Subcellular localization of brain mast cell histamine in developing rat

Blanco, Isaac; Ferrer, Isidre; Toledo, A.; Sabriá, Josefa; Picatoste, Fernando; Rodrı́guez, Ricardo; Brandner, Regina; Rodríguez, José Manuel ́Ramírez; Sentís, Melcior

doi:10.1016/0197-0186(87)90035-0

Cited by 5 publications

(3 citation statements)

References 43 publications

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“…We found in rats kept under both resting and stress conditions that icv administration of histamine and its agonists stimulated the corticosterone response which, in turn, was antagonized by histamine receptor blockers [22,23]. It has been found recently that in rat brain compound 48/80 given icy induces mast cells degranulation and the release of histamine from MC but not from neurons and the nlast cells contribution to rat brain histamine was about 22% [24]. A very similar inhibition of the corticosterone release by compound 48/80 was observed in our experiment by histamine antagonists mepyramine and cimetidine.…”

Section: Discussionmentioning

confidence: 93%

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

Gàdek-Michalska

Chłap²,

Turoń

et al. 1991

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The effect of brain mast cells degranulation by compound 48/80 on the pituitary-adrenocortical activity, measured indirectly through corticosterone secretion, and the involvement of a histaminergic mechanism in that stimulation was investigated in conscious rats. All the drugs were given intracerebroventricularly (icv), histamine antagonists 15 min prior to compound 48/80. Compound 48/80 induced a significant dose- and time-related increase in the serum corticosterone levels. That increase, measured 1 h after administration of compound 48/80, was moderately diminished by icv pretreatment of rats with mepyramine and cimetidine, histamine H1- and H2-receptor antagonists. Three hours after administration of compound 48/80 mast cells of the thalamus and the hypothalamus were completely degranulated. At the same time the thalamus and the whole brain histamine levels were substantially higher than in the saline-treated control rats. The above results suggest that histamine liberated from the brain mast cells and central histamine receptors play a moderate role in increasing the pituitary-adrenocortical activity by compound 48/80.

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Section: Discussionmentioning

confidence: 93%

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

Gàdek-Michalska

Chłap²,

Turoń

et al. 1991

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“…14, 1991 Formerly it was presumed that histamine in the CNS was catabolized only by histidine-N-methyl transferase and by MAO-B, since the presence of histaminase in CNS was not known (Blanco et al, 1987). Recently Desiderio et al (1988) demonstrated the presence of histarninase in the CNS and suggested that this enzyme is of great importance not only in histamine degradation but also in the regulation of polyamine synthesis, as well as in gamma-aminobutyric acid formation.…”

Section: Molecular and Chemical I'leuropathologymentioning

confidence: 99%

“…In the central nervous system (CNS) histamine may be produced in mastocytes, glial cells, and histaminergic neurons (Kapeller-Adler, 1956;Blanco et a!., 1987).…”

Section: Introductionmentioning

confidence: 99%

Decrease in blood histamine in drug-treated Parkinsonian patients

Coelho¹,

Silva²,

Azevedo³

et al. 1991

Molecular and Chemical Neuropathology

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Blood histamine and serum histaminase activity were determined in a group of patients with Parkinson disease (PD) and in a group of healthy controls. Untreated PD patients present significantly higher blood histamine than normal controls. Therapy with L-dopa + cardidopa results in a significant decrease in blood histamine. This decrease becomes more accentuated when anticholinergics are added to this therapy. No significant changes were detected in plasma histaminase. The authors suggest, as a hypothesis, that the CNS contributes to blood histamine concentration and that its rise is the result of increased neuronal destruction.

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