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Modulation of synaptic potentials and cell excitability by dendritic K(IR) and K(As) channels in nucleus accumbens medium spiny neurons: A computational study

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Title Modulation of synaptic potentials and cell excitability by dendritic K(IR) and K(As) channels in nucleus accumbens medium spiny neurons: A computational study
 
Creator JOHN, J
MANCHANDA, R
 
Subject INACTIVATING POTASSIUM CURRENT
HIPPOCAMPAL PYRAMIDAL NEURONS
PREFRONTAL CORTICAL INPUTS
PROJECTION NEURONS
DOPAMINERGIC MODULATION
IN-VIVO
INTEGRATIVE PROPERTIES
MEMBRANE-PROPERTIES
LIMBIC SYSTEM
RAT
Computational model
excitatory post synaptic potential (EPSP)
inward rectifying K(+) (K(IR)) channel
medium spiny neurons
nucleus accumbens slowly inactivating A-type potassium channel (K(As))
spiking
 
Description The nucleus accumbens (NAc), a critical structure of the brain reward circuit, is implicated in normal goal-directed behaviour and learning as well as pathological conditions like schizophrenia and addiction. Its major cellular substrates, the medium spiny (MS) neurons, possess a wide variety of dendritic active conductances that may modulate the excitatory post synaptic potentials (EPSPs) and cell excitability. We examine this issue using a biophysically detailed 189-compartment stylized model of the NAc MS neuron, incorporating all the known active conductances. We find that, of all the active channels, inward rectifying K(+) (K(IR)) channels play the primary role in modulating the resting membrane potential (RMP) and EPSPs in the down-state of the neuron. Reduction in the conductance of K(IR) channels evokes facilitatory effects on EPSPs accompanied by rises in local input resistance and membrane time constant. At depolarized membrane potentials closer to up-state levels, the slowly inactivating A-type potassium channel (K(As)) conductance also plays a strong role in determining synaptic potential parameters and cell excitability. We discuss the implications of our results for the regulation of accumbal MS neuron biophysics and synaptic integration by intrinsic factors and extrinsic agents such as dopamine.
 
Publisher INDIAN ACAD SCIENCES
 
Date 2012-06-26T06:02:04Z
2012-06-26T06:02:04Z
2011
 
Type Article
 
Identifier JOURNAL OF BIOSCIENCES,36(2)309-328
0250-5991
http://dx.doi.org/10.1007/s12038-011-9039-8
http://dspace.library.iitb.ac.in/jspui/handle/100/13995
 
Language English