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Dopamine, serotonin and tachykinin in self-injurious behavior
1Department of Pharmacology & Toxicology, Indiana University School of Medicine, Gary 46408, USA.
Life Sciences
|May 24, 1996
Summary
Self-injurious behavior (SIB) involves dopamine, serotonin, and tachykinin systems. Reduced dopamine and increased serotonin may precede SIB, which is then sustained by dopamine receptor-linked tachykinin activation.
Area of Science:
- Neurobiology
- Neuropharmacology
- Behavioral Neuroscience
Background:
- The neurobiological underpinnings of self-injurious behavior (SIB) in Lesch-Nyhan syndrome and other neuropsychiatric disorders are not fully understood.
- Existing research points to complex interactions within neurotransmitter systems.
Purpose of the Study:
- To review recent findings on SIB induced by the dopamine (DA) uptake inhibitor GBR-12909 (GBR).
- To compare neurochemical data on SIB in neonatal 6-hydroxydopamine (6OHDA) lesioned rats.
Main Methods:
- Administration of GBR-12909 to adult rats and assessment of neurochemical changes and SIB.
- Induction of SIB in neonatal 6OHDA lesioned rats using DA agonists.
- Analysis of striatal dopamine, serotonin turnover, and tachykinin (substance P, neurokinin A) transcription and biosynthesis.
Main Results:
- GBR-induced SIB correlated with reduced striatal DA, increased serotonin turnover, and enhanced tachykinin biosynthesis.
- GBR-induced SIB was blocked by dopaminergic lesions or D1/D2 antagonists.
- In neonatal 6OHDA lesioned rats, DA agonists precipitated SIB via D1 receptor activation, linked to tachykinin induction.
Conclusions:
- A substantial reduction in DA and increased serotonin turnover may create conditions conducive to SIB.
- Dopamine receptor-mediated activation of tachykinin neurons likely sustains SIB.
- A dynamic interplay between DA, serotonin, and tachykinin systems in the basal ganglia influences SIB.