Influence of Intracerebroventricular Administration of Histaminergic Drugs on Morphine State-Dependent Memory in the Step-Down Passive Avoidance Test

Zarrindast, Mohammad Reza; Khalilzadeh, Azita; Rezayat, Seyed Mehdi; Sahebgharani, Mousa; Djahanguiri, B

doi:10.1159/000085590

Cited by 16 publications

(5 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MRS5980, (1S,2R,3S,4R,5S)-4-(2-((5-chlorothiophen-2-yl) ethynyl)-6-(methylamino)-9H-purin-9-yl)-2,3-dihydroxy-N-methylbicyclo [3.1.0]hexane-1-carboxamide (Tosh et al, 2014), was dissolved in dimethyl sulfoxide and adjusted to 30% dimethyl sulfoxide/0.5% methylcellulose/water. Other compounds (vehicles) with references for dose choice are: histamine type 1 receptor (H 1 R) antagonist pyrilamine (saline) (Zarrindast et al, 2005;Kitanaka et al, 2007), H 2 R antagonist zolantidine (saline) (Kitanaka et al, 2007), and H 4 R antagonist JNJ7777120 (10% ethanol in saline) (Cowden et al, 2013). Mice were treated with escalating doses of compound 48/80 in saline on 5 consecutive days as described (Ge et al, 2006).…”

Section: Methodsmentioning

confidence: 99%

Peripheral Adenosine A3 Receptor Activation Causes Regulated Hypothermia in Mice That Is Dependent on Central Histamine H1 Receptors

Carlin

Tosh

Xiao

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

Adenosine can induce hypothermia, as previously demonstrated for adenosine A 1 receptor (A 1 AR) agonists. Here we use the potent, specific A 3 AR agonists MRS5698, MRS5841, and MRS5980 to show that adenosine also induces hypothermia via the A 3 AR. The hypothermic effect of A 3 AR agonists is independent of A 1 AR activation, as the effect was fully intact in mice lacking A 1 AR but abolished in mice lacking A 3 AR. A 3 AR agonist-induced hypothermia was attenuated by mast cell granule depletion, demonstrating that the A 3 AR hypothermia is mediated, at least in part, via mast cells. Central agonist dosing had no clear hypothermic effect, whereas peripheral dosing of a non-brainpenetrant agonist caused hypothermia, suggesting that peripheral A 3 AR-expressing cells drive the hypothermia. Mast cells release histamine, and blocking central histamine H 1 (but not H 2 or H 4 ) receptors prevented the hypothermia. The hypothermia was preceded by hypometabolism and mice with hypothermia preferred a cooler environmental temperature, demonstrating that the hypothermic state is a coordinated physiologic response with a reduced body temperature set point. Importantly, hypothermia is not required for the analgesic effects of A 3 AR agonists, which occur with lower agonist doses. These results support a mechanistic model for hypothermia in which A 3 AR agonists act on peripheral mast cells, causing histamine release, which stimulates central histamine H 1 receptors to induce hypothermia. This mechanism suggests that A 3 AR agonists will probably not be useful for clinical induction of hypothermia.

show abstract

Section: Methodsmentioning

confidence: 99%

Peripheral Adenosine A3 Receptor Activation Causes Regulated Hypothermia in Mice That Is Dependent on Central Histamine H1 Receptors

Carlin

Tosh

Xiao

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

View full text Add to dashboard Cite

show abstract

“…Zarrindast et al recently reported that histamine interacts with opioidergic systems in learning and memory [15] . Histamine reverses the impairment of rat memory recall induced by pretraining administration of morphine, as evaluated by the passive avoidance response [16,17] .…”

