| | Models | Description |
| 1. |
Afferent Integration in the NAcb MSP Cell (Wolf et al. 2005)
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"We describe a computational model of the principal cell in the nucleus accumbens (NAcb), the medium spiny projection (MSP) neuron.
The model neuron, constructed in NEURON, includes all of the known ionic currents in these cells and receives synaptic input from simulated spike trains via NMDA, AMPA, and GABAA receptors.
... results suggest that afferent information integration by the NAcb MSP cell may be compromised by pathology in which the NMDA current is altered or modulated, as has been proposed in both schizophrenia and addiction."
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| 2. |
Computational endophenotypes in addiction (Fiore et al 2018)
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"... here we simulated phenotypic
variations in addiction symptomology and responses to putative
treatments, using both a neural model, based on cortico-striatal
circuit dynamics, and an algorithmic model of reinforcement
learning. These simulations rely on the widely accepted assumption
that both the ventral, model-based, goal-directed system and the
dorsal, model-free, habitual system are vulnerable to
extra-physiologic dopamine reinforcements triggered by addictive
rewards. We found that endophenotypic differences in the balance
between the two circuit or control systems resulted in an inverted
U-shape in optimal choice behavior. Specifically, greater unbalance
led to a higher likelihood of developing addiction and more severe
drug-taking behaviors.
..." |
| 3. |
NAcc medium spiny neuron: effects of cannabinoid withdrawal (Spiga et al. 2010)
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Cannabinoid withdrawal produces a hypofunction of dopaminergic neurons targeting medium spiny neurons (MSN) of the forebrain. Administration of a CB1 receptor antagonist to control rats provoked structural abnormalities, reminiscent of those observed in withdrawal conditions and support the regulatory role of cannabinoids in neurogenesis, axonal growth and synaptogenesis. Experimental observations were incorporated into a realistic computational model which predicts a strong reduction in the excitability of morphologically-altered MSN, yielding a significant reduction in action potential output. These paper provided direct morphological evidence for functional abnormalities associated with cannabinoid dependence at the level of dopaminergic neurons and their post synaptic counterpart, supporting a hypodopaminergic state as a distinctive feature of the “addicted brain”. |
| 4. |
Nicotinic control of dopamine release in nucleus accumbens (Maex et al. 2014)
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Minimal model of the VTA (ventral segmental area) representing two (GABA versus dopamine) neuron populations and two subtypes of nicotinic receptors (alpha4beta2 versus alpha7). The model is used to tell apart circuit from receptor mechanisms in the nicotinic control of dopamine release and its pharmacological manipulation. |
| 5. |
VTA neurons: Morphofunctional alterations in acute opiates withdrawal (Enrico et al. 2016)
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" ... Here we present a biophysical model of a DA VTA neuron based on 3D morphological reconstruction and electrophysiological data, showing how opiates withdrawal-driven morphological and electrophysiological changes could affect the firing rate and discharge pattern...." |
