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Hindi Research Article
Effect of Spine Density on Excitability in Accumbal Medium Spiny Neurons-A Computational Approach
Mrunal Rane1,2* and Rohit Manchanda1
1Department of Biosciences and Bioengineering, IIT Bombay, Mumbai, Maharashtra, India
2Department of Biomedical Engineering, D. J. Sanghvi College of Engineering, Mumbai, Maharashtra, India
- *Corresponding Author:
- Mrunal Rane
Department of Biosciences and Bioengineering
IIT Bombay, Mumbai, Maharashtra, India
Tel: +91-22-25767765
E-mail: mrunal.rane@iitb.ac.in
Received date: June 28, 2017; Accepted date: July 19, 2017; Published date: July 26, 2017
Citation: Rane M, Manchanda R (2017) Effect of Spine Density on Excitability in Accumbal Medium Spiny Neurons-A Computational Approach. J Addict Res Ther 8:337. doi:10.4172/2155-6105.1000337
Copyright: © 2017 Rane M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The nucleus accumbens (NAc), the major subdivision of the ventral striatum plays an important role in the reward pathway. GABAergic Medium Spiny Neurons (MSNs) are the principal cell type of NAc. These neurons receive excitatory synaptic inputs over the numerous spines which are present on their complex dendritic arbours. Alterations in spine density and morphology can affect the integrative properties of MSNs. We developed a biophysically realistic, spiny model of MSN. We found that inclusion of spines in an existing aspiny model changed passive as well as active properties of the cell. The spiny model was tuned to match its properties with that of the earlier aspiny model. We found that a total of 192 inputs from middle and distal dendrites were required to generate a characteristic bimodal behaviour of the membrane potential. Using this model, we investigated the effect of loss of spines on the excitability of the cell. We found that with no spine loss, when only the number of activated inputs was reduced by 15%, spike frequency of the cell reduced to zero, rendering the cell completely inexcitable. However, spine loss of 15% along with 15% reduction in activated synaptic inputs decreased the spike frequency to 1.1 Hz. Our results suggest that when spines are lost along with synaptic inputs, excitability of the cell is not abolished completely, although this might happen when only synaptic inputs are lost. Instead, in such a case the excitability can be increased by slightly enhancing the input connections.
