Neurochemical Responses in Stress: Relationships Between the Hypothalamic-Pituitary-Adrenal and Catecholamine Systems

Dunn, Adrian J.; Kramarcy, Neal R.

doi:10.1007/978-1-4615-7178-0_8

Cited by 54 publications

(50 citation statements)

References 249 publications

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“…4). Because an increased release of corticosterone and brain monoamines are responses characteristic of stress, exposure to the MCC can be considered a stressor (Dunn and Kramarcy, 1984). This would explain why ahCRF slightly elevated the mean time per contact in unrestrained mice (Fig.…”

Section: Discussionmentioning

confidence: 94%

“…Central noradrenergic systems are also activated in stress (Stone, 1975;Dunn and Kramarcy, 1984). In an earlier study, mice administered the +-antagonist idazoxan at a dose (1 .O mg/ kg) that increases both norepinephrine (NE) release (Scheinin and Virtanen, 1986) and neuronal firing in the locus coeruleus (Goldstein et al, 1983) experienced a stress-like decrease in exploratory behavior when tested in the MCC (Berridge and Dunn, 1987b).…”

mentioning

confidence: 99%

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Restraint-stress-induced changes in exploratory behavior appear to be mediated by norepinephrine-stimulated release of CRF

1989

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Exploratory behavior, measured by the time an animal spends investigating objects in a novel environment, has been shown to be sensitive to prior exposure of the animal to stressors. or the number of rears. These results implicate noradrenergic systems in the stress-related changes in this behavior, consistent with our parallel measures of the production of NE catabolites. Thus, both CRF and noradrenergic systems appear to be involved in the effect of restraint on exploratory behavior in this task. Neither DSP-4 nor prazosin had any effect on the CRFinduced decrease in exploratory behavior. However, the CRF antagonist a-helical CRF,,, (20 fig, i.c.v.) reversed the decrease in exploratory behavior induced by phenylephrine. The most likely explanation is that the 2 systems act in tandem such that noradrenergic systems regulate the release of brain CRF via an a,-adrenoreceptor.This arrangement parallels that involved in the release of hypothalamic CRF to activate the pituitary-adrenal axis. The implications of these results for research on stress-related behaviors and for the etiology of depression are discussed.

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Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

Restraint-stress-induced changes in exploratory behavior appear to be mediated by norepinephrine-stimulated release of CRF

1989

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“…In the CNS, the major response occurs in noradrenergic neurons, but responses also occur in dopaminergic and serotonergic neurons [163,164]. The NE response is widespread and appears to affect similarly both the locus coeruleus (A6) system innervating dorsal structures, via the DNAB, and the NTS A1/A2 system via the VNAB.…”

Section: Neurochemical Responses To Infectionsmentioning

confidence: 99%

Effects of cytokines and infections on brain neurochemistry

Dunn

2006

Clinical Neuroscience Research

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283

169

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Administration of cytokines to animals can elicit many effects on the brain, particularly neuroendocrine and behavioral effects. Cytokine administration also alters neurotransmission, which may underlie these effects. The most well studied effect is the activation of the hypothalamopituitary-adrenocortical (HPA) axis, especially that by interleukin-1 (IL-1). Peripheral and central administration of IL-1 also induces norepinephrine (NE) release in the brain, most markedly in the hypothalamus. Small changes in brain dopamine (DA) are occasionally observed, but these effects are not regionally selective. IL-1 also increases brain concentrations of tryptophan, and the metabolism of serotonin (5-HT) throughout the brain in a regionally nonselective manner. Increases of tryptophan and 5-HT, but not NE, are also elicited by IL-6, which also activates the HPA axis, although it is much less potent in these respects than IL-1. IL-2 has modest effects on DA, NE and 5-HT. Like IL-6, tumor necrosis factor-α (TNFα) activates the HPA axis, but affects NE and tryptophan only at high doses. The interferons (IFN's) induce fever and HPA axis activation in man, but such effects are weak or absent in rodents. The reported effects of IFN's on brain catecholamines and serotonin have been very varied. However, interferon-γ, and to a lesser extent, interferon-α, have profound effects on the catabolism of tryptophan, effectively reducing its concentration in plasma, and may thus limit brain 5-HT synthesis.Administration of endotoxin (LPS) elicits responses similar to those of IL-1. Bacterial and viral infections induce HPA activation, and also increase brain NE and 5-HT metabolism and brain tryptophan. Typically, there is also behavioral depression. These effects are strikingly similar to those of IL-1, suggesting that IL-1 secretion, which accompanies many infections, may mediate these responses. Studies with IL-1 antagonists, support this possibility, although in most cases the antagonism is incomplete, suggesting the existence of multiple mechanisms. Because LPS is known to stimulate the secretion of IL-1, IL-6 and TNFα, it seems likely that these cytokines mediate at least some of the responses, but studies with antagonists indicate that there are multiple mechanisms. The neurochemical responses to cytokines are likely to underlie the endocrine and behavioral responses. The NE response to IL-1 appears to be instrumental in the HPA activation, but other mechanisms exist. Neither the noradrenergic nor the serotonergic systems appear to be involved in the major behavioral responses. The significance of the serotonin response is unknown.

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“…As reviewed later, many of the neural systems known to undergo developmental alterations in adolescence are sensitively activated by stressors, including DA projections to PFC as well as to mesolimbic brain regions thought to be critical in modulating the reward value of drugs [1,109,148,251,554]. Receptors for glucocorticoids have been identified in rodent brain on dopaminergic neurons in the ventral tegmental area (VTA) and substantia nigra (SN) as well as in DA terminal regions including the nucleus accumbens (ACC) and PFC [6,90,136,225].…”

Section: Stress and Drug Abuse In Adolescentsmentioning

confidence: 99%

The adolescent brain and age-related behavioral manifestations

Spear

2000

Neuroscience & Biobehavioral Reviews

4,693

110

4,301

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To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence. ᭧

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Neurochemical Responses in Stress: Relationships Between the Hypothalamic-Pituitary-Adrenal and Catecholamine Systems

Cited by 54 publications

References 249 publications

Restraint-stress-induced changes in exploratory behavior appear to be mediated by norepinephrine-stimulated release of CRF

Restraint-stress-induced changes in exploratory behavior appear to be mediated by norepinephrine-stimulated release of CRF

Effects of cytokines and infections on brain neurochemistry

The adolescent brain and age-related behavioral manifestations

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