Effect of Methamphetamine and Imipramine on Cerebral Ischemia-Induced Hyperactivity in Mongolian Gerbils

Araki, Hiroaki; Yamamoto, Takahiko; Kobayashi, Yuri; Futagami, Koujiro; Kawasaki, Hiromu; Gomita, Yutaka

doi:10.1254/jjp.88.293

Cited by 9 publications

(7 citation statements)

References 38 publications

(29 reference statements)

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“…This finding is supported by a paper that showed that a longer duration of transient ischemia led to severer hippocampal damage and locomotor hyperactivity [25]. In addition, many researchers reported that the locomotor activity after transient cerebral ischemia was affected 1 day after I-R [26][27][28][29].…”

Section: Discussionmentioning

confidence: 65%

Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

et al. 2012

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Ischemic damage occurs well in vulnerable regions of the brain, including the hippocampus and striatum. In the present study, we examined neuronal damage/death and glial changes in the striatum 4 days after 5, 10, 15 and 20 min of transient cerebral ischemia using the gerbil. Spontaneous motor activity was increased with the duration time of ischemia-reperfusion (I-R). To examine neuronal damage, we used Fluoro-Jade B (F-J B, a marker for neuronal degeneration) histofluorescence staining. F-J B positive cells were detected only in the 20 min ischemia-group, not in the other groups. In addition, we examined gliosis of astrocytes and microglia using anti-glial fibrillary acidic protein (GFAP) and anti- ionized calcium-binding adapter molecule 1 (Iba-1), respectively. In the 5 min ischemia-group, GFAP-immunoreactive astrocytes were distinctively increased in number, and the immunoreactivity was stronger than that in the sham-group. In the 10, 15 and 20 min ischemia-groups, GFAP-immunoreactivity was more increased with the duration of I-R. On the other hand, the immunoreactivity and the number of Iba-1-immunoreactive microglia were distinctively increased in the 5 and 10 min ischemia-groups. In the 15 min ischemia-group, cell bodies of microglia were largest, and the immunoreactivity was highest; however, in the 20 min ischemia-group, the immunoreactivity was low compared to the 15 min ischemia-group. The results of western blotting for GFAP and Iba-1 were similar to the immunohistochemical data. In brief, these findings showed that neuronal death could be detected only in the 20 min ischemia-group 4 days after I-R, and the change pattern of astrocytes and microglia were apparently different according to the duration time of I-R.

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Section: Discussionmentioning

confidence: 65%

Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

et al. 2012

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“…Growing evidence suggests that a deficit in cholinergic neurotransmission plays an important role in mediating cognitive deficits (Araki et al, 2002; Levin, 2002; Money et al, 2012). This evidence suggests that activation of the nicotinic receptors can be useful in treating some symptoms of schizophrenia particularly the cognitive deficits (Taly et al, 2009; Toyohara and Hashimoto, 2010).…”

Section: Discussionmentioning

confidence: 99%

Cotinine: Beyond that Expected, More than a Biomarker of Tobacco Consumption

Moran¹

2012

Front. Pharmacol.

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A greater incidence of tobacco consumption occurs among individuals with psychiatric conditions including post-traumatic stress disorder (PTSD), bipolar disorder, major depression, and schizophrenia, compared with the general population. Even when still controversial, it has been postulated that smoking is a form of self-medication that reduces psychiatric symptoms among individuals with these disorders. To better understand the component(s) of tobacco-inducing smoking behavior, greater attention has been directed toward nicotine. However, in recent years, new evidence has shown that cotinine, the main metabolite of nicotine, exhibits beneficial effects over psychiatric symptoms and may therefore promote smoking within this population. Some of the behavioral effects of cotinine compared to nicotine are discussed here. Cotinine, which accumulates in the body as a result of tobacco exposure, crosses the blood-brain barrier and has different pharmacological properties compared with nicotine. Cotinine has a longer plasma half-life than nicotine and showed no addictive or cardiovascular effects in humans. In addition, at the preclinical level, cotinine facilitated the extinction of fear memory and anxiety after fear conditioning, improved working memory in a mouse model of Alzheimer’s disease (AD) and in a monkey model of schizophrenia. Altogether, the new evidence suggests that the pharmacological and behavioral effects of cotinine may play a key role in promoting tobacco smoking in individuals that suffer from psychiatric conditions and represents a new potential therapeutic agent against psychiatric conditions such as AD and PTSD.

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“…Rodent models touching on poststroke hyperlocomotion have been mainly of a transient global cerebral ischemia model 6–10 . Neuronal loss confined to the bilateral hippocampus has been claimed to be related to the hyperlocomotion, 6,7 , 9 especially by the acutely injured but still active neurons within the hippocampus 10 .…”

Section: Introductionmentioning

confidence: 99%

Heterogeneous hyperactivity and distribution of ischemic lesions after focal cerebral ischemia in Mongolian gerbils

Katsumata¹,

Kuroiwa

Ishibashi³

et al. 2006

Neuropathology

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Various types of poststroke hyperactivity exist in humans, but studies of each mechanism using animal models are scarce. We aimed to analyze the heterogeneity of postischemic hyperlocomotion and to identify the ischemic lesions responsible for postischemic hyperlocomotion in rodent models of focal ischemia. Mongolian gerbils underwent right common carotid artery occlusion (CCAO) for 10 or 20 min. At 24 h, 2 days, and 7 days postischemia, we performed quantitative and qualitative locomotor analysis and correlated these results with the extent of ischemic lesions. Intermittent explosive hyperlocomotion was induced transiently in a 10-min CCAO group at 24 h after ischemia and continual unexplosive hyperlocomotion persisted for 7 days in the 20-min CCAO animals. Selective neuronal death, confined to the hippocampal cornu ammonis 1 (CA1), was observed in the 10-min CCAO group and widespread cortical and basal ganglia infarction was observed in the 20-min CCAO group. Amyloid precursor protein was transiently observed in the hippocampus at 24 h postischemia in the 10-min CCAO animals, while it was widely distributed over the ischemic regions throughout the 7 days postischemia in the 20-min CCAO animals. Incidence maps and correlation analysis revealed hippocampal neuronal death of the CA1 sector and widespread hemispheric infarction, including the cortex, as the region responsible for the 10-min and 20-min CCAO-induced hyperactivity, respectively. Two distinct types of locomotor hyperactivity were observed that varied with regard to the distribution of the ischemic lesion, that is, hippocampal neuronal death and widespread infarction involving the cortex. These two types of locomotor hyperactivity appear to be models of the different types of poststroke hyperactivity seen in stroke patients.

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Effect of Methamphetamine and Imipramine on Cerebral Ischemia-Induced Hyperactivity in Mongolian Gerbils

Cited by 9 publications

References 38 publications

Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

Neuronal Damage Using Fluoro-Jade B Histofluorescence and Gliosis in the Striatum After Various Durations of Transient Cerebral Ischemia in Gerbils

Cotinine: Beyond that Expected, More than a Biomarker of Tobacco Consumption

Heterogeneous hyperactivity and distribution of ischemic lesions after focal cerebral ischemia in Mongolian gerbils

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