ХОЛИНЕРГИЧЕСКИЕ НЕЙРОНЫ В СУСПЕНЗИОННЫХ И ТКАНЕВЫХ АЛЛОТРАНСПЛАНТАТАХ ЭМБРИОНАЛЬНОГО СПИННОГО МОЗГА КРЫСЫ, РАЗВИВАЮЩИХСЯ В ПОВРЕЖДЕННОМ СЕДАЛИЩНОМ НЕРВЕ

43 unloading, while the MCD-induced increase in H2DCF fluorescence was 
not changed. The data suggest that the MCD application leads to an 
activation of the TRPV1 channels that is implicated in enhancement of 
the spontaneous exocytosis. In addition the stimulation of these 
channels lies downstream of the ROS production in the MCD action. To 
verify a possibility of the ROS-evoked stimulation of the TRPV1 channels 
the Са2+ indicator was used. At the synaptic region, the fluorescence of 
Fluo4 was increased by 10 mM MCD. Capsazepine or antioxidant completely 
inhibits this increase in the fluorescence. Therefore, the activation 
of TRPV1 channels and the rise in [Ca2+]i occur in response to 10 mM MCD 
treatment in a ROS-dependent manner. 
In sum, the exposure to MCD increases the spontaneous exocytosis at 
mouse neuromuscular junction partially through stimulation of NADPHoxidase/ROS/TRPV1
channels pathway. The enhancement of spontaneous 

exocytosis occurs only after strong cholesterol depletion using 10 mM 
MCD [1, 2]. In natural conditions it can be observed at excessive 
synaptic activity [5]. Accordingly, the activation of the NADPHoxidase/ROS/TRPV1-channels pathway due to plasma membrane cholesterol 
depletion may be a sign of the enhanced excitatory synaptic 
transmission. Subsequent intensification of the spontaneous exocytosis 
could limit evoked synaptic transmission via depletion of the synaptic 
vesicle pool, desensitization of the postsynaptic receptors, and 
inhibition of the local protein synthesis [3]. We speculate that such 
mechanism can provide a cholesterol-dependent negative feedback that is 
able to suppress evoked exocytosis via enhancing spontaneous release. 
Further investigations are needed to identify the presence and 
functioning of this regulation. The study was supported for A.M. Petrov 
by RFBR 14-04-00094.
References.
1. Kasimov M.R., Giniatullin A.R., Zefirov A.L., Petrov A.M. // Biochim 
Biophys Acta. 2015. V. 1851. № 5. P. 674-685.
2. Petrov A.M., Naumenko N.V., Uzinskaya K.V. et al. // Neuroscience. 
2011. V. 186. P.1-12.
3. Petrov A.M, Yakovleva A.A., Zefirov A.L. // Journal of Physiology. 
2014. V. 592. № 22, P. 4995-5009.
4. Smith A.J., Sugita S., Charlton M.P. // J. Neurosci. 2010. V. 30. № 
17. P. 6116-6121.
5. Sodero A.O., Weissmann C., Ledesma M.D., Dotti C.G. // Neurobiol 
Aging. 2011. V. 32. № 6. P. 1043-1053.
DOI:10.12737/12445

ХОЛИНЕРГИЧЕСКИЕ НЕЙРОНЫ В СУСПЕНЗИОННЫХ И ТКАНЕВЫХ 

АЛЛОТРАНСПЛАНТАТАХ ЭМБРИОНАЛЬНОГО СПИННОГО МОЗГА КРЫСЫ, 

РАЗВИВАЮЩИХСЯ В ПОВРЕЖДЕННОМ СЕДАЛИЩНОМ НЕРВЕ

Е.С.Петрова, Е.Н.Исаева, Д.Э. Коржевский

ФГБНУ «Институт экспериментальной медицины», Санкт-Петербург

Iemmorphol@yandex.ru