The intracerebroventricularly administered mast cells degranulator compound 48/80 increases the pituitary-adrenocortical activity in rats

Gàdek-Michalska, A; Chłap, Z; Turoń, M; Bugajski, J; Fogel, W. A.

doi:10.1007/bf01980874

Cited by 29 publications

(12 citation statements)

References 28 publications

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“…To understand the underlying mechanism of this phenomenon, we examined the serum corticosterone level of rats exposed to CSD and treated with ranitidine or cimetidine which is significantly lower than that of the rats exposed to CSD and receiving placebo. Cerebral histamine is produced by mastocytes which can activate the HPA axis after stimulation [22]. It is possible that the H 2 receptor antagonists such as ranitidine and cimetidine may affect histamine to activate HPA axis through blocking the H 2 receptor in the brain, which decrease serum corticosterone level and suppress the depression-like behaviors.…”

Section: Discussionmentioning

confidence: 99%

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Zhang

Gao

et al. 2012

PLoS ONE

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Stress contributes to a variety of diseases and disorders such as depression and peptic ulcer. The present study aimed to investigate the correlation between stress ulcer and depression in pathogenesis and treatment by using chronic stress depression (CSD), chronic psychological stress ulcer (CPSU) and water immersion restrain stress models in rats. Our data showed that the ulcer index of the animals after CSD exposure was significantly higher than that of controls. Depression-like behaviors were observed in rat after CPSU exposure. Fluoxetine hydrochloride significantly reduced the ulcer index of rats exposed to CPSU stress, while ranitidine inhibited depression-like behavior of the animals in CSD group. The ulcer index of rats administered with mifepristone after CPSU stress was markedly reduced compared to CPSU group, although there was no significant difference in the depression-like behavior between mifepristone-treated CSD group and naive controls. We also found that the rats exposed to CPSU or CSD stress displayed a lower level of corticosterone than naive controls, however, the acute stress (AS) group showed an opposite result. Additionally, in order to study the relevance of H2 receptors and depression, we treated the CSD group with cimetidine and famotidine respectively. The data showed that cimetidine inhibited depression-like behavior in CSD rats, and famotidine had no impact on depression. Overall our data suggested that the hypothalamic-pituitary-adrenal (HPA) axis dysfunction may be the key role in triggering depression and stress ulcer. Acid-suppressing drugs and antidepressants could be used for treatment of depression and stress ulcer respectively. The occurrence of depression might be inhibited by blocking the central H2 receptors.

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Section: Discussionmentioning

confidence: 99%

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Zhang

Gao

et al. 2012

PLoS ONE

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“…This assumption is confirmed by the fact that in our concurrent experiments the total degranulation of the rat brain mast cells by compound 48/80 administered intracerebroventricularly did not diminish the brain histamine levels. Also the histamine blockers mepyramine and cimetidine given into cere bral ventricles did not considerably change the corticosterone response induced by cen tral administration of compound 48/80 [25], Therefore, these findings indicate that the brain histamine involved in the opioid-in duced increase in corticosterone secretion is located mainly in the neuronal pool. In in vivo experiments on rats the most pro nounced histamine depletion (below 40% of the control value), observed in different brain structures, occurred 2-4 h after sys temic treatment with a-FMH [26,27].…”

Section: Discussionmentioning

confidence: 57%

Alpha-Fluoromethylhistidine Decreases the Leu-Enkephalinamide- and Morphine-Induced Corticosterone Response in Rats

Turoń

Fogel²,

Bugajski³

1991

Pharmacology

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The effect of inhibition of brain histamine synthesis by α-fluoromethylhistidine (α-FMH) on the pituitary adrenocortical activity stimulated by D-Ala-·D-Leu-enkephalinamide (DADL) and morphine was investigated indirectly through corticosterone secretion in conscious rats. α-FMH (20 mg/kg i.p.) drastically reduced the whole brain histamine content, measured 2 h later. The same pretreatment also considerably reduced the corticosterone response induced by DADL or morphine injected into cerebral ventricles, and abolished the response to morphine given intraperitoneally. When α-FMH was administered intracerebroventricularly (50 μg), the maximum inhibition of the corticosterone response to DADL and morphine occurred 4 h after administration, which may suggest a weaker accessibility of α-FMH from the cerebral venticle to the brain structures involved in pituitary-adrenocortical stimulation. The corticosterone responses were not related to the core temperature changes. These results indicate that inhibition of brain histamine synthesis by α-FMH considerably impairs the pituitary-adrenocortical response to the opioid δ- and μ-receptor agonists DADL and morphine. They also suggest that neuronal histamine is significantly involved in the central stimulation of the pituitary-adrenal axis by opioids.

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“…It is known that histamine receptors are densely concentrated in the thalamus (Pillot et al, 2002) and can control presynaptic glutamate release (Garduno-Torres et al, 2007). Moreover, thalamic mast cell degranulation and histamine release coincides with corticosterone secretion (Bugajski et al, 1995), which is reduced by pretreatment with histamine receptor antagonists (Gadek-Michalska et al, 1991). Previously, it has been shown that mast cells can express corticotrophin-releasing factor receptors (Cao et al, 2005) and can even release corticotrophin-releasing factor (Theoharides et al, 2004) and corticosterone (Csaba et al, 1967).…”

Section: Discussionmentioning

confidence: 99%

Thalamic mast cell activity is associated with sign-tracking behavior in rats

Fitzpatrick

Morrow

2017

Brain, Behavior, and Immunity

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Mast cells are resident immune cells in the thalamus that can degranulate and release hundreds of signaling molecules (i.e., monoamines, growth factors, and cytokines) both basally and in response to environmental stimuli. Interestingly, mast cell numbers in the brain show immense individual variation in both rodents and humans. We used a Pavlovian conditioned approach (PCA) procedure to examine whether mast cells are associated with individual variation in the attribution of incentive-motivational value to reward-related cues. During the PCA procedure, a lever response-independently predicts the delivery of a food pellet into a magazine, and over training sessions three conditioned responses (CRs) develop: sign-tracking (lever-directed CRs), goal-tracking (magazine-directed CRs), and an intermediate response (both CRs). In Experiment 1, we measured thalamic mast cell number/activation using toluidine blue and demonstrated that sign-trackers have increased degranulated (activated) but not granulated (inactive) mast cells. In Experiment 2, we infused the mast cell inhibitor, cromolyn (200 µg/rat; i.c.v.), immediately before five daily PCA training sessions and demonstrated that mast cell inhibition selectively impairs the acquisition of sign-tracking behavior. Taken together, these results demonstrate that thalamic mast cells contribute to the attribution of incentive-motivational value to reward-related cues and suggest that mast cell inhibition may be a novel target for addiction treatment.

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The intracerebroventricularly administered mast cells degranulator compound 48/80 increases the pituitary-adrenocortical activity in rats

Cited by 29 publications

References 28 publications

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Bidirectional Crosstalk between Stress-Induced Gastric Ulcer and Depression under Chronic Stress

Alpha-Fluoromethylhistidine Decreases the Leu-Enkephalinamide- and Morphine-Induced Corticosterone Response in Rats

Thalamic mast cell activity is associated with sign-tracking behavior in rats

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