Serotonergic Heterotypic Sprouting in the Unilaterally Dopamine-Depleted Mouse Neostriatum

Yamazoe, Ichiro; Takeuchi, Yoshihiro; Matsushita, Hiroko; Kawano, Hisashi; Sawada, Tadashi

doi:10.1159/000048698

Cited by 14 publications

(8 citation statements)

References 18 publications

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“…This interpretation is supported by the stronger 5-HT labeling observed in the striatal functional territories of recovered monkeys and weaker labeling observed in monkeys with stable motor symptoms than in normal monkeys (Mounayar et al, 2007). This serotoninergic hyperinnervation, often observed in animal models of PD (Zhou et al, 1991;Gaspar et al, 1993;Yamazoe et al, 2001), may be compensatory. Indeed, 5-HT may promote DA release from the remaining dopaminergic fibers (Benloucif and Galloway, 1991;Yadid et al, 1994).…”

Section: Relevance Of Repeated Microdialysis For Investigating Neurocmentioning

confidence: 89%

“…We observed an increase in 5-HT concentration which was greater in the sensorimotor than in the associative-limbic striatum. Ultrastructural studies on 6-OHDA rats (Zhou et al, 1991), MPTP mice (Yamazoe et al, 2001), and MPTP monkeys (Gaspar et al, 1993) have demonstrated that nigrostriatal dopaminergic pathway destruction leads to serotoninergic hyperinnervation of the striatum. These data are consistent with our neurochemical findings and with the negative correlation between TH-positive fiber counts and 5-HT levels in the associative-limbic striatum.…”

Section: Modifications Associated With Motor Symptom Expressionmentioning

confidence: 99%

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Behavioral Recovery in MPTP-Treated Monkeys: Neurochemical Mechanisms Studied by Intrastriatal Microdialysis

Boulet

Mounayar²,

Poupard³

et al. 2008

J. Neurosci.

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Parkinson's disease (PD) patients express motor symptoms only after 60 -80% striatal dopamine (DA) depletion. The presymptomatic phase of the disease may be sustained by biochemical modifications within the striatum. We used an appropriate specific 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkey model (Mounayar et al., 2007) to study the compensatory mechanisms operating in recovery from PD motor symptoms. We assessed the levels of DA and its metabolites (DOPAC, homovanillic acid), GABA, glutamate (Glu), serotonin (5-HT) and its metabolite (5HIAA) by repeated intracerebral microdialysis in awake animals before exposure to MPTP during full expression of the motor symptoms induced by MPTP and after recovery from these symptoms. Measurements were obtained from two functionally and anatomically different striatal areas: the associative-limbic territory and sensorimotor territory. Animals with motor symptoms displayed an extremely large decrease in levels of DA and its metabolites and an increase in Glu and GABA levels, as reported by other studies. However, we show here for the first time that serotonin levels increased in these animals. We found that increases in DA levels in the sensorimotor and/or associative-limbic territory and high levels of 5-HT and of its metabolite, 5HIAA, were associated with recovery from motor symptoms in this model. Determining whether similar changes in DA and 5-HT levels are involved in the compensatory mechanisms delaying the appearance of motor symptoms in the early stages of PD might make it possible to develop new treatment strategies for the disease.

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Section: Relevance Of Repeated Microdialysis For Investigating Neurocmentioning

confidence: 89%

Section: Modifications Associated With Motor Symptom Expressionmentioning

confidence: 99%

Behavioral Recovery in MPTP-Treated Monkeys: Neurochemical Mechanisms Studied by Intrastriatal Microdialysis

Boulet

Mounayar²,

Poupard³

et al. 2008

J. Neurosci.

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“…In several studies in which mouse pups were injected with 6-OHDA, no mention was made about death or reduced body weight in these pups [Shimizu et al, 1987;Fink et al, 1992;Yamazoe et al, 2001]. Their research focus and protocols differed from those presented here, and perhaps they did not notice the stunted growth.…”

Section: Resultsmentioning

confidence: 79%

“…Some authors have suggested that removing DA neurons in neonates provides an opportunity for regenerative mechanisms, particularly among monoaminergic neurons [Björklund et al, 1981;Zigmond and Stricker, 1985;Takeuchi et al, 1991]. For example, it has been reported that neuronal systems containing serotonin further extend their processes into areas otherwise occupied by DA terminals [Imamoto et al, 1980;Stachowiak et al, 1984;Berger et al, 1985;Snyder et al, 1986;Yamazoe et al, 2001]. It is also possible that DA signaling by the remaining neurons is more efficient when lesions 532 Dev Neurosci 2002;24:531-538 Brot/Szczypka/Reavell/Marck/Matsumoto/ Palmiter occur while the dopaminergic system is still developing [Bruno et al, 1987].…”

Section: Introductionmentioning

confidence: 99%

Neonatal 6-Hydroxydopamine Administration to Mice Is Fatal

et al. 2002

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Depletion of dopamine in adult rats by treatment with the neurotoxin 6-hydroxydopamine (6-OHDA) causes severe deficits in feeding, drinking, and movement that often lead to death. However, when neonatal rats are treated similarly, they survive normally, suggesting that compensatory adaptation to dopamine depletion occurs. In contrast, dopamine-deficient mice that have a selective genetic deficiency in dopamine production die 2–4 weeks after birth. Thus, we tested the hypothesis that killing dopaminergic neurons with 6-OHDA might promote survival of dopamine-deficient mice. Body weights, motor coordination, catecholamine levels, and survival were monitored for several weeks after bilateral administrations of 6-OHDA to 3-day-old mice. Some treated mice were raised in a heated chamber to help them conserve energy. The results demonstrate that regardless of genotype or environmental temperature, bilateral neonatal 6-OHDA lesions are lethal to mice.

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“…In contrast, axon sprouting of serotonin fibers appears in the striatum of the experimental animals and generates a markedly dense distribution. These findings suggest that the serotonin neuron system has a strong influence on the dopamine neuron system (Yamazoe, 2001). This phenomenon, called "heterotypic sprouting", is observed particularly between the serotonin neuron and dopamine neuron systems.…”

Section: High Sprouting Capabilitymentioning

confidence: 93%