Related Experiment Video
Updated: Jun 15, 2026

Comprehensive Analysis of Transcription Dynamics from Brain Samples Following Behavioral Experience
Published on: August 26, 2014
The addicted synapse: mechanisms of synaptic and structural plasticity in nucleus accumbens
Scott J Russo1, David M Dietz, Dani Dumitriu
1Fishberg Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029-6574, USA. scott.russo@mssm.edu
Abstract:
Addictive drugs cause persistent restructuring of several neuronal cell types in the limbic regions of brain thought to be responsible for long-term behavioral plasticity driving addiction. Although these structural changes are well documented in nucleus accumbens medium spiny neurons, little is known regarding the underlying molecular mechanisms. Additionally, it remains unclear whether structural plasticity and its synaptic concomitants drive addictive behaviors or whether they reflect homeostatic compensations to the drug not related to addiction per se. Here, we discuss recent paradoxical data, which either support or oppose the hypothesis that drug-induced changes in dendritic spines drive addictive behavior. We define areas where future investigation can provide a more detailed picture of drug-induced synaptic reorganization, including ultrastructural, electrophysiological and behavioral studies.
Related Concept Videos
Drug Abuse and Addiction: Pharmacological Phenomena
Long-term Potentiation
Hebbian LTP
LTP can occur when presynaptic neurons...
Long-term Potentiation
Neuroplasticity
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

