Studies on the long-term developmental effects of in utero cocaine exposure are few and the small number of studies published do not consider the postnatal environment. The present investigation was conducted to quantify the role that postnatal environment played compared to prenatal exposure. Four
Effects of prenatal cocaine exposure upon postnatal development of neostriatal dopaminergic function
โ Scribed by Catherine A. Leslie; Matthew W. Robertson; Anthony B. Jung; Jennifer Liebermann; James P. Bennett Jr.
- Publisher
- John Wiley and Sons
- Year
- 1994
- Tongue
- English
- Weight
- 720 KB
- Volume
- 17
- Category
- Article
- ISSN
- 0887-4476
No coin nor oath required. For personal study only.
โฆ Synopsis
Pregnant rats were injected twice daily with 20 mgkg cocaine (or saline) from gestational day 10 to parturition. Brains from offspring were examined with quantitative receptor autoradiography ED1 receptor (DlR), D2 receptor (D2R) and dopamine transporter (DAT)] and quantitative in situ hybridization [DlR mRNA, D2R mRNA, preproenkephalin (PPE) mRNA1 for markers of neostriatal dopaminergic function. Prenatal cocaine exposure did not alter postnatal development of striatal D1R sites, but D1R mRNA levels were reduced by a third at days 14 and 35. D2R sites were increased over control in lateral striatum by day 6, and remained elevated through postnatal day 35. Total D2R mRNA was increased over control in both medial and lateral striatum at 7 and 14 days but was equal to control at 35 days. Prenatal cocaine exposure increased DAT density at postnatal days 1 through 5, but reduced it at days 14 and 35; PPE mRNA expression was reduced at days 7,14 and 35. Many of these results are similar to those found in experimental animals and humans following cocaine withdrawal.
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