Prenatal Ethanol Exposure on Reactivity of Dopamine Receptor

· TGI - Gestation

This study represents the first functional demonstration that prenatal exposure to a relatively high-dose EtOH leads to the persistent emergence of abnormal LTP instead of LTD via altering D1R and D2R functions in the DL striatum of young male rat offspring.

To support this conclusion authors provided the major observations as follows.

First, PD 30 or PD 40 control offspring expressed LTD, while the same-aged EtOH offspring showed LTP instead of LTD.

Second, in comparison with control offspring, EtOH offspring showed a D1R-mediated potentiation of basal synaptic transmission through increasing presynaptic glutamate release.

Third, D1R antagonist SCH23390 blocked the induction of LTP in EtOH-exposed offspring.

Fourth, D2R agonist quinpirole could rescue the D1R- and mGluR-dependent LTD induction in EtOH-exposed offspring.

The present study found that LTP was induced in the DL striatum of PD 15 control rats, while LTD was elicited in PD 30 or PD 40 control rats by the same HFS protocol. Consistent with our results, Partridge et al. (2000) have reported that in the developing rat striatum the conversion from LTP to LTD occurs during the postnatal third week [21]. Tepper and associates (1998) have shown that the third week of postnatal maturation in rat striatum is an intense period of electrophysiological and morphological change [22]. This discriminating pattern of synaptic development may give rise to functional differences in integrating afferent input during this stage of striatal development. LTP is a predominant form of plasticity when synapses are beginning to come on-line in striatum [21]. The emergence of LTD later in development is thought to help to fine-tune synaptic efficacy to refine movement and behavioral sequencing [16][42]. This is in line with the fact that LTD predominates during a time period when movement patterns are changing from more neonatal to more adult-like[21]. LTP appearing in the early development has been considered to depend on NMDAr activation[21]. Studies in the review by Costa et al. (2000) have shown prenatal EtOH exposure led to a decrease in either NMDAR expression or function in various regions of the brain [43]. Therefore, we speculated the impairment of LTP in PD15 EtOH-exposed offspring might be the consequence of NMDAr down-regulation. Furthermore, in the present study, prenatal EtOH exposure resulted in LTP but not LTD of synaptic plasticity at PD 30 even if at the older age, when LTD was generally induced in the same-aged control rats. The loss of LTD in the mature DL striatum of adult animals has been reported to be accompanied by the motor abnormality [44]. This observation, together with the findings presented here, suggests that this abnormal synaptic plasticity in the DL striatum might be the important mechanism underlying movement disorders caused by in utero exposure to EtOH.

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