Section: Introductionmentioning

confidence: 99%

Ameliorating effect of histamine on impairment of cued fear extinction induced by morphine withdrawal in histidine decarboxylase gene knockout mice

et al. 2010

View full text Add to dashboard Cite

Aim: Histamine plays an important role in morphine addiction and memory-dependent behavior. However, little is known about the effect of histamine on the impairment of memory after morphine withdrawal. This study was designed to investigate the effect of histamine on memory impairment induced by morphine withdrawal in histidine decarboxylase knockout (HDC-KO) and wild-type (WT) mice. Methods: WT and HDC-KO mice were given subcutaneous morphine or saline twice daily for 5 consecutive days. The mice received a cued or contextual fear conditioning session 7 days after the last injection. During subsequent days, mice received 4 cued or contextual extinction sessions (one session per day). Western blot was used to assess extracellular signal-regulated kinase (ERK) phosphorylation in the amygdala and hippocampus. Results: Morphine withdrawal did not affect the acquisition of cued or contextual fear responses. It impaired cued but not contextual fear extinction. The acquisition of cued and contextual fear responses was accelerated in HDC-KO mice. Histamine deficiency aggravated the impairment of cued fear extinction induced by morphine withdrawal, whereas histamine (icv, 5 µg/mouse) reversed this effect. Morphine withdrawal decreased ERK phosphorylation in the amygdala after cued fear extinction, especially in HDC-KO mice. Conclusion: These results suggest that morphine withdrawal specifically impairs cued fear extinction and histamine ameliorates this impairment. Its action might be mediated by the modulation of ERK phosphorylation in the amygdala. Histamine should be explored for possible roles in the prevention or treatment of morphine abuse and relapse.

show abstract

“…Moreover, activation of the opioid receptors present on the mast cells has been shown to cause the release of histamine and has thus been shown to mediate a number of pharmacological effects of opioid agonists [29,30]. Moreover, phospholipase C and calcium‐linked transduction systems have been shown to be associated with opioid receptor activation [31–37].…”

Section: Discussionmentioning

confidence: 99%

Amisulpride‐Induced Seizurogenic Effect: A Potential Role of Opioid Receptor‐Linked Transduction Systems

Rehni

Singh

Chand

2010

Basic Clin Pharma Tox

View full text Add to dashboard Cite

This study was designed to investigate the role of opioid receptors, gamma-aminobutyric acid (GABA) receptors, mast cells and histamine receptors (H 1 subtype) in the seizurogenic effect of amisulpride on mice. A single injection of amisulpride (180 mg ⁄ kg) was employed to evaluate the seizurogenicity of the drug in mice. Seizures were assessed in terms of a composite seizure severity score (SSS), time of the onset of straub-like tail, onset of jerky movements of whole body, convulsions and death. Amisulpride administration (180 mg ⁄ kg) induced a significant pro-convulsant effect in mice as measured in terms of the SSS (21.12 € 2.71) and a significant decrease in the time latency of the onset of straub-like tail (132.45 € 12.31), jerky movements of whole body (153.28 € 14.12), convulsions (184.97 € 13.11) and death (100%). Moreover, prior administration of naloxone, cetrizine, sodium cromoglycate and gabapentin, respectively, attenuated this seizurogenic activity that amisulpride exerted on mice (p < 0.05). Therefore, it may be suggested that amisulpride exerts a seizurogenic effect on mice possibly via an opioid receptor activation-dependent release of histamine from the mast cells and a simultaneous inhibition of GABA release.

show abstract

Influence of Intracerebroventricular Administration of Histaminergic Drugs on Morphine State-Dependent Memory in the Step-Down Passive Avoidance Test

Cited by 16 publications

References 64 publications

Peripheral Adenosine A3 Receptor Activation Causes Regulated Hypothermia in Mice That Is Dependent on Central Histamine H1 Receptors

Peripheral Adenosine A3 Receptor Activation Causes Regulated Hypothermia in Mice That Is Dependent on Central Histamine H1 Receptors

Ameliorating effect of histamine on impairment of cued fear extinction induced by morphine withdrawal in histidine decarboxylase gene knockout mice

Amisulpride‐Induced Seizurogenic Effect: A Potential Role of Opioid Receptor‐Linked Transduction Systems

Contact Info

Product

Resources

About