Effects of prenatal exposure to alcohol on activity, anxiety, motor coordination, and memory in young adult Wistar rats.

The objective of the present study was to examine the effects of prenatal exposure to ethanol on motor performance, emotionality, learning and memory in young-adult, male Wistar rats. Alcohol was delivered to the pregnant dams intragastrically, throughout gestation days (GD) 7-20, at the dose of 6 g/kg/day resulting in the peak blood alcohol concentration (BAC) of 350 mg/dl as assessed on GD 20. Isocaloric intubation and untreated control groups were included. Alcohol exposed rats were not impaired in the rotarod/accelerod tests. Their behavior in the open field and plus maze suggested increased neophobia. Hyperactivity was not observed. In the spatial-navigation task in the water maze, by the middle of the training, fetal alcohol rats showed a tendency towards a slower place acquisition compared to controls, but statistical analysis of the data did not yield between-group differences significant. Towards the end of the training, all rats reached a similar performance level. No detectable between-group differences were noted either in memory retention after a delay, in reversal learning, or in working memory task. Our findings demonstrate that the adverse behavioral effects of a binge-like alcohol administration during half of the first and throughout the second trimester equivalent are difficult to be disclosed in young-adult male Wistar rats. The possible reasons of the lack of significant behavioral deficits in the fetal-alcohol rats observed in the present study are discussed.

The gene encoding polyneuridine aldehyde esterase of monoterpenoid indole alkaloid biosynthesis in plants is an ortholog of the alpha/betahydrolase super family.

The biosynthesis of the anti-arrhythmic alkaloid ajmaline is catalysed by more than 10 specific enzymes. In this multistep process polyneuridine aldehyde esterase (PNAE) catalyses a central reaction by transforming polyneuridine aldehyde into epi-vellosimine, which is the immediate precursor for the synthesis of the ajmalane skeleton. PNAE was purified from cell suspension cultures of Rauvolfia serpentina. The N-terminal sequence and endoproteinase LysC fragments of the purified protein were used for primer design and for the amplification of specific PCR products leading to the isolation of PNAE-encoding cDNA from a R. serpentina library. The PNAE cDNA was fused with a C-terminal His-tag, expressed in Escherichia coli and purified to homogeneity using Ni-affinity chromatography. The pure enzyme shows extraordinary substrate specificity, completely different to other esterases. Sequence alignments indicate that PNAE is a new member of the alpha/beta hydrolase super family.

Modification of avoidance responding by amphetamine and dopamine receptor antagonists.

This study was designed to investigate the effects of preferential D1 (SCH 23390) and D2 (haloperidol) dopamine (DA) receptor antagonists and their interaction with low-dose (1 mg kg) D-amphetamine during the acquisition of two-way shuttle avoidance in rats. In the course of training, the dissociation of drug effects on response latencies was observed. Haloperidol (0.05 mg/kg) caused significant reduction in the frequency of short-latency avoidance responses that was only partially compensated by concomitant amphetamine administration. In contrast, SCH 2339 (0.025 mg/kg) did not affect the frequency of short-latency responses but lowered probability of avoidances emitted toward the end of 5 s interval between the onsets of conditoned and unconditioned stimuli (CS-UCS interval). Amphetamine compensated for this impairment by increasing frequency of short-latency avoidances well above the control level. These results argue for different nature of short- and long-latency avoidance responses, and suggest involvement of DA D2 receptors in the process of response initiation facilitated by amphetamine. Interestingly, a profound behavioral breakdown was observed under higher dose of SCH 23390 (0.05 mg/kg), but only when applied together with amphetamine. The latter result seems to confirm the notion that behavioral output of dopaminergic transmission may depend more on the balance between D1 and D2 receptors than on the independent modulation of particular receptor system.