Stimulant-induced adaptations in neostriatal matrix and striosome systems: Transiting from instrumental responding to habitual behavior in drug addiction
Abstract
Converging evidence indicates that repeated exposure to motor stimulants such as cocaine and amphetamine produces marked alterations in network responsiveness of striatal neurons to subsequent challenge with the same stimulant drug. Such alterations, which correlate with persistent patterns of repetitive behavior, associate with distinct compartmental changes in the neostriatum. Striatal matrix system neurons undergo "silencing" following repeated drug challenges, allowing striosome system neurons to exhibit preferential activation. Matrix neurons are innervated by sensory and motor areas of neocortex and are activated in the course of on-going, adaptive behavior. Inactivation of matrix neurons by chronic stimulant exposure may therefore constrain sensorimotor and cognitive processing. In turn, the striosomes are anatomically connected through re-entrant loops with limbic prefrontal and allocortical structures, such as anterior cingulate cortex, orbital frontal cortex, and basolateral amygdala, all of which play a part in stimulant-induced reinforcement and relapse to drug-taking. Moreover, functional evidence links striosome system neurons, which are responsible for providing inhibitory regulatory feedback to midbrain dopamine neurons, with reinforcement-based processes. In considering such evidence, we postulate that recurrent matrix inactivation and recruitment of striosome-based pathways by chronic stimulant exposure represent neural end-points of the transit from action-outcome associative behavior to conditioned habitual responding. Within this theoretical framework, habitual behavior can be elicited by both interoceptive cues and exteroceptive conditioned stimuli to promote the automatic execution of learned responses.
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Many aspects of drug-seeking behaviors become automatized, complicating treatment of drug addiction.
“For example, a complicating factor in treating drug addiction is that many aspects of drug-seeking behaviors become automatized [79–82].”
From Cortical and basal ganglia contributions to habit learning and automaticity (2010) · cites this paper as [82]
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- Authors
- CANALES, J.
- Affiliations
- Universitat de València (ES)
- Corresponding author
- CANALES, J
- ORCID
- CANALES, J
- Venue
- Neurobiology of Learning and Memory
- Publisher
- Elsevier BV
- Published
- 2005-03
- Volume
- 83
- Issue
- 2
- Pages
- 93-103
- ISSN
- 1074-7427 (ISSN-L)
- OpenAlex
- W2065786707
- Cited by
- 95
- References
- 87
- Citations by year
- 2026: 2 · 2023: 1 · 2022: 1 · 2021: 1 · 2020: 6 · 2019: 2 · 2018: 1 · 2017: 3 · 2016: 4 · 2015: 6 · 2014: 2 · 2013: 7 · 2012: 4
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurobiology of Learning and Memory (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- neostriatum, striosomes, striatal matrix, cocaine, amphetamine, drug addiction, habitual behavior, instrumental responding, anterior cingulate cortex, orbitofrontal cortex, basolateral amygdala, dopamine, relapse, conditioned stimulus, interoceptive cues, action-outcome learning
- MeSH terms
- Amphetamine, Central Nervous System Stimulants, Animals, Arousal, Basal Ganglia, Cerebral Cortex, Cocaine, Conditioning, Operant, Habituation, Psychophysiologic, Humans, Limbic System, Nerve Net, Neurons, Receptors, Dopamine, Neostriatum, Amphetamine-Related Disorders, Cocaine-Related Disorders
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