Histamine H3 receptor agonist- and antagonist-evoked vacuous chewing movements in 6-OHDA-lesioned rats occurs in an absence of change in microdialysate dopamine levels

Nowak, Przemysław; Dąbrowska, Jolanta; Bortel, Aleksandra; Biedka, I.; Szczerbak, G.; Słomian, Grzegorz; Kostrzewa, Richard M.; Brus, Ryszard

doi:10.1016/j.ejphar.2006.08.092

Cited by 10 publications

(5 citation statements)

References 52 publications

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“…The studies were conducted in: (i) normal rats treated with NaCl (vehicle) or RAMH (10 mg/kg body weight/day) 23,24 for 1 week; and (ii) BDL rats that, immediately after BDL, 27 were treated for 1 week with daily I.P. injections of NaCl, RAMH (10 mg/kg body weight/day), 28 thioperamide maleate (5 mg/kg body weight) 25,26 or histamine (0.5 mg/kg body weight) 15,29 in the absence or presence of thioperamide maleate for 1 week. The doses of RAMH, thioperamide maleate and histamine used in the present studies were similar to those used in other studies in rodents.…”

Section: Animal Modelmentioning

confidence: 99%

“…The doses of RAMH, thioperamide maleate and histamine used in the present studies were similar to those used in other studies in rodents. 15,25,26,28,29 Liver blocks, serum and cholangiocytes were obtained at the end of the selected treatments. We evaluated body and liver weight from the selected groups of animals.…”

Section: Animal Modelmentioning

confidence: 99%

“…22 The rationale for studying the role of H3R in the regulation of cholangiocyte growth in BDL rats is first based on the fact that H3R exerts their effects by coupling to Ga i/o proteins with inhibition of adenylyl cyclase, 21,22 a key factor in the regulation of cholangiocyte growth. [1][2][3]5 The aims of our study were to: (i) evaluate the presence of H3R protein in bile ducts from normal and BDL rat liver sections; (ii) study the expression of H3R mRNA in purified cholangiocytes from normal and BDL rats; (iii) determine the in vivo effect of (a) the H3R agonist, (R)-(a)-(À)-methylhistamine dihydrobromide (RAMH), 23,24 (b) the H3 HR antagonist, thioperamide maleate 25,26 and (c) histamine, in the absence or presence of thioperamide maleate, on cholangiocyte proliferation in BDL rats; and (iv) to elucidate, in purified BDL cholangiocytes, the transduction mechanisms by which RAMH regulates the proliferation of these cells.…”

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confidence: 99%

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H3 histamine receptor agonist inhibits biliary growth of BDL rats by downregulation of the cAMP-dependent PKA/ERK1/2/ELK-1 pathway

Francis

Franchitto

Ueno

et al. 2007

Laboratory Investigation

152

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Histamine regulates many functions by binding to four histamine G-coupled receptor proteins (H1R, H2R, H3R and H4R). As H3R exerts their effects by coupling to Ga i/o proteins reducing adenosine 3 0 , 5 0 -monophosphate (cAMP) levels (a key player in the modulation of cholangiocyte hyperplasia/damage), we evaluated the role of H3R in the regulation of biliary growth. We posed the following questions: (1) Do cholangiocytes express H3R? (2) Does in vivo administration of (R)-(a)-(À)-methylhistamine dihydrobromide (RAMH) (H3R agonist), thioperamide maleate (H3R antagonist) or histamine, in the absence/presence of thioperamide maleate, to bile duct ligated (BDL) rats regulate cholangiocyte proliferation? and (3) Does RAMH inhibit cholangiocyte proliferation by downregulation of cAMP-dependent phosphorylation of protein kinase A (PKA)/extracellular signal-regulated kinase 1/2 (ERK1/2)/ets-like gene-1 (Elk-1)? The expression of H3R was evaluated in liver sections by immunohistochemistry and immunofluorescence, and by real-time PCR in cholangiocyte RNA from normal and BDL rats. BDL rats (immediately after BDL) were treated daily with RAMH, thioperamide maleate or histamine in the absence/presence of thioperamide maleate for 1 week. Following in vivo treatment of BDL rats with RAMH for 1 week, and in vitro stimulation of BDL cholangiocytes with RAMH, we evaluated cholangiocyte proliferation, cAMP levels and PKA, ERK1/2 and Elk-1 phosphorylation. Cholangiocytes from normal and BDL rats express H3R. The expression of H3R mRNA increased in BDL compared to normal cholangiocytes. Histamine decreased cholangiocyte growth of BDL rats to a lower extent than that observed in BDL RAMH-treated rats; histamine-induced inhibition of cholangiocyte growth was partly blocked by thioperamide maleate. In BDL rats treated with thioperamide maleate, cholangiocyte hyperplasia was slightly higher than that of BDL rats. In vitro, RAMH inhibited the proliferation of BDL cholangiocytes. RAMH inhibition of cholangiocyte growth was associated with decreased cAMP levels and PKA/ERK1/2/Elk-1 phosphorylation. Downregulation of cAMP-dependent PKA/ERK1/2/Elk-1 phosphorylation (by activation of H3R) is important in the inhibition of cholangiocyte growth in liver diseases.

