Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex

Crayton, John W.; Joshi, Ira; Gulati, Anil; Arora, Ramesh; Wolf, William A.

doi:10.1016/0006-8993(96)00189-8

Cited by 28 publications

(15 citation statements)

References 21 publications

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“…Marked differences were observed between these serotonergic receptor populations that may represent functional differences in these regions with respect to regulation of the HPA axis (hypothalamus), cognitive processes (frontal cortex), or both (hippocampus). In the frontal cortex, the changes in density of 5-HT 1A receptors due to corticosterone concentration in young animals correlated with previous findings (Crayton et al, 1996) but were not as pronounced as those in the hippocampus. In contrast to the limited corticosterone-mediated responses in the hippocampus and frontal cortex found in the oldest group, an upregulation of 5-HT 1A receptor density in the hypo- Hypothalamic 5-HT 1A receptor density is increased in both 3 and 18 month LC groups as compared to age-matched MC groups; a significant age-dependent increase in 5-HT 1A density was observed in the 18 month LC group as compared to the 3 month LC group.…”

Section: Discussionsupporting

confidence: 88%

Age-dependent loss of corticosterone modulation of central serotonin 5-HT1A receptor binding sites

Dugar

et al. 1998

J. Neurosci. Res.

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A loss of endocrine and neurotransmitter system interactions, including corticosterone regulation of 5-HT1A receptors, may underlie the age-related deficits in the hypothalamic-pituitary-adrenal (HPA) axis including adapting to stress. In this study, female Fischer 344 rats, (ages 3, 13, and 18 months), were bilaterally adrenalectomized and supplemented for 3 weeks with placebo or corticosterone (200 mg or 600 mg) containing 21 day sustained-release pellets implanted subcutaneously (LC, MC, or HC, respectively). Scatchard analysis using the 5-HT1A receptor agonist [3H]8-hydroxy-2-(di-N-propylamino) tetralin (8-OH-DPAT) demonstrated a significant decrease in hippocampal receptor density in 3 month and 13 month MC groups (-35.2 and -32.1%, respectively) as compared to age-matched LC groups; a significant decline in 5-HT1A receptor density in 3 month and 13 month HC groups was found compared to age-matched MC groups (-16.7 and -22.0%, respectively). However, these hormone treatments (LC or HC) failed to alter hippocampal 5-HT1A binding site density in the 18 month groups. Cortical 5-HT1A receptor densities were altered in a similar age-dependent manner. In contrast, the density of hypothalamic 5-HT1A receptors in the 18 month LC group was significantly increased above that in the 3 month LC group. An additional indicator of the hippocampal response to corticosterone, the distribution of glial fibrillary acidic protein (GFAP), revealed an age-related decline in responsiveness to hormone treatment in the oldest group. The present study has identified an age-associated deficit in the regulation of hippocampal 5-HT1A receptors by corticosterone which may underly the diminished capacity of the aging HPA axis to cope with stress.

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Section: Discussionsupporting

confidence: 88%

Age-dependent loss of corticosterone modulation of central serotonin 5-HT1A receptor binding sites

Dugar

et al. 1998

J. Neurosci. Res.

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“…Obviously, the simultaneous occurrence of elevated plasma cortisol and increased neural activity need not imply that a causal relationship exists. It should also be kept in mind that glucocorticoids influence both the synthesis and release of monoamine neurotransmitters, as well as receptor densities [Chaouloff, 1993;Stanford, 1993;Crayton et al, 1996;Piazza et al, 1996], so the direction of causality is not immediately obvious.…”

Section: Discussionmentioning

confidence: 99%

Short-Term Effects of Fights for Social Dominance and the Establishment of Dominant-Subordinate Relationships on Brain Monoamines and Cortisol in Rainbow Trout

Øverli

Harris

Winberg³

1999

Brain Behav Evol

379

213

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We report changes in brain serotonergic, noradrenergic and dopaminergic activity, along with plasma cortisol concentrations, occurring during the initial 24-h period following the establishment of dominant-subordinate relationships in pairs of rainbow trout. Immediately (within 5 min) after the termination of staged fights for social dominance, a large increase in blood plasma cortisol was observed in both fight losers (future subordinate fish) and winners (future dominant fish). In dominant fish, cortisol decreased rapidly (within 3 h) to the level of unstressed controls, while continuing to increase in subordinate fish. At 3 h following fights, the brain serotonergic system was activated in both dominant fish and subordinate fish, at least in some brain regions (telencephalon). This effect was reversed in dominant individuals within 24 h of social interaction, whereas in subordinate fish a substantial activation of the serotonergic system was manifest in all brain regions by 24 h. Similarly, a strong increase in brain catecholaminergic activation was indicated after 24 h of social interaction in subordinate fish, but not in dominant fish. Relationships between plasma cortisol and brain serotonergic and noradrenergic activity in the various experimental groups suggest that these systems influence cortisol secretion under normal conditions and during moderate or short-term stress.

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“…Whatever the precise mechanism of action, intra-mPFC actions of 5-HT1A-Rs (and as described later, other serotonin receptors) is a critical means of system-level regulation of the serotonergic response to stress. In this regard, a loss in mPFC 5-HT1A-R binding following stress or glucocorticoid excess (Crayton et al, 1996;Preece et al, 2004) (cf. Arborelius et al, 2004) could significantly impact this form of regulation.…”

Section: Role Of 5-ht1a Receptorsmentioning

confidence: 99%

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

Holmes

2008

Neuroscience & Biobehavioral Reviews

249

166

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The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase 1 and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research.

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Effect of corticosterone on serotonin and catecholamine receptors and uptake sites in rat frontal cortex

Cited by 28 publications

References 21 publications

Age-dependent loss of corticosterone modulation of central serotonin 5-HT1A receptor binding sites

Age-dependent loss of corticosterone modulation of central serotonin 5-HT1A receptor binding sites

Short-Term Effects of Fights for Social Dominance and the Establishment of Dominant-Subordinate Relationships on Brain Monoamines and Cortisol in Rainbow Trout

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

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