Neuronal activity and stress differentially regulate hippocampal and hypothalamic corticotropin-releasing hormone expression in the immature rat

Hatalski, Carolyn G.; Brunson, Kristen L.; Tantayanubutr, B.; Chen, Y; Baram, Tallie Z.

doi:10.1016/s0306-4522(00)00386-9

Cited by 47 publications

(60 citation statements)

References 65 publications

(167 reference statements)

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“…This has been found in both adult [133] and immature [55] rat hippocampal interneurons, and may be a result of 'release-coupled synthesis' [34]. A similar mechanism has been described in immature hypothalamus and amygdala [154,56].…”

Section: Stress Induces Release Of Crh Into the Hippocampal Intercellmentioning

confidence: 59%

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Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

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Whereas genetic factors contribute crucially to brain function, early-life events, including stress, exert long-lasting influence on neuronal function. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning and memory. Using a novel immaturerodent model, we describe the deleterious consequences of chronic early-life 'psychological' stress on hippocampus-dependent cognitive tasks. We review the cellular mechanisms involved and discuss the roles of stress-mediating molecules, including corticotropin releasing hormone, in the process by which stress impacts the structure and function of hippocampal neurons. KeywordsNeonatal; Rat; Human; Stress; Memory; Hippocampus; Corticotropin releasing hormone; CRF; Hypothalamic pituitary adrenal axis; Neuroplasticity Early-life events interact with genetic factors to influence hippocampal function long-termBrain function and dysfunction throughout life are determined by the interaction of genetic factors with 'acquired' environmental events, signals and stimuli [100]. Events that occur early in life are capable of exerting effects that persist throughout adulthood. Here, we focus on the hippocampus as the target of these early-life events because of its crucial role in learning, memory storage and retrieval, and general cognitive function [105,41,65]. Indeed, early-life events, via complex interactions with genetic factors [106,120], have been suspected to be a major determinant of smaller hippocampal volume and long-term cognitive dysfunction in preterm infants [111,17] and may play a role in certain affective and dementing disorders in the adult and aging human [100,26,120]. This review focuses on the mechanisms by which certain early-life events influence populations of hippocampal neurons acutely, and impact the function and integrity of the hippocampus long-term. Studying early-life stress may be used to probe the molecular mechanisms involved in experience-evoked hippocampal neuroplasticityStress may provide a salient example of early-life experience that might exert long-lasting influence on the brain, because (1) over 50% of the world's children are exposed to stress [139] and (2) evidence from both human and animal studies suggests that early-life stress has profound effects on cognitive function and emotional health.Stress has been shown to influence the hippocampus in a number of important ways. Whereas acute mild stress rapidly enhances synaptic efficacy and learning and memory processes [131,45,91,123], chronic or severe activation of the stress response early in life has been shown to be potentially injurious in both humans [6,120,147] and experimental animals [120,31]. For example, severe childhood psychological stress (neglect and abuse) correlates with a higher incidence of learning disabilities later in life, including those learning and memory functions requiring an intact hippocampus [121,50]. Further, MRI studies have suggested that adults subjected to abuse (a measure of chronic stress) ...

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Section: Stress Induces Release Of Crh Into the Hippocampal Intercellmentioning

confidence: 59%

“…From amygdala outflow nuclei [112], selected stress signals project to the hippocampus (via mono-and poly-synaptic projections), evoking IEG expression [55] and enhancing synaptic efficacy [146,20].…”

Section: Early-life Events Interact With Genetic Factors To Influencementioning

confidence: 99%

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Fenoglio¹,

Brunson²,

Baram³

2006

Frontiers in Neuroendocrinology

192

138

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“…77,78 The effects of stress on hippocampal neurons during development have been less studied. 79 This is somewhat surprising, because both human and animal model studies suggest that the consequences of earlylife stress on the function and structure of the hippocampus might differ significantly depending on the age at which the stress is experienced.…”

Section: Discussionmentioning

confidence: 99%

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

et al. 2006

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The effects of stress, including their putative contribution to pathological psychiatric conditions, are crucially governed by the age at which the stress takes place. However, the cellular and molecular foundations for the impact of stress on neuronal function, and their change with age, are unknown. For example, it is not known whether 'psychological' stress signals are perceived by similar neuronal populations at different ages, and whether they activate similar or age-specific signaling pathways that might then mediate the spectrum of stress-evoked neuronal changes. We employed restraint and restraint/noise stress to address these issues in juvenile (postnatal day 18, [P18]) and adult rats, and used phosphorylation of the transcription factor CREB (pCREB) and induction of c-fos as markers of hippocampal neuronal responses. Stress-activated neuronal populations were identified both anatomically and biochemically, and selective blockers of the stress-activated hippocampal peptide, corticotropin-releasing hormone (CRH) were used to probe the role of this molecule in stressinduced hippocampal cell activation. Stress evoked strikingly different neuronal response patterns in immature vs adult hippocampus. Expression of pCREB appeared within minutes in hippocampal CA3 pyramidal cells of P18 rats, followed by delayed induction of Fos protein in the same cell population. In contrast, basal pCREB levels were high in adult hippocampus and were not altered at 10-120 min by stress. Whereas Fos induction was elicited by stress in the adult, it was essentially confined to area CA1, with little induction in CA3. At both age groups, central pretreatment with either a nonselective blocker of CRH receptors or the CRF 1 -selective antagonist, NBI 30775, abolished stress-evoked neuronal activation. In conclusion, hippocampal neuronal responses to psychological stress are generally more rapid and robust in juvenile rats, compared to fully mature adults, and at both ages, CRH plays a key role in this process. Enhanced hippocampal response to stress during development, and particularly the activation of the transcription factor CREB, may contribute to the enduring effects of stress during this period on hippocampal function.

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“…[22][23][24] The limbic neuroendocrine and behavioral circuit A second major stress-transducing circuit consists of limbic pathways that are more sensitive to stressors involving higher-order sensory processing ( Figure 1b). [25][26][27] These pathways are preferentially activated by stimuli that require assembly and processing of signals from multiple modalities (as opposed to stressors that are an immediate physiological threat). Substantial 28,30 However, the precise nature of the effector neurotransmitters/neuromodulators involved in the limbic stress circuit is still not fully understood.…”

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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Neuronal activity and stress differentially regulate hippocampal and hypothalamic corticotropin-releasing hormone expression in the immature rat

Cited by 47 publications

References 65 publications

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Hippocampal neuroplasticity induced by early-life stress: Functional and molecular aspects

Cellular and molecular mechanisms of hippocampal activation by acute stress are age-dependent

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

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