Nicotinic receptor stimulation protects nigral dopaminergic neurons in rotenone‐induced Parkinson's disease models

Takeuchi, Hiroki; Yanagida, Takashi; Inden, Masatoshi; Takata, Kazuyuki; Kitamura, Yoshihisa; Yamakawa, Kentaro; Sawada, Hideyuki; Izumi, Yasukatsu; Yamamoto, Norio; Kihara, Takeshi; Uemura, Kazunori; Inoue, Haruhisa; Taniguchi, Takashi; Akaike, Akinori; Takahashi, Ryōsuke; Shimohama, Shun

doi:10.1002/jnr.21869

Cited by 100 publications

(73 citation statements)

References 55 publications

(62 reference statements)

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“…Previous studies have suggested that a4b2 and a6b2 subtypes of nicotinic acetylcholine receptors (nAChRs) contribute to the neuroprotective effects of the stimulant, although other nicotinic subunits also likely contribute (Ryan et al, 2001;Khwaja et al, 2007;Takeuchi et al, 2009;Quik et al, 2011). For example, a4b2 antagonist administration inhibits the protection afforded by nicotine in rotenonetreated mice (Takeuchi et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Vieira-Brock

McFadden

Nielsen

et al. 2015

J Pharmacol Exp Ther

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Repeated methamphetamine (METH) administrations cause persistent dopaminergic deficits resembling aspects of Parkinson's disease. Many METH abusers smoke cigarettes and thus selfadminister nicotine; yet few studies have investigated the effects of nicotine on METH-induced dopaminergic deficits. This interaction is of interest because preclinical studies demonstrate that nicotine can be neuroprotective, perhaps owing to effects involving a4b2 and a6b2 nicotinic acetylcholine receptors (nAChRs). This study revealed that oral nicotine exposure beginning in adolescence [postnatal day (PND) 40] through adulthood [PND 96] attenuated METH-induced striatal dopaminergic deficits when METH was administered at PND 89. This protection did not appear to be due to nicotine-induced alterations in METH pharmacokinetics. Short-term (i.e., 21-day) high-dose nicotine exposure also protected when administered from PND 40 to PND 61 (with METH at PND 54), but this protective effect did not persist. Short-term (i.e., 21-day) high-dose nicotine exposure did not protect when administered postadolescence (i.e., beginning at PND 61, with METH at PND 75). However, protection was engendered if the duration of nicotine exposure was extended to 39 days (with METH at PND 93). Autoradiographic analysis revealed that nicotine increased striatal a4b2 expression, as assessed using [125 I]epibatidine. Both METH and nicotine decreased striatal a6b2 expression, as assessed using [125 I]aconotoxin MII. These findings indicate that nicotine protects against METH-induced striatal dopaminergic deficits, perhaps by affecting a4b2 and/or a6b2 expression, and that both age of onset and duration of nicotine exposure affect this protection.

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Section: Introductionmentioning

confidence: 99%

“…For example, a4b2 antagonist administration inhibits the protection afforded by nicotine in rotenonetreated mice (Takeuchi et al, 2009). Furthermore, the protective effect of chronic nicotine against 6-hydroxy-DA was lost in a4-knockout mice (Ryan et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Vieira-Brock

McFadden

Nielsen

et al. 2015

J Pharmacol Exp Ther

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“…Attempts to lesion other animal species such as mice or monkeys have not been successful at all [72,92]. However, recent studies by two groups have demonstrated that oral administration of rotenone to mice causes nigral degeneration, a decrease of striatal dopamine levels, and motor dysfunction [85,93,94]. They also demonstrated α-synuclein aggregation in different areas of the brain [95].…”

Section: Rotenonementioning

confidence: 99%

The Effect of Treadmill Exercise on Expression of α-synuclein and miRNA in MPTP Induced-mouse Models of Parkinson’s Disease

Moon¹,

Choi²,

Oh³

et al. 2017

Exerc Sci

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Neurological disorders can be modeled in animals so as to recreate specific pathogenic events and behavioral outcomes. Parkinson's Disease (PD) is the second most common neurodegenerative disease of an aging population, and although there have been several significant findings about the PD disease process, much of this process still remains a mystery. Breakthroughs in the last two decades using animal models have offered insights into the understanding of the PD disease process, its etiology, pathology, and molecular mechanisms. Furthermore, while cellular models have helped to identify specific events, animal models, both toxic and genetic, have replicated almost all of the hallmarks of PD and are useful for testing new neuroprotective or neurorestorative strategies. Moreover, significant advances in the modeling of additional PD features have come to light in both classic and newer models. In this review, we try to provide an updated summary of the main characteristics of these models as well as the strengths and weaknesses of what we believe to be the most popular PD animal models. These models include those produced by 6-hydroxydopamine (6-OHDA), 1-methyl-1,2,3,6-tetrahydropiridine (MPTP), rotenone, and paraquat, as well as several genetic models like those related to alpha-synuclein, PINK1, Parkin and LRRK2 alterations.

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“…Found to activate the AMPK/SIRT1/autophagy pathway in cellular models of PD [172], reseveratrol and idebenone have been shown to increase longevity and delay agerelated deterioration of motor functions in HtrA2 knockout PD mice [180].…”

Section: Resveratrol and Idebenonementioning

confidence: 99%

Animal Models of Parkinson's Disease: A Gateway to Therapeutics?

Sayana

Jankovic

2014

Neurotherapeutics

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Parkinson's disease (PD) is a progressive, neurodegenerative disorder of unknown etiology, although a complex interaction between environmental and genetic factors has been implicated as a pathogenic mechanism of selected neuronal loss. A better understanding of the etiology, pathogenesis, and molecular mechanisms underlying the disease process may be gained from research on animal models. While cell and tissue models are helpful in unraveling involved molecular pathways, animal models are much better suited to study the pathogenesis and potential treatment strategies. The animal models most relevant to PD include those generated by neurotoxic chemicals that selectively disrupt the catecholaminergic system such as 6-hydroxydopamine; 1-methyl-1,2,3,6-tetrahydropiridine; agricultural pesticide toxins, such as rotenone and paraquat; the ubiquitin proteasome system inhibitors; inflammatory modulators; and several genetically manipulated models, such as α-synuclein, DJ-1, PINK1, Parkin, and leucine-rich repeat kinase 2 transgenic or knock-out animals. Genetic and nongenetic animal models have their own unique advantages and limitations, which must be considered when they are employed in the study of pathogenesis or treatment approaches. This review provides a summary and a critical review of our current knowledge about various in vivo models of PD used to test novel therapeutic strategies.

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Nicotinic receptor stimulation protects nigral dopaminergic neurons in rotenone‐induced Parkinson's disease models

Cited by 100 publications

References 55 publications

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

Chronic Nicotine Exposure Attenuates Methamphetamine-Induced Dopaminergic Deficits

The Effect of Treadmill Exercise on Expression of α-synuclein and miRNA in MPTP Induced-mouse Models of Parkinson’s Disease

Animal Models of Parkinson's Disease: A Gateway to Therapeutics?

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