Effect of Amphetamine on the Metabolism and Incorporation of [&lt;sup&gt;3&lt;/sup&gt;H]-Thymidine into DNA of Developing Rat Brain

Béndek, G.; Hahn, Z.

doi:10.1159/000112741

Cited by 7 publications

(2 citation statements)

References 13 publications

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“…proliferation of neural cells (Huot, 1974;Bendek and Hahn, 1981;Miller and Nowakowski, 1991;Stiene-Martin and Hauser, 1993;Levin and Slotkin, 1998). However, the present study, to our knowledge, is the first that demonstrates the ability of the developing brain to support a significant compensatory burst of proliferative activity following suppression of cell division by one such drug.…”

Section: Discussionmentioning

confidence: 63%

Effect of Cocaine on Cell Proliferation in the Cerebral Wall of Monkey Fetuses

Lidow

Song²

2001

Cerebral Cortex

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This study examined the effect of cocaine on cell proliferation in the fetal monkey cerebral wall. Pregnant monkeys received cocaine daily (10 mg/kg, orally, in fruit treats, at 07.00 h and 19.00 h) beginning on the 40th day of pregnancy (E40). The control animals received fruit treats only. One set of monkeys was used to examine the state of cell proliferation in the fetal cerebral wall at peak cocaine levels. These animals were injected with [(3)H]thymidine intravenously on E73, 1.5 h after the morning drug or placebo administration. Another set of monkeys was used to determine the state of cell proliferation after cocaine concentration declined to ineffective levels. These animals were injected with [(3)H]thymidine on the same day of pregnancy 10 h after the treatment. Cesarean sections were performed 40 min after the radioisotope injection. The right hemispheres were processed for autoradiography. The left hemispheres were used for biochemical analysis of the radioisotope incorporation into DNA. The third set of monkeys was used to determine whether chronic cocaine treatment extends the timing of neocortical neuronogenesis. These monkeys received their final cocaine treatment on E102 (the last day of normal neocortical neuronogenesis) and were injected with [(3)H]thymidine 24 h later. On E113, the fetal brains were processed for emulsion autoradiography. We found a significant decrease in the density of [(3)H]thymidine-labeled cells and in the levels of this radioisotope incorporation into DNA in the fetal cerebral wall 1.5 h after cocaine administration. In contrast, 10 h after cocaine administration we detected a significantly elevated density of radiolabeled cells, and abnormally high levels of [(3)H]thymidine incorporation into DNA. This suggests that chronic intermittent administration of cocaine results in significant periodic fluctuations in cell production within the fetal cortical proliferative zones. We detected no cocaine-induced extension in neocortical neuronogenesis.

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Section: Discussionmentioning

confidence: 63%

Effect of Cocaine on Cell Proliferation in the Cerebral Wall of Monkey Fetuses

Lidow

Song²

2001

Cerebral Cortex

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“…Probably the most important difference between adult administration of psychostimulants and the results of the present study is the period of development when MA was administered. For instance, neonatal amphetamine exposure has been shown to produce a reduction in synapses in the hippocampus that appears to be related to decreased cell proliferation (Bendek & Hahn, 1981). Neonatal drug administration, especially during the time period that MA was administered in the present study, may affect synaptogenesis and result in long‐term changes in brain function.…”

Section: Discussionmentioning

confidence: 99%

Neonatal methamphetamine administration induces region‐specific long‐term neuronal morphological changes in the rat hippocampus, nucleus accumbens and parietal cortex

Williams¹,

Brown²,

Vorhees³

2004

Eur J of Neuroscience

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Previous studies have demonstrated that rats exposed to methamphetamine (MA) during the neonatal period display deficits in spatial learning and memory. The underlying correlates are unknown; therefore, this study was devised to determine whether neuronal changes occur in the dentate gyrus (DG), nucleus accumbens (NAcc) and cortex of adult rats exposed to 10 mg/kg MA administered four times daily from P11-20 using Golgi-Cox staining [Gibb, R. & Kolb, B. (1998) J. Neurosci. Meth., 79, 1-4]. The DG and NAcc demonstrated a decrease in the number of spines per neuron and the NAcc showed an associated decrease in dendritic length. Selective changes in cortex were observed because increased dendritic length in the parietal cortex occurred with no change in the number of spines, and no differences were noted for either dendritic length or spines in the medial frontal cortex. The data suggest a potential cause for the learning and memory deficits induced by neonatal MA exposure; however, the underlying mechanism that produces these neuronal changes is unknown.

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