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НАРУШЕНИЕ СЕНСОМОТОРНОЙ ИНТЕГРАЦИИ У ДЕТЕЙ С СДВГ

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Основная коллекция
Артикул: 623531.01.99
Сапина, Е. А. НАРУШЕНИЕ СЕНСОМОТОРНОЙ ИНТЕГРАЦИИ У ДЕТЕЙ С СДВГ / Е. А. Сапина. - Текст : электронный // Znanium.com. - 2017. - №1-12. - URL: https://znanium.com/catalog/product/534707 (дата обращения: 24.04.2024)
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disfunctions. Also we have found the decreased levels of DA degradation 
products: dihydroxyphenylacetic acid (DOPAC) and homovanillic acid 
(HVA). The ratio metabolite/neurotransmitter is thought to be an 
integral rate of neurotransmitter turnover. These ratios were increased 
in MPTP treated group: up to 150% for DOPAC/DA and up to 224% for 
HVA/DA 
vs. 
control, 
that 
is 
the 
indication 
of 
activated 

neurotransmission in survived DA-ergic axons in striatum.

DA content in the SN was reduced by 29%, DOPAC content – by 26% 

and HVA –
by 30%, that conclude that metabolic disfunctions in the 

developed model of PD also occur in the bodies of DA-ergic neurons.

We also estimated DA and its metabolites concentrations in the 

motor cortex, olifactory bulbs and brainstem, because PD is knows as 
the systemic disease, with neurodegeneration affecting other brain 
regions. There werent any changes in DA levels observed in any analyzed 
brain structure. However, the ratio DOPAC/DA was decreased by 61% and 
HVA/DA –
by 83% in olyfactory bulb, containing a group of DA-ergic 

neurons. There werent any changes in DOPAC/DA and HVA/DA ratios found 
in the brainstem and motor cortex that is the indication of absent 
metabolic 
disfunctions 
in 
these 
structures 
at 
this 
stage 
of 

parkinsonism in mice.

Thus new prolonged chronic model of the early symptomatic stage of 

the parkinsonism were developed in mice with the MPTP and this model 
was used to analyse the changes in DA metabolism in various brain 
regions.
References
1.
Agid Y. Parkinson's disease: pathophysiology. // Lancet. 1991. V. 

337. P. 1321-1324.
2.
Dunnett S.B., Björklund A. Prospects for new restorative and 

neuroprotective treatments in Parkinson's disease // Nature. 1999. V, 
399 (6738 Suppl): A32-9.
3.
Haas B.R., Stewart T.H., Zhang J. Premotor biomarkers for 

Parkinson's disease -a promising direction of research // Transl. 
Neurodegener. 2012. V. 1(1). P. 11.
4.
Alvarez-Fischer D., Guerreiro S., Hunot S. et al. Modelling 

Parkinson-like neurodegeneration via osmotic minipump delivery of MPTP 
and probenecid // J. Neurochem. 2008. V. 107. P. 701-711. 
5.
Bezard E., Dovero S., Bioulac B. et al. Kinetics of nigral 

degeneration in a chronic model of MPTP-treated mice // Neurosci. Lett. 
1997. V. 234. P. 47-50.
DOI:10.12737/12456

НАРУШЕНИЕ СЕНСОМОТОРНОЙ ИНТЕГРАЦИИ У ДЕТЕЙ С СДВГ

Сапина Е.А.

Федеральное государственное бюджетное научное учреждение «Научно
исследовательский институт молекулярной биологии и биофизики», 

Новосибирск

cdoastrum@mail.ru