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Differential development of autoreceptor subsensitivity and enhanced dopamine release during amphetamine
M E Wolf1, F J White, R Nassar
1Department of Psychiatry, Wayne State University School of Medicine, Detroit, Michigan.
The Journal of Pharmacology and Experimental Therapeutics
|January 1, 1993
Summary
Autoreceptor subsensitivity in dopamine neurons is transient and may contribute to amphetamine sensitization. Enhanced dopamine release appears later, potentially sustaining sensitization after longer withdrawal periods.
Area of Science:
- Neuroscience
- Pharmacology
- Behavioral Science
Background:
- Repeated d-amphetamine use leads to behavioral sensitization.
- Changes in dopamine neuron function are hypothesized to cause sensitization.
Purpose of the Study:
- To investigate the role of somatodendritic autoreceptor sensitivity and dopamine release in amphetamine sensitization.
- To differentiate mechanisms after short (3-4 days) and long (10-14 days) withdrawal periods.
Main Methods:
- Single-unit recording in rat ventral tegmental area to assess autoreceptor sensitivity.
- In vivo microdialysis in rat nucleus accumbens to measure extracellular dopamine levels.
- Behavioral assessment of locomotor stimulant effects of d-amphetamine.
Main Results:
- Amphetamine-treated rats showed robust behavioral sensitization.
- Short withdrawal (3-4 days): Autoreceptor subsensitivity observed, but dopamine release unchanged.
- Long withdrawal (10-14 days): Autoreceptor sensitivity normalized, but amphetamine-induced dopamine release increased.
Conclusions:
- Autoreceptor subsensitivity is a transient mechanism potentially involved in early sensitization.
- Enhanced dopamine release may contribute to the persistence of sensitization after longer withdrawal periods.