Aggravation of ischemic neuronal damage in the rat hippocampus by impairment of histaminergic neurotransmission

Adachi, Naoto; Oishi, Ryozo; Itano, Yoshitaro; Yamada, Teruo; Hirakawa, Masahisa; Saeki, Kiyomi

doi:10.1016/0006-8993(93)90259-p

Cited by 33 publications

(26 citation statements)

References 23 publications

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“…␣-FMH treatment has increased ischemic neuronal damage, this effect being mediated through H 1 and H 3 receptors (Adachi et al, 1993). The H 3 receptor acts as an autoreceptor regulating histamine synthesis and release (Arrang et al, 1983;Takeshita et al, 1998;Torrent et al, 2005), and through its heteroreceptor it may inhibit release of other neurotransmitters (e.g., glutamate and GABA) (Brown and Haas, 1999;Korotkova et al, 2002).…”

Section: Mechanisms Of Histamine-mediated Neuroprotective Effectmentioning

confidence: 99%

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

Kukko‐Lukjanov

Soini²,

Taira³

et al. 2006

J. Neurosci.

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The central histaminergic neuron system inhibits epileptic seizures, which is suggested to occur mainly through histamine 1 (H 1 ) and histamine 3 (H 3 ) receptors. However, the importance of histaminergic neurons in seizure-induced cell damage is poorly known. In this study, we used an organotypic coculture system and confocal microscopy to examine whether histaminergic neurons, which were verified by immunohistochemistry, have any protective effect on kainic acid (

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Section: Mechanisms Of Histamine-mediated Neuroprotective Effectmentioning

confidence: 99%

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

Kukko‐Lukjanov

Soini²,

Taira³

et al. 2006

J. Neurosci.

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“…The H3 agonist α-methylhistamine significantly aggravates the delayed neuronal death following ischemia caused by 10 min of 4-vessel occlusion in rats. 25 We recently found that mice treated with the H3 antagonists thioperamide or clobenpropit, and H3 receptor knockout mice showed less impairment of neurological function and a reduced infarct area after MCAO (unpublished data). However, we were interested to find that the protection after H3 receptor blockade also occurs in HDC knockout mice, which suggests that blockade of H3 receptors has a protective mechanism other than up-regulating histamine.…”

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

confidence: 92%

“…Rats pretreated with α-FMH show significantly more necrotic hippocampal CA1 pyramidal cells than controls after cerebral ischemia caused by 10 min of 4-vessel occlusion. 25 Moreover, in gerbils, α-FMH also aggravates the death of hippocampal CA2 neurons after 3 min ischemia, while the histamine content of the brain is significantly reduced. 26 In addition, we found that the histamine from mast cells protects against neuronal death induced by oxygen-glucose deprivation, which is an in vitro model of ischemia.…”

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

confidence: 98%

“…However, in a previous study, the H1 receptor was found to participate in delayed neuronal death caused by cerebral ischemia. 25 Excitotoxicity is a predominant reason for neuronal death in the early phase after cerebral ischemia, due to the accumulation of extracellular glutamate and the activation of N-methyl-Daspartate (NMDA) receptors. Blockade of H1 receptors by terfenadine, chlorpheniramine, oxatomide, or triprolidine enhances the excitotoxic response of NMDA receptors, which is prevented by histamine.…”

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

confidence: 99%

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Role of Histamine and Its Receptors in Cerebral Ischemia

Chen

2012

ACS Chem. Neurosci.

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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.

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“…Under ischemic conditions, increased levels of HA have been reported in certain brain parts [15], but also in the extracellular fluid, the microvessels and the venous plasma [16]. Thus, this suggests a continuos glial/endothelial cooperation; the uptake of HA into astroglial cells (in the vicinity of synapses) and its release at the 'end-feet', is followed by an uptake into the endothelium at the abluminal site.…”

Section: Histamine Uptake Into Cerebral Endothelial Cellsmentioning

confidence: 94%

Histamine uptake into non-neuronal brain cells

Huszti¹

2003

Inflammation Research

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IntroductionThe main function of various transport systems is to maintain the cellular concentrations of the physiological substances. However, transport also contributes to various mechanisms in clearing and scavenging substances from the interstitial spaces. In the CNS, the termination of many neurotransmitters involves rapid removal from the synapse; mainly by uptake either into presynaptic terminal or into the surrounding glia through specialised transport systems.Histamine (HA) is a regulator of the vascular permeability through cerebrovascular endothelium as well as being a central neurotransmitter. However, no neuronal uptake of HA has been detected in vertebrates [1]. In invertebrates, HA is taken up into the photoreceptor terminals and surrounding glia and replenishes HA stores by an activitydependent fashion [2]. In mammalian neurones, a polyspecific cation transporter (hOCT 2 ) can transport HA along with monoamines [3] but as it shows a low affinity for HA (K M in mM range), it is not assumed to play a considerable role in HA inactivation.Besides inactivation, the possibility of a clearance mechanism in which glial and cerebral endothelial HA uptake are co-operatively involved, has also been considered. We have focused our research on HA uptake by CNS-resident nonneuronal cells (including mast cells) bearing physiological significance. Histamine uptake by astroglial cellsAstrocytes perform a variety of CNS functions, including uptake of a number of neurotransmitters. In 1985, we showed that HA is taken up and slowly metabolised by chick astroglial cells [4]. In chick astroglial cells (grown as monolayer culture), uptake was found to be saturable, with high affinity for HA and relatively low capacity (K M = 0.24 mM; V max = 0.31 pmol/mg protein/min), showing energy-requirements and strong sensitivity to extracellular Na + concentration. The uptake vs [Na + ] curve was saturable, fitted the Michaelis-Menten equation and resulted in a K M of 172 mM for Na + . HA taken up into these cells was slowly metabolised and/or released ('reversed uptake'), dependent on the shift of the Na + /K + gradient [5].Bidirectonal uptake could also be detected in astroglial cultures from postnatal (P 0 -P 6 ) rat brains with similar affinity for HA (K M = 0.19 mM) but with 10 times higher capacity (V max = 3.12 pmol/mg protein/min) [6]. It was noteworthy that partial dissipations of the inward oriented Na + (in < out) and the outward oriented K + (in > out) gradient could reverse the inward-directed HA uptake resulting in a carrier-mediated release of HA. The release of HA was increased by high [K + ] and K + channel blockers which might depolarise the cells, suggesting an electrogenic transporter for the uptake. The HA analogues, 2-meHA and 4-me-HA showed significant inhibition while well-known uptake inhibitors (imipramine and cocaine) did not show much effect on the uptake [6]. Impromidine and the impromidine derivative, VUF 8407 [9] showed potent inhibitory effects on HA uptake and antagonistic actions on the H 3 auto-r...

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Aggravation of ischemic neuronal damage in the rat hippocampus by impairment of histaminergic neurotransmission

Cited by 33 publications

References 23 publications

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

Histaminergic Neurons Protect the Developing Hippocampus from Kainic Acid-Induced Neuronal Damage in an Organotypic Coculture System

Role of Histamine and Its Receptors in Cerebral Ischemia

Histamine uptake into non-neuronal brain cells

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