Shesharao M Wanjerkhede

Publications (3)4.63 Total impact

• Article: Role of CAMKII in reinforcement learning: a computational model of glutamate and dopamine signaling pathways.

  Shesharao M Wanjerkhede, Raju S Bapi
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  ABSTRACT: Timely release of dopamine (DA) at the striatum seems to be important for reinforcement learning (RL) mediated by the basal ganglia. Houk et al. (in: Houk et al (eds) Models of information processing in the basal ganglia, (1995) proposed a cellular signaling pathway model to characterize the interaction between DA and glutamate pathways that have a role in RL. The model simulation results, using GENESIS KINETIKIT simulator, point out that there is not only prolongation of duration as proposed by Houk et al. (1995), but also an enhancement in the amplitude of autophosphorylation of CaMKII. Further, the autophosphorylated form of CaMKII may form a basis for the "eligibility trace" condition required in RL. This simulation study is the first of its kind to support the comprehensive theoretical proposal of Houk et al. (1995).
  Biological Cybernetics 06/2011; 104(6):397-424. · 1.59 Impact Factor
• Conference Proceeding: A Computational study of pre-synaptic re-uptake of dopamine on phosphorylation of DARPP-32.

  Shesharao M. Wanjerkhede, Raju S. Bapi
  International Joint Conference on Neural Networks, IJCNN 2009, Atlanta, Georgia, USA, 14-19 June 2009; 01/2009
• Article: Modeling the sub-cellular signaling pathways involved in reinforcement learning at the striatum.

  Shesharao M Wanjerkhede, Raju S Bapi
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  ABSTRACT: A general discussion of various levels of models in computational neuroscience is presented. A detailed case study of modeling at the sub-cellular level is undertaken. The process of learning actions by reward or punishment is called 'Instrumental Conditioning' or 'Reinforcement Learning' (RL). Temporal difference learning (TDL) is a mathematical framework for RL. Houk et al. (1995) proposed a cellular signaling model for interaction of dopamine (DA) and glutamate activities at the striatum that forms the basis for TDL. In the model, glutamatergic input generates a membrane depolarization through N-methyl-d-aspartate (NMDA), alpha-amino-5-hydroxy-3-methyl-4-isoxazole propionic acid (AMPA), metabotropic glutamate receptors (mGluR), and opens calcium two plus ion (Ca(2+)) channels resulting in the influx of Ca(2+) into the dendritic spine. This raises the postsynaptic calcium concentration in the dendritic spine leading to the autophosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII). The timely arrival of the DA input at the neck of the spine head generates a cascade of reactions which then leads to the prolongation of long-term potentiation (LTP) generated by the autophosphorylation of CaMKII. Since no simulations were done so far to support this proposal, we undertook the task of computational verification of the model. During the simulations it was found that there was enhancement and prolongation of autophosphorylation of CaMKII. This result verifies Houk's proposal for LTP in the striatum. Our simulation results are generally in line with the known biological experimental data and also suggest predictions for future experimental verification.
  Progress in brain research 02/2008; 168:193-206. · 3.04 Impact Factor