ReviewCerebellum (London, England)2009
Pogo: a novel spontaneous ataxic mutant mouse.
Review in Cerebellum (London, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Perampanel increases seizure threshold in pentylenetetrazole-kindled mice and improves behavioral dysfunctions by modifying mRNA expression levels of BDNF/TrkB and inflammatory markers.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2024Article
- Protein expression pattern in cerebellum of Cav2.1 mutant, tottering-6j mice.Experimental animals · 2016Article
- Motor learning of mice lacking cerebellar Purkinje cells.Frontiers in neuroanatomy · 2013Article
- Animal models of human cerebellar ataxias: a cornerstone for the therapies of the twenty-first century.Cerebellum (London, England) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Pogo (pogo/pogo) mouse is a naturally occurring neurological mutant from a Korean wild-type mouse characterized by loss of balance and motor coordination due to dysfunction of the cerebellum. The Pogo mutation is believed to be an allele of P/Q-type calcium channel mutants such as tottering, leaner, and rolling mouse Nagoya. These mutants have been served as mouse models for a group of neurodegenerative diseases. The overall aim of this minireview is to summarize our current understanding of the ataxic Pogo mouse. To address this issue, we first describe the discovery of Pogo mouse and its morphological and behavioral defects. Then, we focus on the abnormal expression of several molecules in the Pogo cerebellum, including tyrosine hydroxylase, glutamate, corticotrophin-releasing factor, and 5-hydroxytryptamine. Much of this review is concerned with the functional implications of these ectopic molecules in the Pogo cerebellum.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.