Behavioural Brain Research: The role of the synth dopamine-like body D2 in motion coordination and balance: an understanding of the pathogenesis of DYT1 dystamism disorder

Dystatic dysfunction is a movement disorder characterized by persistent or intermittent muscle contractions that causes abnormal, frequently repeated movements, postures, or both.
may be caused by genetic mutations, brain damage, or side effects of drugs.
DYT1 or DYT-TOR1A is the most common early-oncological systemic dystatic dystatic disorder with symptoms aged 5-28 years.
most individuals affected by DYT1 dystain share a trinucleotide deficiency in the exon 5 of the DYT1 or TOR1A gene, resulting in the loss of glutamate amino acid residues in TorsinA.
other mutations in the gene have also been reported in rare cases.
mutations in DYT1 cause stunting and movement disorders, and torsinA expresses higher levels during early brain development, especially among neurons located in the substrate.
generally believes that dystia is not a muscle disease, but is caused by a brain defect.
Deep brain stimulation (DBS), which targets the pale ball inner core (GPi) or hyalthyclycerine nucleus (STN), can improve dystachia symptoms and indicate a change in the function of the substrate circuit.
symposomes control movement by balancing the symposome circuits between choline-energy intermediate neurons (ChIs) and black dopamine.
changes in choline energy systems play a key role in the pathophysiology of DYT1 dystiosis disorder.
anticholinental drugs such as triamid benzene (THP) are effective in clinically treating DYT1 dystamitis, suggesting that DYT1 dystroma is abnormal in choline energy.
synth dopamine D2 subject (D2R) binding activity and expression levels have been reduced in patients with DYT1 dystase disorder.
reduction in synth D2R is the result or cause of DYT1 dystow disorder is not clear.
this paper presents a model that linkes D2R signal reduction on ChIs, elevated acetylcholine levels, LTD damage, and abnormal movement of DYT1 dystachia.
paper uses ChI-specific Drd2 condition knock-out mice (Drd2 ChKO) to verify the role of D2R in chIs directly involved in the pathogenesis of DYT1 dystachia disorder.
analysis of the ratchet neuron (MSN) specific Drd2 condition knock-out mice (Drd2-sKO) to explore the role of D2R in MSN's motor performance.
to study whether the decrease in D2R on ChIs causes movement disorders similar to those in Dyt1 KI mice.
Drd2-ChKO mice were obtained using the Mendel ratio (p-0.999, camong tests), indicating that Drd2-ChKO mice were neither embryos nor newborns.
did not have significant developmental delays as drd2-ChKO mice grew into adults.
to evaluate the knock-off of D2R, the self-releasing electrical properties of ChIs in Drd2-ChKO and the regulatory effect of D2R astrist quinaro were measured.
, Drd2 ChKO and ChDHet mice had significantly increased discharge frequencies compared to control mice.
treatment, the discharge frequency of all genotypes was significantly reduced.
ChIs resting membrane in Drd2 ChKO and ChDHet mice did not change compared to control mice.
these results show a successful knock-out of D2Rs on ChIs.
protein levels of chat and AChE, two key metabolic enzymes of acetylcholine, were measured to detect whether the selective knock-out of D2R on ChIs led to changes in the synth choline energy system.
results showed that the Drd2-ChKO syroids had no ChI neurodegenerative degeneration, consistent with most mouse models of DYT1 dystase disorder.
the motion performance of Drd2 ChKO mice was measured.
strong reflexes when turning over in Drd2-ChKO mice and ChDHet mice, and did not exhibit any significant stress disorder behavior in the body type assessment.
MSNs can regulate the activity of ChIs.
D2Rs on MSNs in indirect pathways also contribute to synth plasticity of synapses.
found a decrease in synth D2R in both DYT1 patients and animal models.
individual selective knock-out or reduction of D2R on ChI can lead to the same age-dependent beam movement defects observed in Dyt1-KI mice.
, D2R on ChIs plays a key role in the pathophysiology of DYT1 dystia Yuning Liu, Hong Xing, Fumiaki Yokoi, David E. Vaillancourt, Yuqing Li, Investigationing the role of striatal dopamine receptor 2 in motor coordinate and balance: Insights into the pathogenesis of dyT1 dystonia, Behavioural Brain Research, Volume 403, 2021, MedSci Original Source: MedSci Original Copyright Statement: All noted on this website "Source: Met Medical" or "Source: MedSci Original" Copyright is owned by Mace Medical and may not be reproduced by any media, website or individual without authorization, with the following "Source: Met Medical" stated at the time of reprint.
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