Long-term depression in the nucleus accumbens: a neural correlate of behavioral sensitization to cocaine

@article{Thomas2001LongtermDI,
  title={Long-term depression in the nucleus accumbens: a neural correlate of behavioral sensitization to cocaine},
  author={Mark J. Thomas and Corinne Beurrier and Antonello Bonci and Robert C. Malenka},
  journal={Nature Neuroscience},
  year={2001},
  volume={4},
  pages={1217-1223}
}
A compelling model of experience-dependent plasticity is the long-lasting sensitization to the locomotor stimulatory effects of drugs of abuse. Adaptations in the nucleus accumbens (NAc), a component of the mesolimbic dopamine system, are thought to contribute to this behavioral change. Here we examine excitatory synaptic transmission in NAc slices prepared from animals displaying sensitization 10–14 days after repeated in vivo cocaine exposure. The ratio of AMPA (α-amino-3-hydroxy-5-methyl-4… 

Enhanced Inhibition of Synaptic Transmission by Dopamine in the Nucleus Accumbens during Behavioral Sensitization to Cocaine

It is hypothesized that the enhanced inhibitory effects of DA on synaptic transmission in the NAc are one of a number of adaptations that contribute to a decrease in excitatory drive to NAc after exposure to drugs of abuse.

Ethanol attenuation of long-term depression in the nucleus accumbens can be overcome by activation of TRPV1 receptors.

EtOH modulation of synaptic plasticity in the NAc is dependent upon a complex interplay between NMDARs, eCBs, and TRPV1 receptors and enhanced eCB signaling rescued NAc-LTD expression in the presence of EtOH through a distinct mechanism requiring activation of TRPv1 receptors.

Nucleus Accumbens Long-Term Depression and the Expression of Behavioral Sensitization

Long-term depression of α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)–mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory.

In Vivo Chronic Intermittent Ethanol Exposure Reverses the Polarity of Synaptic Plasticity in the Nucleus Accumbens Shell

The acute in vitro and in vivo effects of ethanol in medium spiny neurons from the shell NAc subregion of slices of C57BL/6 mice are studied and alterations in this synaptic process may constitute a neural adaptation that contributes to the induction and/or expression of ethanol dependence.

Cocaine Withdrawal Impairs Metabotropic Glutamate Receptor-Dependent Long-Term Depression in the Nucleus Accumbens

It is shown that animals withdrawn from repeated cocaine exposure have a selective deficit in the ability to elicit metabotropic glutamate receptor (mGluR)-dependent long-term depression (LTD) in the shell of the NAc in response to bath application of the group I mGLUR agonist (S)-3,5-dihydroxyphenylglycine (DHPG).

Neuroplastic alterations in the limbic system following cocaine or alcohol exposure.

Evidence that drugs of abuse are powerful modulators of synaptic plasticity is reviewed, finding that dopaminergic neurons of the ventral tegmental area as well as medium spiny neurons in nucleus accumbens show enhanced excitatory synaptic strength following passive or active exposure to drugs such as cocaine and alcohol.

Cocaine Experience Enhances Thalamo-Accumbens N-Methyl-D-Aspartate Receptor Function

The role of D-serine as co-agonist of NMDA receptors in the nucleus accumbens: relevance to cocaine addiction

It is found that reduced D-serine levels play a crucial role in synaptic plasticity relevant to cocaine addiction, and this finding opens new perspectives for therapeutic approaches to treat this addictive state.

Cocaine Experience Controls Bidirectional Synaptic Plasticity in the Nucleus Accumbens

It is demonstrated that a progression of bidirectional changes in glutamatergic synaptic strength occurs after repeated in vivo exposure to cocaine, and enduring modifications in AMPAR-mediated responses and plasticity may provide a neural substrate for disrupted processing of drug-related stimuli in drug-experienced individuals.

Temporally Dependent Changes in Cocaine-Induced Synaptic Plasticity in the Nucleus Accumbens Shell are Reversed by D1-Like Dopamine Receptor Stimulation

D1DRs gate the stability of these cocaine-induced changes at glutamatergic synapses in the accumbens shell by utilizing multiple temporally distinct mechanisms, which has implications for the treatment of cocaine craving and addiction.
...

References

SHOWING 1-10 OF 49 REFERENCES

Modulation of Long-Term Depression by Dopamine in the Mesolimbic System

It is found that both sets of synapses express LTD but that their basic triggering mechanisms differ, and that DA blocks the induction of LTD in the midbrain via activation of D2-like receptors but has minimal effects on LTD inThe NAc.

Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons

It is shown that a prominent form of synaptic plasticity can be elicited by a single in vivo exposure to cocaine and therefore may be involved in the early stages of the development of drug addiction.

The role of excitatory amino acids in behavioral sensitization to psychomotor stimulants

  • M. Wolf
  • Biology, Psychology
    Progress in Neurobiology
  • 1998

Repeated administration of cocaine or amphetamine alters neuronal responses to glutamate in the mesoaccumbens dopamine system.

Whether repeated psychomotor stimulant administration can alter responsiveness of the mesoaccumbens dopamine (DA) system to glutamate is determined and sensitization appears to be associated with alterations in glutamate transmission at both the origin and termination of the MesoaccUMens DA pathway.

Fear conditioning induces a lasting potentiation of synaptic currents in vitro

One of the first in vitro measures of synaptic plasticity resulting from emotional learning by whole animals is reported, reporting a long-lasting increase in the synaptic efficacy of the MGN–LA pathway attributable to fear-conditioning itself, rather than an electrically induced model of learning.

Alterations in dopaminergic and glutamatergic transmission in the induction and expression of behavioral sensitization: a critical review of preclinical studies

The distinctions between drugs in the induction and expression of sensitization indicate that behavioral sensitization can arise from multiple neuroadaptations in multiple brain nuclei, not only the result of distinct molecular targets for the drugs, but may also include a differential involvement of learned associations.

Whole-Cell Plasticity in Cocaine Withdrawal: Reduced Sodium Currents in Nucleus Accumbens Neurons

It is found that nucleus accumbens neurons are less excitable in cocaine withdrawn rats because of a novel form of plasticity: reduced whole-cell sodium currents.

Repeated cocaine augments excitatory amino acid transmission in the nucleus accumbens only in rats having developed behavioral sensitization

It is indicated that repeated cocaine administration increases EAA transmission in the nucleus accumbens only in rats that develop behavioral sensitization to cocaine.

Persistent Structural Modifications in Nucleus Accumbens and Prefrontal Cortex Neurons Produced by Previous Experience with Amphetamine

The ability of amphetamine to alter patterns of synaptic connectivity in brain regions that mediate its psychomotor activating and rewarding effects may contribute to some of the long-term behavioral consequences of repeated amphetamine use, including amphetamine psychosis and addiction.

Psychostimulants depress excitatory synaptic transmission in the nucleus accumbens via presynaptic D1-like dopamine receptors

DA and psychostimulants (acting indirectly by increasing endogenous extracellular DA levels) reduce excitatory synaptic transmission in the NAc by activating presynaptic DA receptors with D1-like properties.