Histamine responses of large neostriatal interneurons in histamine H1 and H2 receptor knock-out mice

Ogawa, Shuji; Yanai, Kazuhiko; Watanabe, Takeshi; Wang, Zhi Ming; Akaike, Hironari; Ito, Yushi; Akaike, Norio

doi:10.1016/j.brainresbull.2008.10.016

Cited by 21 publications

(9 citation statements)

References 25 publications

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“…However, it is postulated that leptin may exert at least part of its influence through a pathway linked to H1-receptor, reducing food intake [44]. In fact leptin-induced food intake appears suppressed in H1 knockout mice [45, 46]. This data suggests that hypothalamic histamine is a modulator of leptin activity.…”

Section: Introductionmentioning

confidence: 99%

The Role of Leptin in Antipsychotic-Induced Weight Gain: Genetic and Non-Genetic Factors

et al. 2012

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Schizophrenia is a chronic and disabling mental illness affecting millions of people worldwide. A greater proportion of people with schizophrenia tends to be overweight. Antipsychotic medications have been considered the primary risk factor for obesity in schizophrenia, although the mechanisms by which they increase weight and produce metabolic disturbances are unclear. Several lines of research indicate that leptin could be a good candidate involved in pathways linking antipsychotic treatment and weight gain. Leptin is a circulating hormone released by adipocytes in response to increased fat deposition to regulate body weight, acting through receptors in the hypothalamus. In this work, we reviewed preclinical, clinical, and genetic data in order to infer the potential role played by leptin in antipsychotic-induced weight gain considering two main hypotheses: (1) leptin is an epiphenomenon of weight gain; (2) leptin is a consequence of antipsychotic-induced “leptin-resistance status,” causing weight gain.

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Section: Introductionmentioning

confidence: 99%

The Role of Leptin in Antipsychotic-Induced Weight Gain: Genetic and Non-Genetic Factors

et al. 2012

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“…To verify this hypothesis, pharmacological experiments using receptor-gene knockout mice should be conducted. Previous studies have shown that histaminergic neurons have inhibitory effects on behavioral sensitization and rewarding using histamine H 1 /H 2 receptor-gene doubleknockout mice (10,11), histidine decarboxylase-gene knockout mice (12), and brain-lesion methods in rats (13). However, further studies are needed to clearly determine whether the histaminergic neuron system has inhibitory effects on behavioral sensitization and rewarding.…”

Section: Introductionmentioning

confidence: 99%

Methamphetamine- and 3,4-Methylenedioxymethamphetamine–Induced Behavioral Changes in Histamine H3–Receptor Knockout Mice

et al. 2009

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Abstract. Histamine H 3 receptors inhibit the release of not only histamine itself, but also other neurotransmitters including dopamine. Previous papers have reported that histaminergic neurons inhibit psychostimulant-induced behavioral changes. To examine whether deficiency in histamine H 3 receptors influences psychostimulant-induced behavioral sensitization and reward, we examined locomotor activity, conditioned place preference (CPP), and c-Fos expression in histamine H 3 receptor-gene knockout mice (H3KO) and their wild-type (WT) counterparts before and after treatment with methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA). The increase in locomotion induced by treatment with METH or MDMA was lower in histamine H3KO mice than in WT mice, while the locomotor sensitization was developed by METH or MDMA in both strains. However, no significant difference in METH-and MDMA-induced preference scores of CPP between histamine H3KO mice and WT mice was observed. Following treatment with METH, the number of c-Fos-positive neurons in the the caudate-putamen of histamine H3KO mice was lower than that in the caudate-putamen of WT mice. In contrast, there was no significant difference in the number of the psychostimulant-induced c-Fos-positive cells in the nucleus accumbens between the two strains of mice. These findings suggest that deficiency in histamine H 3 receptors may have inhibitory effects on psychostimulant-induced increase in locomotion, but insignificant effects on the reward.

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“…Indeed, Hdc −/− mice showed stronger methamphetamine-induced stimulation of locomotor activity than wild-type controls (Kubota et al, 2002;Iwabuchi et al, 2004;Acevedo and Raber, 2011). This may be due to a lack of H 1 R-and H 2 R stimulation, because increased sensitivity to methamphetamine was also reported for H 1 R/H 2 R double knockouts (Iwabuchi et al, 2004;Ogawa et al, 2009). Moreover, metamphetamine-induced conditioned place preference (CPP) was stronger in Hrh1 −/− mice than in wild-type controls .…”

Section: Dopaminergic Reward System and Other Neurotransmitter Systemsmentioning

confidence: 86%

Modulation of behavior by the histaminergic system: Lessons from HDC-, H3R- and H4R-deficient mice

Schneider

Neumann

Seifert

2014

Neuroscience & Biobehavioral Reviews

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Histamine responses of large neostriatal interneurons in histamine H1 and H2 receptor knock-out mice

Cited by 21 publications

References 25 publications

The Role of Leptin in Antipsychotic-Induced Weight Gain: Genetic and Non-Genetic Factors

The Role of Leptin in Antipsychotic-Induced Weight Gain: Genetic and Non-Genetic Factors

Methamphetamine- and 3,4-Methylenedioxymethamphetamine–Induced Behavioral Changes in Histamine H3–Receptor Knockout Mice

Modulation of behavior by the histaminergic system: Lessons from HDC-, H3R- and H4R-deficient mice

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