Abstract
The AS/AGU rat has a recessive single point mutation in the gene coding for the gamma isoform of protein kinase C (PKC-γ) resulting in a failure to release dopamine in the striatum and impaired movement including a staggering gait, difficulty in initiating movement and a slight whole body tremor. This study examined the levels tyrosine hydroxylase, ubiquitin and parkin in individual SNC cell bodies, there was no evidence of a reduction in tyrosine hydroxylase levels although levels of ubiquitin and parkin were elevated in the cytoplasm. The findings support the hypothesis that the initial bar to dopamine availability in the striatum is reduced release, with substantia nigra cell death being a later phenomenon.
Highlights
The AS/AGU rat originated as a recessive mutation in a closed colony of Albino Swiss (AS) rats
This study examined the levels tyrosine hydroxylase, ubiquitin and parkin in individual SNC cell bodies
There is no evidence that they lack the ability to synthesise dopamine— whole tissue micropunches of the midbrain and striatum have shown that dopamine levels remain normal until six months or more [22]
Summary
The AS/AGU rat originated as a recessive mutation (agu) in a closed colony of Albino Swiss (AS) rats. The mutation is in the gene coding for the gamma isoform of protein kinase C [1]. The rats are characterized by a movement impairments including rigidity of the hind limbs, a staggering gait, a tendency to fall over every few steps, a slight whole body tremor and difficulty in initiating movements [2,3] by progressive dysfunction of the nigro-striatal dopaminergic (DA) and raphe-striatal serotonergic (5-HT) systems. The chief defect in both systems is a failure to release transmitter within the striatum under normal physiological conditions. There is loss of aminergic cell bodies [7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
