Rapid synaptic plasticity of glutamatergic synapses on dopamine neurons in the ventral tegmental area in response to acute amphetamine injection
Drugs of abuse activate the reward circuitry of the mesocorticolimbic system, and it has been hypothesized that drug exposure triggers synaptic plasticity of glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area. Here, we show that just a 2 h in vivo exposure to amphetamine...
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| Veröffentlicht in: | Neuropsychopharmacology (New York, N.Y.) N.Y.), 2004-12, Vol.29 (12), p.2115-2125 |
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| creator | FALEIRO, Lavina J JONES, Susan KAUER, Julie A |
| description | Drugs of abuse activate the reward circuitry of the mesocorticolimbic system, and it has been hypothesized that drug exposure triggers synaptic plasticity of glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area. Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio. We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine. We also examined the possibility of increased AMPA receptor insertion in the membrane, but did not detect a significant increase in biotinylated surface GluR1. We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse. |
| doi_str_mv | 10.1038/sj.npp.1300495 |
| format | Article |
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Here, we show that just a 2 h in vivo exposure to amphetamine is sufficient to potentiate these synapses, measured as an increase in the synaptic AMPAR/NMDAR ratio. We tested the prediction that an increase in GluR1-containing AMPA receptors would result in an increase in GluR1 homomeric receptors at synapses, but were unable to observe any evidence of the predicted rectification in DA neurons from animals treated with amphetamine. We also examined the possibility of increased AMPA receptor insertion in the membrane, but did not detect a significant increase in biotinylated surface GluR1. We conclude that amphetamine induces rapid changes in synaptic AMPAR/NMDAR ratios, suggesting that potentiation of glutamatergic synapses is a relatively early event in the series of neuroadaptations in response to drugs of abuse.</abstract><cop>New York, NY</cop><pub>Nature Publishing</pub><pmid>15150533</pmid><doi>10.1038/sj.npp.1300495</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Neuropsychopharmacology (New York, N.Y.), 2004-12, Vol.29 (12), p.2115-2125 |
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| subjects | 2-Amino-5-phosphonovalerate - pharmacology Age Factors alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid - pharmacology Amphetamine - pharmacology Animals Animals, Newborn Behavior, Animal Behavioral psychophysiology Biological and medical sciences Blotting, Western - methods Central Nervous System Stimulants - pharmacology Dopamine - metabolism Drug Interactions Excitatory Amino Acid Agonists - pharmacology Excitatory Amino Acid Antagonists - pharmacology Excitatory Postsynaptic Potentials - drug effects Female Fundamental and applied biological sciences. Psychology Glutamic Acid - metabolism In Vitro Techniques Male Membrane Potentials - drug effects Motor Activity - drug effects N-Methylaspartate - pharmacology Neuronal Plasticity - drug effects Neurons - drug effects Neurotransmission and behavior Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Rats Rats, Sprague-Dawley Receptors, AMPA - metabolism Receptors, N-Methyl-D-Aspartate Substance Withdrawal Syndrome Synapses - drug effects Time Factors Transferrin - metabolism Ventral Tegmental Area - cytology |
| title | Rapid synaptic plasticity of glutamatergic synapses on dopamine neurons in the ventral tegmental area in response to acute amphetamine injection |
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