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Comment
. 2017 Nov 3:10:364.
doi: 10.3389/fnmol.2017.00364. eCollection 2017.

Commentary: Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinioid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons

Hada Fong-Ha Ieong  1
Affiliations
Comment

Commentary: Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinioid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons

Hada Fong-Ha Ieong. Front Mol Neurosci. .
No abstract available

Keywords: addiction; cannabinoid receptors; eCB system; early adversity; glutamate; mGluR; positive reinforcement; reward system.

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Figures

Figure 1
Figure 1
PE-induced alterations of eCB signaling and excitatory synaptic plasticity in VTA DA neuron underlie positive reinforcement. (A) Under normal conditions, eCB-LTD is induced by afferent stimulation, resulting in eCB synthesis. eCBs then activate CB1 receptors. (B) PE exposure persistently alters eCB signaling, impairs eCB-LTD, downregulates CB1 receptors, and thus results in the enhanced excitability of VTA DA neurons that underlie positive reinforcement states that promote addiction-related behaviors. Upregulation of AMPA receptors, including the polyamine-lacking receptors, and the decreased glutamate stimulation further contribute to an occlusion effect on the eCB signaling. (C) Drug-induced adaptations can be counteracted by using mGlu receptor agonists, signaling eCB production, leading to rescue of eCB-LTD and restoration of augmented excitatory synaptic strength in VTA DA neurons.
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