Biomedical subjects
Publications and source records attributed to G Bignami.
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Higher-tier tests for the assessment of early treatment effects should be aimed at providing specific information on the behavior processes affected, rather than simply at extending the descriptive data base. The contrast between positive and negative results can be useful to point out possible mechanisms of action. For example, late prenatal oxazepam exposure of mice produced a reduction of the amphetamine hyperactivity at the end of the second postnatal week, but did not significantly affect the response to scopolamine at the end of the third week. An impairment of active locomotor avoidance was observed at the young adult stage, which contrasted with the absence or scarcity of changes in passive avoidance and extinction responding in the same go-no go tests. These changes in response-activating mechanisms appear to be in agreement with the medium- and long-term effects on CNS monoamine metabolism described in the literature. As concerns statistical analysis, dichotomous or polytomous data obtained, e.g., by the Fox battery are not yet amenable to an adequate processing, due to the shortcomings of the available nonparametric tests. By contrast, mixed-model ANOVAs can cope with complex data obtained, e.g., in activity and learning tests. However, the available checks on various assumptions (normality, homogeneity of variance, sphericity) are not valid when nested factors, block factors and repeated measures coexist. Finally, the more usual cross-fostering procedures provide adequate information on some aspects (e.g., separation of main effects of prenatal treatments from postnatal maternal effects) but not on others.(ABSTRACT TRUNCATED AT 250 WORDS)
In the rat, behavioral changes during lactation are in several ways similar to those produced by benzodiazepines (BDZ). Moreover, an increased activity at the GABA/BDZ receptor complex has been found in both conditions. We tested the hypothesis that early manipulation of this neurochemical system by prenatal BDZ exposure should affect typical responses of lactating dams, such as maternal aggression. Outbred CD-1 mice were treated with either oxazepam (15 mg/kg PO twice/day on days 12-16 of fetal life) or vehicle and fostered at birth to untreated dams. Female offspring were subsequently mated at the young-adult stage and used to assess maternal aggressive responses towards a male intruder. In a first 5-min test on postpartum day 6, the prenatal oxazepam animals showed a reduced Latency to the First Attack, a markedly enhanced frequency of several offensive scores (such as Fighting Episodes, Attacks, and Offensive Upright, On Top, and Kicking Postures), a decrease of Submissive Postures and a reduced duration of time spent lying still (Out of the Nest). The tests were repeated 48 h later after IP treatment by either chlordiazepoxide (10 mg/kg) or saline. The drug significantly enhanced locomotor activity as well as the frequency of Fighting Episodes and of Attacks, while decreasing the number of Submissive Postures and the time spent On Nest. These effects were not significantly modified by prenatal oxazepam exposure. This suggests that long-term and acute effects of benzodiazepines are produced either by changes in different regulatory systems or by different types of changes in the same system.
The positively reinforcing and activity enhancing effects of IP cocaine (0, 5, or 25 mg/kg) were assessed at three ages (14-17, 21-24, and 28-31 days) in outbred CD-1 mouse pups treated prenatally by either oxazepam (OX, 15 mg/kg PO twice/day on days 12-16 of pregnancy) or vehicle (VEH). A 4-day unbiased conditioned place preference (CPP) procedure was used with combined visual and tactile cues (white walls and wide-mesh metal floor versus black walls and narrow-mesh floor). A single 25 mg/kg cocaine dose produced CPP in both prenatal groups of 28-31 day-old mice. At the two younger ages, a significant cocaine CPP was found in prenatal OX mice but not in vehicle animals; the latter apparently developed CPP less readily than the offspring of indisturbed dams in a previous experiment. On the other hand, prenatal OX did not produce substantial changes in the developmental profile of cocaine effects on locomotor activity, consisting of a dose-related response enhancement which is much more marked at 22 and 29 days than before weaning.
CD-1 mice were continuously exposed to ozone (O3) from 6 days before the formation of breeding pairs to Day 17 of pregnancy. The concentrations used were 0, 0.2, 0.4, and 0.6 ppm; the lowest-observed-effect levels for eye irritation and respiratory function are in the range of 0.08-0.2 ppm for both humans and animals (47). Ozone failed to produce significant effects on either reproductive performance, postnatal somatic and neurobehavioral development (as assessed by a Fox test battery) or adult motor activity (including within-session habituation). In social interaction tests performed in the pre-juvenile period (23-25 days) and the juvenile period (43-45 days), social response endpoints were not modified in O3 mice, but exploration and self-grooming showed concentration dependent effects (decrease and increase, respectively). Performance at 84-98 days in an eight-arm radial maze with water reinforcement was initially impaired in O3 mice, but the results were not entirely consistent; e.g., the data failed to show a concentration dependence of the effects. Overall, the data confirm previous results of an experiment with more limited exposure [pregnancy Days 7-17 (6)] by showing that prenatal O3 exposure, even when extended to include a period before the start of pregnancy and the preimplantation phase, does not produce major or widespread somatic and neurobehavioral effects. Some of the results, however, point to subtle or borderline behavioral deficits which deserve to be considered both in further animal experiments and in the assessment of risk to developing humans.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: The aim of the study was to present the results of a citation analysis concerned with the impact of Italian researchers and institutions in psychiatry and psychology upon the international scientific community. METHOD: The analysis has been performed using a database of the Institute for Scientific Information (ISI): All scientific papers which were published between 1981 and 1998 in psychiatric and psychological journals included in the Science Citation Index (SCI) and the Social Sciences Citation Index (SSCI) were considered. The most cited Italian papers, authors and institutions are reported, as well the most frequently utilised journals. RESULTS: Publications concerned with neuropsychology, psychopharmacology and biological psychiatry were the most cited. This prevalence also affected the ranking of the most cited authors, even though, in this case, research groups in disciplines such as clinical psychology and epidemiological psychiatry appeared to be strong. The four most productive Italian Universities were characterized by the presence of both a School of Medicine and a School of Psychology. The Journal of Neurology, Neurosurgery and Psychiatry and Psychopharmacology were the most frequent vehicles of scientific communication. CONCLUSIONS: The results entail important implications for Italian research in psychology and psychiatry. On a general level, these analyses appear to be helpful for monitoring scientific production by granting agencies and for comparing different individual researchers. On a more specific level the analysis has identified the leading trends in research of Italian psychiatry and psychology.
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Repeated injection of paraoxon to pretrained rats 2 hr before avoidance sessions, at a dose causing considerable intoxication symptoms and reduction of brain acetylcholinesterase (0.125 mg/kg SC daily), induced marked performance depression followed by progressive development of tolerance. Additional groups treated either after each session (i.e., 23.5 hr before each subsequent session), or treated and not tested, showed a substantial depression when shifted to treatment 2 hr before sessions after achievement of tolerance by the animals tested from the beginning of the experiment at the time of maximal paraoxon effect. This indicates that chronic paraoxon tolerance cannot be ascribed entirely to metabolic and/or physiological changes occurring as a consequence of repeated treatment per se, but must be explained at least in part by postulating a behaviorally augmented (or "learned") component. In an additional experiment chronic paraoxon animals (0.1 mg/kg SC daily) were indistinguishable from control rats with respect to acquisition of light/go, noise-light/no go discrimination, i.e., of an active-passive avoidance task known to be highly sensitive to the disrupting (response-disinhibiting) effect of antimuscarinics. Therefore, the enhanced sensitivity to antimuscarinics in organophosphate tolerant rats, which is usually ascribed to cholinergic receptor changes, does not appear to be associated with a spontaneous "antimuscarinic-like" syndrome.