The developmental profile of the corticotropin releasing factor receptor (CRF2) in rat brain predicts distinct age-specific functions

Eghbal-Ahmadi, Mariam; Hatalski, Carolyn G.; Lovenberg, Timothy W.; Avishai-Eliner, Sarit; Chalmers, Derek T.; Baram, Tallie Z.

doi:10.1016/s0165-3806(98)00002-9

Cited by 50 publications

(48 citation statements)

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“…31 Indeed, CRHexpressing neurons and CRH receptors are found in select amygdala nuclei, other limbic relay centers, and all hippocampal fields. [32][33][34][35][36][37][38][39] Furthermore, administration of receptor-blockers of CRH into the key regions in this limbic circuit, such as ACe 40 blocks stressinduced responses. In addition, CRH-containing cells constitute a significant neuronal population in ACe, and send efferent projections to the bed nucleus of the stria terminalis, which then projects to CRH-expressing cells in PVN.…”

Section: Neuronal Circuitry and Crh-mediated Transduction Of The Respmentioning

confidence: 99%

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

et al. 2001

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Over the last few decades, concepts regarding the presence of hormonal and molecular responses to stress during the first postnatal weeks in the rat and the role of the neuropeptide corticotropin releasing hormone (CRH) in these processes, have been evolving. CRH has been shown to contribute critically to molecular and neuroendocrine responses to stress during development. In turn the expression of this neuropeptide in both hypothalamus and amygdala is differentially modulated by single and recurrent stress, and is determined also by the type of stress (eg, psychological or physiological). A likely transcriptional regulatory factor for modulating CRH gene expression, the cAMP responsive element binding protein CREB, is phosphorylated (activated) in the developing hypothalamus within seconds of stress onset, preceding the transcription of the CRH gene and initiating the activation of stress-induced cellular and neuroendocrine cascades. Finally, early life stress may permanently modify the hypothalamic pituitary adrenal axis and the response to further stressful stimuli, and recent data suggest that CRH may play an integral role in the mechanisms of these long-term changes. Molecular Psychiatry (2001) 6, 647-656.

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Section: Neuronal Circuitry and Crh-mediated Transduction Of The Respmentioning

confidence: 99%

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

et al. 2001

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“…However, the density and location of CRH receptors is altered through development. Some brain regions exhibit a decline in CRHr1 and r2 expression as the animal matures, whereas other regions show increased gene expression during specific stages of development (Avishai-Eliner et al, 1996;Eghbal-Ahmadi et al, 1998). To our knowledge, the expression of CRH binding protein early in development has not been described (Eckart et al, 2002) and the modulation of these CRH-related molecules by stress has been relatively unexplored during development.…”

Section: Introductionmentioning

confidence: 98%

Brain corticotropin-releasing hormone (CRH) circuits in the developing rat: Effect of maternal deprivation

et al. 2006

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Early in life, there is a delicate and critical balance aimed to maintain low hormone responses derived from the stress responsive hypothalamic-pituitary-adrenal axis (HPA). However, in the infant rat hypothalamic corticotrophin-releasing hormone (CRH) stress responses to environmental events are clearly seen even though other elements of the HPA axis may have limited responses. In view of the role of CRH in mediating behavior associated with stress and anxiety, we considered the ontogeny and the effects of prolonged maternal deprivation (DEP) in brain areas that express CRH-related molecules outside the hypothalamus. We hypothesized that DEP would alter the ontogeny of CRH, CRH binding protein and CRH receptor 1 in prefrontal cortex, amygdala, septum and hippocampus, areas that are part of the CRH extra hypothalamic system, and that a differential modulation would be observed in response to restraint. We compared non-deprived animals to animals subjected to 24 h of DEP at 6, 12 and 18 days of life. We found (1) developmental patterns, which were idiosyncratic to the anatomical area examined, and (2) a temporal response of mRNA levels which was also site specific. The genomic changes are not always related to maternal deprivation status, in fact DEP enhanced, suppressed or had no consequence on the underlying ontogenic progression and restraint response of these CRH-related molecules. We conclude that the extra hypothalamic CRH system is a dynamic system responding to developmental and environmental demands challenging the basic assumption of stress hypo responsiveness in the infant rat. This modulation may have important repercussions on morphological organization and events leading to neuroprotection.

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“…In addition, abnormally high CRH levels at the synapse may lead to excessive excitability and contribute to some developmental seizures (7). CRH functions via activation of specific membrane-spanning Gprotein coupled receptors, and both CRH-expressing cells and target neurons possessing these specific receptors (CRF 1 and CRF 2 ) are abundant throughout the limbic system (3,(16)(17)(18)22,53).…”

Section: Introductionmentioning

confidence: 99%

Corticotropin-Releasing Hormone (CRH) Downregulates the Function of Its Receptor (CRF1) and Induces CRF1 Expression in Hippocampal and Cortical Regions of the Immature Rat Brain

Brunson

Grigoriadis

Lorang

et al. 2002

Experimental Neurology

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In addition to regulating the neuroendocrine stress response, corticotropin-releasing hormone (CRH) has been implicated in both normal and pathological behavioral and cognitive responses to stress. CRH-expressing cells and their target neurons possessing CRH receptors (CRF 1 and CRF 2 ) are distributed throughout the limbic system, but little is known about the regulation of limbic CRH receptor function and expression, including regulation by the peptide itself. Because CRH is released from limbic neuronal terminals during stress, this regulation might play a crucial role in the mechanisms by which stress contributes to human neuropsychiatric conditions such as depression or posttraumatic stress disorder. Therefore, these studies tested the hypothesis that CRH binding to CRF 1 influenced the levels and mRNA expression of this receptor in stress-associated limbic regions of immature rat. Binding capacities and mRNA levels of both CRF 1 and CRF 2 were determined at several time points after central CRH administration. CRH downregulated CRF 1 binding in frontal cortex significantly by 4 h. This transient reduction (no longer evident at 8 h) was associated with rapid increase of CRF 1 mRNA expression, persisting for >8 h. Enhanced CRF 1 expression-with a different time course-occurred also in hippocampal CA3, but not in CA1 or amygdala, CRF 2 binding and mRNA levels were not altered by CRH administration. To address the mechanisms by which CRH regulated CRF 1 , the specific contributions of ligand-receptor interactions and of the CRH-induced neuronal stimulation were examined. Neuronal excitation without occupation of CRF 1 induced by kainic acid, resulted in no change of CRF 1 binding capacity, and in modest induction of CRF 1 mRNA expression. Furthermore, blocking the neuroexcitant effects of CRH (using pentobarbital) abolished the alterations in CRF 1 binding and expression. These results indicate that CRF 1 regulation involves both occupancy of this receptor by its ligand, as well as "downstream" cellular activation and suggest that stress-induced perturbation of CRH-CRF 1 signaling may contribute to abnormal neuronal communication after some stressful situations.

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The developmental profile of the corticotropin releasing factor receptor (CRF2) in rat brain predicts distinct age-specific functions

Cited by 50 publications

References 61 publications

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

Neurobiology of the stress response early in life: evolution of a concept and the role of corticotropin releasing hormone

Brain corticotropin-releasing hormone (CRH) circuits in the developing rat: Effect of maternal deprivation

Corticotropin-Releasing Hormone (CRH) Downregulates the Function of Its Receptor (CRF1) and Induces CRF1 Expression in Hippocampal and Cortical Regions of the Immature Rat Brain

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