Thesis (Ph.D.)--University of Wyoming, 2008. / Title from PDF title page (viewed on August 9, 2009). Includes bibliographical references.

Thesis (Ph. D.)--University of California, San Diego, 2001. / Vita. Includes bibliographical references (leaves 122-132).

Huang, Hui. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 141-154). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Thesis (M.S.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains viii, 138 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 105-134).

Thesis (Ph. D.)--West Virginia University, 1999. / Title from document title page. Document formatted into pages; contains xiv, 223 p. : ill. Vita. Includes abstract. Includes bibliographical references (p. 187-220).

Lors d’un stress, l’activation de l’axe hypothalamo-hypophyso-surrénalien (HHS) conduit à une augmentation de la production de glucocorticoïdes (tel que la corticostérone) par les glandes surrénales. Le rôle de la corticotropin-releasing hormone (CRH), à l’origine de l’activation de l’axe HHS, est encore méconnu. En effet, les récepteurs à la CRH sont présents aussi bien au niveau du système nerveux central (SNC), notamment au niveau du cervelet, qu’au niveau du système immunitaire (SI). Cela suggère donc une action directe possible de cette hormone sur ces deux systèmes. Au cours de ce projet, nous avons étudié les régulations des SNC et SI lors d’un stress, et plus particulièrement le rôle de la CRH et de ses récepteurs dans ces régulations. Suite à des injections chroniques de corticostérone, mimant un stress, nous avons observé une altération des fonctions locomotrices qui semble être reversée lorsque le CRH-R1 est inhibé avec un antagoniste. Ces premiers résultats permettent de mettre en avant un éventuel rôle de la CRH dans la régulation des fonctions motrices au niveau du cervelet en conditions de stress. En parallèle, d’autres études in vitro réalisées sur des splénocytes murins stimulés avec de la CRH ont montré une diminution de la viabilité des lymphocytes B (LB). Suite à ces résultats, nous avons caractérisé pour la première fois la présence de récepteurs à la CRH sur cette population de LB murins. Ces résultats montrent l’importance de la CRH dans les régulations des SNC et SI en condition de stress et le rôle de cette hormone dans les interactions entre les deux systèmes / In stress conditions, the Hypothalamo-Pituitary-Adrenal (HPA) axis activation leads to an overproduction of glucocorticoïds (such as corticosterone in rodent) by adrenal glands and this activation is well characterized. However, various questions remain about the precise role of corticotropin-releasing hormone (CRH), which is at the beginning of the HPA activation. Indeed, CRH receptors are presents both in central nervous system (CNS), especially in cerebellum, and in immune system (IS). This suggest a possible direct action of this hormone on both system. In this project, we studied the regulations on CNS and IS in stress conditions and more particularly the CRH role and these receptors in these regulations. After chronic corticsterone injections, to mimic a stress, we observed a locomotor alteration which seems to be inverted when CRH-R1 were inhibited with an antagonist. These first results show an possible CRH role in locomotor regulation in cerebellum under stress condition. In parallel, others in vitro studies performed on murine splenocytes stimulated with CRH showed a B lymphocyte (LB) viability decrease. Furthermore, we are the first to characterise the CRH receptors on murine LB. This work show the CRH importance in CNS and IS regulations under stress conditions and its role in interactions between the two systems

Leung Tse Ngong. / Thesis (M.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 169-197). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web.

