Despite diverse acute pharmacological actions, all drugs of abuse produce many similar
behaviors, such as psychomotor sensitization, conditioned drug taking, drug seeking,
and relapse (
1
). The development of these addiction-related behaviors is thought to arise from diverse
molecular and cellular adaptations, which collectively result in convergent long-term
functional alterations of the striatum. However, at the cellular level, on the one
hand, exposure to different classes of drugs, such as stimulants versus opioids (
2
), induces distinct and often opposing forms of adaptations in striatal medium spiny
neurons (MSNs). On the other hand, exposure to alcohol promotes alcohol consumption
by simultaneously activating both excitatory and inhibitory synaptic signaling, two
seemingly opposing mechanisms, in the striatum (
3
,
4
). It remains underexplored how such opposing synaptic mechanisms contribute to the
same behavioral states induced by drugs of abuse.To read this article in full you will need to make a payment
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References
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Article info
Publication history
Accepted:
February 13,
2017
Received:
February 11,
2017
Identification
Copyright
© Society of Biological Psychiatry, 2017.
ScienceDirect
Access this article on ScienceDirectLinked Article
- Distinct Synaptic Strengthening of the Striatal Direct and Indirect Pathways Drives Alcohol ConsumptionBiological PsychiatryVol. 81Issue 11
- PreviewRepeated exposure to addictive drugs or alcohol triggers glutamatergic and gamma-aminobutyric acidergic (GABAergic) plasticity in many neuronal populations. The dorsomedial striatum (DMS), a brain region critically involved in addiction, contains medium spiny neurons (MSNs) expressing dopamine D1 or D2 receptors, which form direct and indirect pathways, respectively. It is unclear how alcohol-evoked plasticity in the DMS contributes to alcohol consumption in a cell type–specific manner.
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