Experimental cerebral infarction in primates: Regional changes in brain histamine content

Subramanian, N.; Theodore, Deepa R.; Abraham, Jacob

doi:10.1007/bf01249144

Cited by 21 publications

(7 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increases in MCs and/or histamine have been identified in other brain injury models. For example, histamine levels, postulated to be derived from MCs, increase in the basal ganglia after focal brain ischemia [Subramanian et al, 1981]. Following fluid percussion injury to the cortex, MCs infiltrate the damaged region [Lozada et al, 2005;Strbian et al, 2006].…”

Section: Discussionmentioning

confidence: 99%

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Jin¹,

Silverman²,

Vannucci

2007

Dev Neurosci

View full text Add to dashboard Cite

Perinatal hypoxic-ischemic (HI) brain damage is a major cause of mortality and neurological morbidity in infants and children. Using an established model of unilateral hypoxia-ischemia in neonatal rats, the present study focused on mast cells (MCs), important regulators of inflammatory processes, as potential contributors to HI damage. MCs are present in the pia of the neonatal rat, entering the central nervous system (CNS) during cerebral development along penetrating blood vessels. Following hypoxia-ischemia, MC numbers increased dramatically in the ipsilateral (ischemic) hemisphere (p < 0.01). In animals exposed to hypoxia only, the numbers of MCs were elevated in both hemispheres to an extent equal to that observed in the contralateral hemisphere of HI animals (p < 0.05 vs. control). Within damaged areas (ipsilateral only), MCs were observed in regions of activated microglia and astroglia that characterize the ischemic hemisphere. Using a triple-label paradigm, MCs were observed along elongating blood vessels, some of which express the GLUT1 isoform of the glucose transporter protein, indicative of blood-brain barrier vessels. To determine whether MC activation has a role in HI brain damage, rat pups were treated with the MCs stabilizer, disodium cromoglycate (cromolyn),prior to and/or following hypoxia-ischemia. The cromolyn treatment inhibited MC migration into the CNS (p < 0.05) and limited brain damage more than 50% (p < 0.01) vs. saline controls. These data support the hypothesis that MCs are key contributors to the extent of brain damage due to hypoxia-ischemia in the immature animal.

show abstract

Section: Discussionmentioning

confidence: 99%

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Jin¹,

Silverman²,

Vannucci

2007

Dev Neurosci

View full text Add to dashboard Cite

show abstract

“…The histaminergic fibers emanating from the tuberomamillary nucleus project to the cerebral cortex, thalamus, basal ganglia, basal forebrain, and hypothalamus (Haas et al , 2008). Histamine content in the brain has been reported to increase transiently after cerebral ischemia in primates (Subramanian et al , 1981) and rodents (Adachi et al , 1992). We also showed that histamine level increased up to 6 hours after reperfusion in the I.C.…”

Section: Discussionmentioning

confidence: 99%

Targeted Disruption of Organic Cation Transporter 3 (Oct3) Ameliorates Ischemic Brain Damage through Modulating Histamine and Regulatory T Cells

Zhu

Hata

Ogasawara

et al. 2012

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

The organic cation transporters OCT1, 2, and 3 (SLC22A1-3) have been implicated in the elimination of biogenic amines such as histamine. Among them, OCT3 was identified as an uptake-2 transporter, responsible for clearance of histamine. Because increasing evidence suggests the involvement of histamine in cerebral ischemia, we investigated the effects of targeted disruption of organic cation transporter-3 (Oct3) on the severity of ischemic brain damage. Transient focal ischemia for 1 hour was induced by occlusion of the middle cerebral artery (MCA) of homozygous Oct3-deficient mice and their wild-type (Wt) littermates. Although targeted disruption of Oct3 did not affect physiological parameters after MCA occlusion, this disruption significantly increased histamine content in the ischemic cortex and significantly reduced the infarct volume after cerebral ischemia. Furthermore, targeted disruption of Oct3 prevented the reduction of regulatory T-cell proportion after cerebral ischemia while this disruption did not affect Th1 and Th2 cells proportions after ischemia. Since repeated administration of L-histidine (a precursor of histamine) to Wt mice also showed the same effects, our observations suggested that OCT3 is the molecule responsible for clearance of ischemia-induced histamine in the brain and targeted disruption of Oct3 ameliorated ischemic brain damage through an increase in regulatory T cells.

show abstract

“…17 In the primate Macaca radiata, a rise in cerebral histamine level was also found following experimental infarction induced in the basal ganglia by coagulation of the middle cerebral artery. 18 Adachi et al reported that histamine release is markedly reversed by preischemic administration of alpha-fluoromethylhistidine (α-FMH, 100 mg/kg), an irreversible inhibitor of HDC, which generates histamine from L-histidine. 17 α-FMH depletes histaminergic neurons of their histamine within the first few hours after treatment, since the turnover rate of neuronal histamine (half-life, <1 h) is more rapid than that of mast cell histamine (half-life, several days).…”

Section: ■ Alteration Of Histamine Content and Its Receptors After Cementioning

confidence: 99%

“…Moreover, Subramanian et al also reported that the elevation of histamine level in the basal ganglia after infarction in this region is probably due to the proliferation of mast cells. 18 Therefore, where the histamine comes from may depend on the ischemic region.…”

Section: ■ Alteration Of Histamine Content and Its Receptors After Cementioning

confidence: 99%

Role of Histamine and Its Receptors in Cerebral Ischemia

Chen

2012

ACS Chem. Neurosci.

View full text Add to dashboard Cite

Histamine is recognized as a neurotransmitter or neuromodulator in the brain, and it plays a major role in the pathogenic progression after cerebral ischemia. Extracellular histamine increases gradually after ischemia, and this may come from histaminergic neurons or mast cells. Histamine alleviates neuronal damage and infarct volume, and it promotes recovery of neurological function after ischemia; the H1, H2, and H3 receptors are all involved. Further studies suggest that histamine alleviates excitotoxicity, suppresses the release of glutamate and dopamine, and inhibits inflammation and glial scar formation. Histamine may also affect cerebral blood flow by targeting to vascular smooth muscle cells, and promote neurogenesis. Moreover, endogenous histamine is an essential mediator in the cerebral ischemic tolerance. Due to its multiple actions, affecting neurons, glia, vascular cells, and inflammatory cells, histamine is likely to be an important target in cerebral ischemia. But due to its low penetration of the blood-brain barrier and its wide actions in the periphery, histamine-related agents, like H3 antagonists and carnosine, show potential for cerebral ischemia therapy. However, important questions about the molecular aspects and pathophysiology of histamine and related agents in cerebral ischemia remain to be answered to form a solid scientific basis for therapeutic application.

show abstract

Experimental cerebral infarction in primates: Regional changes in brain histamine content

Cited by 21 publications

References 16 publications

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Mast Cell Stabilization Limits Hypoxic-Ischemic Brain Damage in the Immature Rat

Targeted Disruption of Organic Cation Transporter 3 (Oct3) Ameliorates Ischemic Brain Damage through Modulating Histamine and Regulatory T Cells

Role of Histamine and Its Receptors in Cerebral Ischemia

Contact Info

Product

Resources

About