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Neurobiochemical changes in tardive dyskinesia.
L M Gunne1, J E Häggström, P Johansson
1Psychiatric Research Center, Ulleråker Hospital, Uppsala, Sweden.
L'Encephale
|September 1, 1988
Summary
Altered levels of gamma-aminobutyric acid (GABA) in the substantia nigra may cause dyskinetic movements. Long-term neuroleptic treatment may lead to withdrawal dyskinesia due to changes in GABA neurons.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- GABAergic system's role in motor control.
- Dyskinetic movements associated with neuroleptic treatment.
Purpose of the Study:
- Investigate the role of nigral GABA in dyskinesia.
- Hypothesize mechanisms of neuroleptic-induced dyskinesia.
Main Methods:
- Intranigral infusion of GABA agonists and antagonists in rats.
- Assessment of nigral GAD activity.
- Measurement of striatal and nigral substance P levels.
Main Results:
- GABA agonists induced stereotyped behaviors.
- GABA antagonists induced vacuous chewing movements.
- Reduced nigral GAD activity linked to irreversible dyskinesia.
Conclusions:
- Nigral GABAergic system modulation is implicated in dyskinesia.
- Neuroleptic treatment may alter striatonigral GABA neurons, leading to withdrawal dyskinesia.
- Changes in the GABA system correlate with substance P alterations.