DocumentCode
1928090
Title
Different inhibitory effects by dopaminergic modulation and global suppression of activity
Author
Hayashi, Takuji ; Araki, Osamu ; Ikeguchi, Tohm
Author_Institution
Dept. of Appl. Phys., Tokyo Univ. of Sci., Japan
Volume
4
fYear
2003
fDate
20-24 July 2003
Firstpage
2563
Abstract
In the dopaminergic network system of prefrontal cortex (PFC)-ventral tegmental area (VTA), physiological experiments have been reported that the D2 neurons inhibit the spontaneous activity of PFC neurons. However, the functional role of D2 suppression is not understood well. Is the effect of modulatory D2 inhibition different from that of GABAergic inhibition? The aim of this research is to reveal the difference between modulatory suppression of D2 and global inhibition by interneurons. To compare the effects, we construct two alternative models: (1) all GABAergic interneurons of PFC are modulated by a D2 system, or (2) a global interneuron depolarizes; all of PFC pyramidal cells. In computer simulations, we exemplify each of the models using a spiking neural network model with sparse and random synaptic connections. The simulation result shows that model-(1) keeps high correlation between spatial patterns of mean firing rates and the network structure despite the suppression of activity, while model-(2) reduces the correlation. This result suggests that modulatory suppression of D2 is more than a global suppression and may play a role in memory retrieval function.
Keywords
learning (artificial intelligence); neural nets; D2 neurons; D2 suppression; dopaminergic modulation; dopaminergic network system; global suppression; inhibitory effects; memory retrieval function; prefrontal cortex ventral tegmental area; random synaptic connections; spiking neural network model; Brain modeling; Chemicals; Computational modeling; Computer networks; Computer simulation; Lead; Learning; Neural networks; Neurons; Physics;
fLanguage
English
Publisher
ieee
Conference_Titel
Neural Networks, 2003. Proceedings of the International Joint Conference on
ISSN
1098-7576
Print_ISBN
0-7803-7898-9
Type
conf
DOI
10.1109/IJCNN.2003.1223969
Filename
1223969
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