalamic inflammation. Inflammation in EHC chicks was manifested, following lipopolysaccharide (LPS) challenge on day 10 post-hatch, by reduced febrile response and reduced expression of LITAF and NFκB compared to controls, as well as nuclear localization and activation of NFκB in the hypothalamus. Since the crosstolerance effect was long-lasting, we assumed that epigenetic mechanisms are involved. We focused on the role of ten-eleven translocation (TET) family enzymes, which are the mediators of active CpG demethylation. Here, TET transcription during early life stress was found to be necessary for stress resilience later in life. The expression of the TET family enzymes in the midbrain during conditioning increased in parallel to an elevation in concentration of their cofactor α-ketoglutarate. In-ovo inhibition of TET activity during EHC, by the α-ketoglutarate inhibitor bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulfide (BPTES), resulted in reduced total and locus specific CpG demethylation in 10-day-old chicks and reversed both thermal and inflammatory resilience. In addition, EHC attenuated the elevation in expression of the stress markers HSP70, CRHR1, and CRHR2, during heat challenge on day 10 post-hatch. This reduction in expression was reversed by BPTES. Similarly, the EHC-dependent reduction of inflammatory gene expression during LPS challenge was eliminated in BPTES-treated chicks. Thus, TET family enzymes and CpG demethylation are essential for the embryonic induction of stress cross-tolerance in the hypothalamus.

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Section: Resultsmentioning

confidence: 99%

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

et al. 2020

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“…The projection from PVN to nHpC may involve both CRH and AVT, as AVT + terminals have been described in nHpC and it expresses V1aR, V1bR, CRHR1 and CRHR2 receptors (although the latter two could be for detection of locally-released CRH; Kadhim et al, 2020 ; Montagnese et al, 2016 ; Nagarajan et al, 2017a ). There is currently no known mammalian equivalent of the nHpC, although the mammalian medial or triangular septal nuclei have been suggested as candidates ( Kadhim et al, 2019 , 2020 ). nHpC contains CRH + neurons, which are activated in response to acute restraint stress ( Ball et al, 1989 ; Nagarajan et al, 2014 ).…”

Section: Hypothalamic and Subpallial Telencephalic Afferents To The Pvnmentioning

confidence: 99%

“…In response to food deprivation, the CRH expression in nHpC increases initially, but then drops again after 4–8 h, while CRH in PVN increases steadily throughout this period. This indicates that nHpC may play a role in the initial activation of the HPA axis (at least in response to food deprivation) ( Kadhim et al, 2019 ; Nagarajan et al, 2017b ). Electrical stimulation in the nHpC of ducks ( Anas platyrhynchos ) results in defecation, which could be in response to an acute stress response, although no other fear behaviours were observed ( Phillips, 1964 ).…”

Section: Hypothalamic and Subpallial Telencephalic Afferents To The Pvnmentioning

confidence: 99%

“…These CRH + neurons do not seem to have axons projecting to the median eminence ( Knapp and Silver, 1995 ), and therefore do not contribute directly to the HPA axis. nHpC expresses GR, and levels of GR expression are low when CRH expression is high, and vice versa ( Kadhim et al, 2019 ). However, dexamethasone does not seem to be able to suppress CRH release in vitro ( Nagarajan et al, 2017a ), so the relationship between GCH, GR expression and CRH release in the nHpC is still unclear.…”

Section: Hypothalamic and Subpallial Telencephalic Afferents To The Pvnmentioning

confidence: 99%

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Telencephalic regulation of the HPA axis in birds

Smulders

2021

Neurobiology of Stress

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The hypothalamo-pituitary-adrenal (HPA) axis is one of the major output systems of the vertebrate stress response. It controls the release of cortisol or corticosterone from the adrenal gland. These hormones regulate a range of processes throughout the brain and body, with the main function of mobilizing energy reserves to improve coping with a stressful situation. This axis is regulated in response to both physical (e.g., osmotic) and psychological (e.g., social) stressors. In mammals, the telencephalon plays an important role in the regulation of the HPA axis response in particular to psychological stressors, with the amygdala and part of prefrontal cortex stimulating the stress response, and the hippocampus and another part of prefrontal cortex inhibiting the response to return it to baseline. Birds also mount HPA axis responses to psychological stressors, but much less is known about the telencephalic areas that control this response. This review summarizes which telencephalic areas in birds are connected to the HPA axis and are known to respond to stressful situations. The conclusion is that the telencephalic control of the HPA axis is probably an ancient system that dates from before the split between sauropsid and synapsid reptiles, but more research is needed into the functional relationships between the brain areas reviewed in birds if we want to understand the level of this conservation.

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“…In chicken, CRH neurones in the nucleus of the hippocampal commissure initiate, while PVN CRH neurones sustain the early response of the HPA axis to stress (Kadhim et al 2019). In rodents and humans, through mineralocorticoid receptors, hippocampus is highly involved in negative feedback regulation of the HPA axis (Reul et al 1990).…”

Section: Cortical Areasmentioning

confidence: 99%

Brain corticotropin releasing hormone and stress reactivity

Bánrévi

Chaves

Correia

et al. 2021

Integrative Physiology

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The hypothalamic-pituitary-adrenocortical axis is one of the main components of stress adaptation. Corticotropin-releasing hormone (CRH) coming from the nucleus paraventricularis hypothalami (PVN) is the canonical central regulator of the axis. This CRH acts on the CRH-R1 receptors of the pituitary, and, through adrenocorticotropin, stimulates glucocorticoid release from the adrenal cortex. However, it may be synthetized in other parts of the brain as well, and may act both on CRH-R1 and CRH-R2 receptors. These areas form the central CRH network. Many of them are also stress reactive and participate in physical and psychological stress response. The central nucleus of the amygdala and bed nucleus of stria terminalis are two areas best known for their role in emotions, while hippocampus is mostly involved in glucocorticoid feedback as well as memory formation, all heavily connected to stress adaptation. Among others, the brainstem raphe nuclei get dense CRHergic innervation that, through CRH-R1 receptors, may influence the serotoninergic tone of the brain. Both stress and serotonin are strongly implicated in depression, therefore, it is not surprising that CRH-R1 antagonists were developed as therapeutic tools that extensively act on the brain CRH system. Our review suggests a general role of brain CRH network in stress adaptation which is not restricted to PVN.

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Differential and temporal expression of corticotropin releasing hormone and its receptors in the nucleus of the hippocampal commissure and paraventricular nucleus during the stress response in chickens (Gallus gallus)

Cited by 23 publications

References 42 publications

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

Telencephalic regulation of the HPA axis in birds

Brain corticotropin releasing hormone and stress reactivity

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