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Section: Animal Modelmentioning

confidence: 99%

Section: Animal Modelmentioning

confidence: 99%

mentioning

confidence: 99%

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H3 histamine receptor agonist inhibits biliary growth of BDL rats by downregulation of the cAMP-dependent PKA/ERK1/2/ELK-1 pathway

Francis

Franchitto

Ueno

et al. 2007

Laboratory Investigation

152

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“…The H 3 receptor predominately modulates histamine exocytosis. Thioperamide, an antagonist of H 3 receptors, enhances histamine release (Arrang et al, 1983(Arrang et al, , 1987Schwartz et al, 1991), and modulates the central dopaminergic system (Molina-Hernández et al, 2000;Nowak et al, 2006Nowak et al, , 2008Nowak et al, , 2009a. H 3 receptors represent an alternative target in treatment of the motor dysfunction of Parkinson's disease.…”

Section: Brain Regionmentioning

confidence: 98%

Thioperamide, an H3 Receptor Antagonist Prevents [3H]Glucose Uptake in Brain of Adult Rats Lesioned as Neonates with 5,7-Dihydroxytryptamine

et al. 2010

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As a first attempt at exploring an association between histaminergic and serotoninergic neuronal phenotypes in glucose regulation, the influence of the histamine H₃ receptor antagonist thioperamide on glucose uptake by brain was determined in rats in which the serotoninergic innervations of brain was largely destroyed perinatally. Male Wistar rats were initially treated on the 3rd day after birth with the serotoninergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) (75 μg icv) or saline vehicle (10 μl icv). At 8 weeks lesioned and control rats were terminated in order to validate the effectiveness of 5,7-DHT: reduction in 5-HT and 5-HIAA by 83-91% and 69-83% in striatum, frontal cortex, and hippocampus (HPLC/ED method). Other groups of rats were pretreated with thioperamide (5.0 mg/kg ip) or saline vehicle 60 min prior to 6-[³H]-D-glucose (500 μCi/kg ip). Fifteen-min later rats were decapitated and brains were excised and dissected to remove frontal cortex, striatum, hippocampus, thalamus/hypothalamus, pons, and cerebellum. Liquid scintillation spectroscopy was used to determine that [³H]glucose uptake, which was enhanced in 5,7-DHT lesioned rats in cortex (by 88%), hippocampus, thalamus/hypothalamus, pons and cerebellum (each by 47-56%), and in striatum (by 35%). In contrast, thioperamide prevented the enhancement in [³H]glucose uptake in all brain regions of 5,7-DHT neonatally lesioned rats; and [³H]glucose levels were significantly different in all brain regions (except thalamus/hypothalamus) in thioperamide-versus saline-treated rats. These findings indicate a functional association between histaminergic and serotoninergic systems in brain in relation to glucose regulation.

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“…Our previous studies and one by Selley have reported that high doses of simvastatin pronouncedly increased dopamine D1/D2 and NMDA receptors in the prefrontal cortex while also altering dopamine content in various brain regions (Selley 2005;Wang et al 2005a;Wang et al 2009). Considering dopamine receptors and histaminergic receptors are all GPCR and the interactions between the histaminergic and dopaminergic systems are well documented (Anichtchik et al 2001;Anichtchik et al 2000;Nowak et al 2006), we considered it reasonable to propose that chronic treatment with simvastatin may affect the expression of H1 receptors in the rat brain.…”

Section: Introductionmentioning

confidence: 99%

Effects of simvastatin and 6-hydroxydopamine on histaminergic H1 receptor binding density in rat brains

Deng

Mackovski

et al. 2010

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Statins have been widely used for the treatment of a variety of medical conditions including psychoneurological disorders beyond their original use in lowering cholesterol. Histamine receptors play an important role in the regulation of neural activity, however, it is unknown whether statins act on histamine receptors, particularly for their neural regulatory effects. This study examined the effects of simvastatin and 6-hydroxydopamine (6-OHDA) lesions on histamine H1 receptors using [3H] pyrilamine binding autoradiography. Compared to the saline group, simvastatin (1 mg/kg/day) significantly decreased H1 receptor bindings in the primary motor cortex (M1), ventromedial hypothalamic nucleus (VMH), caudate putamen (CPu), accumbens core (AcbC) and prefrontal cortex (PfC) (all pb0.05); however 10 mg/kg/day simvastatin increased H1 receptor density only in the medial amygdaloid nucleus (Mep) (pb0.05), but had no significant effect in other regions examined. The 6-OHDA lesion did not alter H1 receptor binding density in most brain areas, except a trend decrease in the hippocampus (p=0.07) and a trend increase in the cingulate cortex (p=0.06). These results suggested that simvastatin has different effects on the H1 receptors in different rat brain regions depending on the doses. Therefore, simvastatin can modulate histaminergic neurotransmission in the brain, and support the role of H1 receptors in psychoneurological disorders.

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Histamine H3 receptor agonist- and antagonist-evoked vacuous chewing movements in 6-OHDA-lesioned rats occurs in an absence of change in microdialysate dopamine levels

Cited by 10 publications

References 52 publications

H3 histamine receptor agonist inhibits biliary growth of BDL rats by downregulation of the cAMP-dependent PKA/ERK1/2/ELK-1 pathway

H3 histamine receptor agonist inhibits biliary growth of BDL rats by downregulation of the cAMP-dependent PKA/ERK1/2/ELK-1 pathway

Thioperamide, an H3 Receptor Antagonist Prevents [3H]Glucose Uptake in Brain of Adult Rats Lesioned as Neonates with 5,7-Dihydroxytryptamine

Effects of simvastatin and 6-hydroxydopamine on histaminergic H1 receptor binding density in rat brains

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