Increased preproenkephalin mRNA and preprotachykinin mRNA in the striatum of Rolling mouse Nagoya

Taniwaki, Takayuki; Shinoda, Hisaharu; Kaseda, Yumiko; Kato, Motohiro; Goto, Ikuo

doi:10.1016/0006-8993(95)01577-9

Cited by 5 publications

(2 citation statements)

References 16 publications

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“…Increased local cerebral glucose utilization (indicating enhanced neuronal activity) in the basal ganglia (including the globus pallidus, entopeduncular nucleus, substantia nigra reticulate, and subthalamic nucleus) as well as electrophysiological abnormalities recorded in the globus pallidus have led to the hypothesis that motor disturbances of RN mice may perhaps in the end be not so much due to cerebellar dysfunction but rather due to striatial dysfunction [ 19 , 36 ]. In addition, radiochemical studies have shown increased preproenkephalin and preprotachykinin mRNA in the striatum [ 37 ]. More research is clearly needed to shed light on how (combined) striatal and cerebellar dysfunction causes motor dysfunction in RN mice.…”

Section: Morphological Studies Of Rolling Nagoya Cmentioning

confidence: 99%

The Ataxic Cacna1a-Mutant Mouse Rolling Nagoya: An Overview of Neuromorphological and Electrophysiological Findings

2009

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Homozygous rolling Nagoya natural mutant mice display a severe ataxic gait and frequently roll over to their side or back. The causative mutation resides in the Cacna1a gene, encoding the pore-forming α 1 subunit of Ca v 2.1 type voltage-gated Ca 2+ channels. These channels are crucially involved in neuronal Ca 2+ signaling and in neurotransmitter release at many central synapses and, in the periphery, at the neuromuscular junction. We here review the behavioral, histological, biochemical, and neurophysiological studies on this mouse mutant and discuss its usefulness as a model of human neurological diseases associated with Ca v 2.1 dysfunction.

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Section: Morphological Studies Of Rolling Nagoya Cmentioning

confidence: 99%

The Ataxic Cacna1a-Mutant Mouse Rolling Nagoya: An Overview of Neuromorphological and Electrophysiological Findings

2009

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“…Increased local cerebral glucose utilization (indicating enhanced neuronal activity) in the basal ganglia (including the globus pallidus, entopeduncular nucleus, substantia nigra reticulate, and subthalamic nucleus) as well as electrophysiological abnormalities recorded in the globus pallidus have led to the hypothesis that motor disturbances of RN mice may perhaps be also due to striatal dysfunction (Kato et al 1982;Tomoda et al 1992). In addition, radiochemical studies have shown increased preproenkephalin and preprotachykinin mRNA in the striatum (Taniwaki et al 1996). On the basis of these results, it may be speculated that the RN mouse is an experimental model for basal ganglia dysfunction, besides being a model for cerebellar ataxia.…”

Section: Histological Analyses Of Rolling Nagoya Brain Areasmentioning

confidence: 99%

Rolling Nagoya Mouse

Tolner

Maagdenberg

Plomp

2021

Handbook of the Cerebellum and Cerebellar Disorders

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The natural mutant mouse rolling Nagoya has an uncoordinated gait and frequently displays sideways body rolls. The mutation underlying this autosomal recessively inherited severely ataxic motor phenotype is present in Cacna1a, the gene encoding the pore-forming α 1 subunit of Ca V 2.1 type voltage-gated Ca 2+ channels. This type of channel is crucially involved in neuronal Ca 2+ signaling and in neurotransmitter release from nerve terminals at many central synapses and, in the periphery, at the neuromuscular junction. This chapter reviews the phenotypic, motor behavioral, histological, biochemical, neurophysiological, and electrophysiological findings in this mouse mutant. Human neurological diseases exist which are associated with Ca V 2.1 dysfunction ("Ca 2+ -channelopathy"), either due to a CACNA1A mutation or an autoimmune attack of Ca V 2.1 channels. The relevance of the rolling Nagoya mouse mutant as a model for these diseases is discussed.

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