The stress response is an evolutionarily conserved mechanism critical for survival that requires orchestration of different systems in the body. Corticotropin-releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus (PVN) represent the final common pathway leading to HPA axis activation in response to stress. Noradrenergic inputs to CRH neurons in the PVN provide a powerful drive to activate the HPA axis. Previous anatomical studies have shown that noradrenergic afferents synapse directly on CRH neurons, but electrophysiological analyses indicate that the noradrenergic activation of CRH neurons is mediated primarily by the stimulation of presynaptic glutamatergic neurons. Here, using whole cell patch clamp recordings in identified CRH neurons, I demonstrate that norepinephrine (NE) stimulates excitatory synaptic inputs by activating postsynaptic α1 adrenergic receptors in CRH neurons and inducing the release of the retrograde messenger nitric oxide, which drives upstream glutamate neurons to elicit spike-dependent synaptic glutamate release onto the CRH neurons. Notably, the NE effect is dependent on ATP transmission and astrocytic function, suggesting that astrocytes serve as an intermediary in the retrograde activation of glutamateregic synaptic inputs to the CRH neurons. In addition, I also show that the NE-induced excitation of CRH neurons is stress-status sensitive and corticosterone dependent, in that stress-induced corticosterone causes internalization of membrane α1 adrenergic receptors to desensitize the CRH neurons to NE. Taken together, my findings provide evidence that NE excites CRH neurons in a stress state-dependent manner by a retrograde NO stimulation of local glutamate circuits that is dependent on glial activation. This retrograde trans-neuronal-glial regulation of excitatory synaptic inputs to CRH neurons by NE provides a mechanism for the NE activation of the HPA axis in the early stage of stress response. The stress-/corticosterone-induced desensitization of CRH neurons to NE modulation by the internalization of α1 adrenergic receptors confers a stress state-dependent resistance of the CRH neurons to repeated noradrenergic activation, which provides a mechanism for the negative feedback regulation of the CRH neurons and the HPA axis by stress and glucocorticoids, and a means to restore neuroendocrine homeostasis after stress exposure. / acase@tulane.edu

The neuropeptides arginine-vasotocin (AVT) and corticotropin-releasing hormone (CRH) are involved in the hypothalamic-pituitary-interrenal (HPI) axis. During stress, the HPI axis is activated and cortisol is released into the blood. In addition to their role in the HPI axis, AVT and CRH also have behavioural effects. The roles of AVT and CRH in stress responses and agonistic behaviour were studied in this thesis, using two different models. In the first model, two strains of rainbow trout (Onchorhynchus mykiss) divergent in stress-induced release of cortisol were investigated. This was done by observing behaviour and stress responses under different conditions. These strains were found to have divergent stress coping strategies based on the observed behaviour and levels of plasma cortisol. This divergence in behaviour could be associated with the CRH system, since the mRNA levels of CRH differed between the strains during stress. However, no differences between strains were observed in AVT or its receptor expressions. In the second model, non-selected rainbow trout were paired and the effect of intracerebroventricular (icv) injections of an active substance (AVT, CRH or the CRH related peptide Urotensin-I (UI)) on fights for dominance was investigated. One fish of the pair received the active substance icv and the other received saline icv. Fish receiving AVT became subordinate in accordance with the suggestion that AVT attenuates aggression in territorial vertebrates. Fish receiving CRH became subordinate whereas UI showed no effect on fights for dominance. Further, both CRH and UI induced an anxiety-related behaviour similar to non-ambulatory motor activity in rats. In addition, CRH appeared to affect the dopaminergic and serotonergic systems. In this thesis, it is suggested that CRH is involved in the behavioural modulation of the stress coping strategies in teleost fish. Further, AVT and CRH seem to act inhibitory on aggressive behaviour.

The involvement of corticotropin-releasing hormone (CRH) and neuropeptide Y (NPY) in the pathophysiology of anxiety and anxiety-related disorders is well established. The objective of this study is to explore the genetic variations in the CRH and NPY genes in a well-documented behavioral animal model, the vervet monkey (Chlorocebus aethiops sabaeus), in order to uncover a possible association between these polymorphisms and behavioral traits quantitatively extracted following analysis of social behavior and responses to novelty challenges. / The vervet CRH and NPY genes were amplified and sequenced; the priority was given to the regions expanding from -1kb upstream of the transcription initiation site (where most of the regulatory elements are found in both genes) through the second exon. / Polymorphism discovery analysis revealed the presence of 9 vervet CRH SNPs and 9 vervet NPY SNPs; the SNPs are relatively evenly distributed across the regions covered. An association between one intronic NPY SNP and "defensive aggression" was detected. / These results are coherent with other reports implicating NPY in defensive aggressive behavior, and support the notion that fear responses are fundamental behavioral traits for the dissection of anxiety.