Effect of isolation stress on brain mast cells and brain histamine levels in rats

Aj, Bugajski; Chłap, Z; Gadek-Michalska,; Bugajski, J

doi:10.1007/bf02007774

Cited by 43 publications

(22 citation statements)

References 6 publications

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“…The possible relationship of mast cells to behavioral states is suggested by the fact that brain mast cell activation can occur in response to isolation stress, 94 to restraint stress, 48 subordination stress, and during courtship after isolation of male doves. 95 The potential pathophysiological role of brain mast cells triggered by acute stress has been reviewed.…”

Section: Significancementioning

confidence: 98%

Chronic Fatigue Syndrome, Mast Cells, and Tricyclic Antidepressants

Theoharides¹,

Papaliodis²,

Tagen³

et al. 2005

Journal of Clinical Psychopharmacology

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Section: Significancementioning

confidence: 98%

Chronic Fatigue Syndrome, Mast Cells, and Tricyclic Antidepressants

Theoharides¹,

Papaliodis²,

Tagen³

et al. 2005

Journal of Clinical Psychopharmacology

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“…Stressed mice had increased inflammatory spinal cord lesions and developed autoimmune antibodies to MBP [299]. Mast cell activation was shown to occur in response to isolation stress [300], restraint stress [278], subordination stress [301], and during courtship following isolation of male doves [302]. …”

Section: Multiple Sclerosismentioning

confidence: 99%

Mast cells and inflammation

Theoharides

Alysandratos

Angelidou

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

652

531

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Mast cells are well known for their role in allergic and anaphylactic reactions, as well as their involvement in acquired and innate immunity. Increasing evidence now implicates mast cells in inflammatory diseases where they are activated by non-allergic triggers, such as neuropeptides and cytokines, often exerting synergistic effects as in the case of IL-33. Mast cells can also release pro-inflammatory mediators selectively without degranulation. In particular, IL-1 induces selective release of IL-6, while corticotropin-releasing hormone secreted under stress induces the release of vascular endothelial growth factor. Many inflammatory diseases involve mast cells in cross-talk with T cells, such as atopic dermatitis, psoriasis and multiple sclerosis, which all worsen by stress. How mast cell differential responses are regulated is still unresolved. Preliminary evidence suggests that mitochondrial function and dynamics control mast cell degranulation, but not selective release. Recent findings also indicate that mast cells have immunomodulatory properties. Understanding selective release of mediators could explain how mast cells participate in numerous diverse biologic processes, and how they exert both immunostimulatory and immunosuppressive actions. Unraveling selective mast cell secretion could also help develop unique mast cell inhibitors with novel therapeutic applications.

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“…An early study by Persinger showed that simple gentle handling of rat pups decreased numbers of mast cells in the brain developmentally, most likely representing an increase in degranulation (25). Psychological stressors induced through social defeat and isolation stress increased the number of mast cells in the brain (26,63). Last, gonadal hormones from conspecifics during mating also increase mast cell number and activation in the brain (23,62,64).…”

Section: Mast Cells Are Active Both Constitutively and Following Stimmentioning

confidence: 99%