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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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References

    1. Abel E. L., Bush R., Dintcheff B. A. (1981). Exposure of rats to alcohol in utero alters drug sensitivity in adulthood. Science 212, 1531–1533. 10.1126/science.7233243 - DOI - PubMed
    1. Adermark L., Jonsson S., Ericson M., Söderpalm B. (2011). Intermittent ethanol consumption depresses endocannabinoid-signaling in the dorsolateral striatum of rat. Neuropharmacology 61, 1160–1165. 10.1016/j.neuropharm.2011.01.014 - DOI - PubMed
    1. Araque A., Castillo P. E., Manzoni O. J., Tonini R. (2017). Synaptic functions of endocannabinoid signaling in health and disease. Neuropharmacology 124, 13–24. 10.1016/j.neuropharm.2017.06.017 - DOI - PMC - PubMed
    1. Baer J. S., Sampson P. D., Barr H. M., Connor P. D., Streissguth A. P. (2003). A 21-year longitudinal analysis of the effects of prenatal alcohol exposure on young adult drinking. Arch. Gen. Psychiatry 60, 377–385. 10.1001/archpsyc.60.4.377 - DOI - PubMed
    1. Basavarajappa B. S., Hungund B. L. (1999). Chronic ethanol increases the cannabinoid receptor agonist anandamide and its precursor N-arachidonoylphosphatidylethanolamine in SK-N-SH Cells. J. Neurochem. 72, 522–528. 10.1046/j.1471-4159.1999.0720522.x - DOI - PubMed

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