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This paper describes an educational card game designed to help high school students (grade 10, 15−16 years old) understand, as opposed to memorize, the periodic table. The game may also be used to identify different chemical elements found in daily life objects. As an additional value, students learn the names and symbols of the displayed elements and may recognize typical compounds formed by them. The game is well received by students and engages them more intensely and for a longer period than the other activities with which it is compared.

The study reported here was conducted to investigate the perceptions of high school students on the use of educational games as a tool for teaching the periodic table of elements in a chemistry class in Spain. The 127 students who participated in this study came from six different classes in grade 10 (15−16 years old). The students' perceptions of the usefulness of a series of 13 specifically designed games as educational tools was assessed. This was achieved in a survey containing 13 items using a 5point Likert-type scale, which was completed by the students at the end of the unit. The results of the study reveal that the students who participated had positive perceptions regarding the use of educational games. Students usually found the educational games to be an interesting tool to make the learning process more enjoyable. It can be observed that the students' perceptions of the games are more favorable than for other class tasks used in the control group. The opinions indicate that games also stimulated their participation in classroom activities. Moreover, educational games are considered to help students better understand some of the main concepts presented and discussed throughout the unit.

The purpose of this study was to examine the time course effects of extinction of cocaine self-administration behavior on proenkephalin (PENK) gene expression in caudateputamen nucleus (ST), nucleus accumbens (Acc), olfactory tubercle (Tu), piriform cortex (Pir), ventromedial hypothalamic nucleus (VMN), and central amygdala (Ce) as measured by in situ hybridization histochemistry. Seventy-two littermate male Lewis rats were randomly assigned in triads to one of three conditions: (1) contingent intravenous self-administration of 1 mg/kg/injection of cocaine (CONT); (2) noncontingent injections of either 1 mg/kg/injection of cocaine (NONCONT); or (3) saline yoked (SALINE) to the intake of the self-administering subject. The self-administering rats were trained to selfadminister cocaine under a FR5 schedule of reinforcement for a minimum of 3 weeks. After stable baseline levels of drug intake had been reached, saline was substituted for drug. Following this first extinction period, cocaine selfadministration was reinstated for an additional period of 2 weeks. Immediately after cessation of the last session of cocaine self-administration (day 0) and 1-, 5-, and 10-day after the second extinction period, animal brains in eachCocaine abuse and dependence remain major public health and social problems. Cocaine abuse results from a complex interplay of behavioral, pharmacological, and neurobiological determinants. The main pharmacological effect of cocaine is to inhibit the reuptake of monoamines dopamine, norepinephrine, and serotonin at presynaptic terminals. As a consequence of these ac- (Hadfield et al. 1980;Heikkila et al. 1975;Ross and Renyi 1969). The major behavioral effect of cocaine is a psychomotor stimulant action with reinforcing addictive properties. This behavioral effect is produced primarily by inhibition of dopamine uptake, thereby increasing extracellular concentrations of released dopamine (Ritz et al. 1987; for a review see Kuhar et al. 1991;Spanagel and Weiss 1999). However, a recent study using mice lacking dopamine transporter proposed other mechanisms, such as increases in serotonin transmission, may mediate the reinforcing effects of cocaine (Rocha et al. 1998).Several studies have shown that cocaine also affects the expression of opioid peptides and opioid receptors. For example, chronic cocaine administration leads to increases in circulating ␤ -endorphin levels (Moldow and Fischman 1987), striatal preprodynorphin mRNA levels (Hurd et al. 1992;Daunais et al. 1993;Daunais and McGinty, 1995;Spangler et al. 1993Spangler et al. , 1996Spangler et al. , 1997, and striatonigral dynorphin content (Sivam 1989;Smiley et al. 1990) in rats and to decreases in preproenkephalin mRNA levels in rhesus monkeys (Daunais et al. 1997) and humans (Hurd and Herkenham 1993). Repeated administration of cocaine can also regulate the activity of opioid receptors in discrete brain regions of rats. Indeed, it has been shown that 2 weeks of either continuous administration of cocaine via subcutaneously implanted osmotic...

This study examined behavioural signs that occur during tolerance development to cannabinoid treatment and hormonal and gene expression alterations induced by spontaneous cannabinoid withdrawal in mice. Tolerance to CP-55,940 treatment developed for hypothermia, ambulatory and exploratory locomotor activity. Cessation of cannabinoid treatment resulted in a behavioural withdrawal syndrome characterized by a pronounced increase in ambulatory activity and rearings. Corticosterone plasma concentrations dramatically increased 24 and 72 h after cessation of cannabinoid treatment. Similarly, an increase (40%) in cannabinoid [ 35 S]GTPcS binding autoradiography was detected on days 1 and 3 of abstinence. Spontaneous cannabinoid withdrawal produced time-related significant alterations in gene transcription: (i) decreased (20%) tyrosine hydroxylase (TH) mRNA levels in the ventral tegmental area and increased (50%) in substantia nigra; (ii) increased proenkephalin (PENK) gene expression more than 100% in caudate-putamen, nucleus accumbens, olfactory tubercle and piriform cortex; (iii) increased (20-40%) pro-opiomelanocortin (POMC) gene expression in the arcuate nucleus of the hypothalamus. These results suggest that spontaneous cannabinoid withdrawal occur after cessation of CP-55,940 treatment. This 'syndrome' includes behavioural, hormonal and gene transcription alterations that seems to be part of the regulation of neuronal plasticity induced by spontaneous cannabinoid withdrawal. Keywords: cannabinoid, opioid, proenkephalin, pro-opiomelanocortin, tyrosine hydroxilase, withdrawal. A number of studies using D 9 -tetrahydrocannabinol (THC) or cannabinoid synthetic derivatives have contributed in the last decade to a substantial progress in understanding the pharmacology and neurobiological mechanisms produced by cannabinoid receptor activation. This significant advance in cannabinoid pharmacology has been driven in part by an increasing interest of medical societies and governments from European and North American countries to consider cannabinoid pharmaceutical preparations as potential therapeutic drugs in a variety of clinical conditions (British

Em certas situações, a Didática das Ciências transmite como mitos algumas crenças que não estão suficientemente sustentadas pela investigação que ela própria produz. Este artigo mostra dois desses mitos relacionados com os motivos que se costumam apontar para incluir a Natureza da Ciência no ensino das ciências, como sejam a suposta relação entre a prática docente e as crenças sobre a Natureza da Ciência, e a crença de que a sua compreensão é um fator chave na hora de tomar melhores decisões cívicas em questões tecnocientíficas de interesse social. A análise que se apresenta realizou-se mediante a revisão de diversos resultados de investigações procedentes da própria Didática das Ciências e também da Psicologia das Decisões. A conclusão aponta para considerar que outros fatores influenciam mais, tornando muito menos lineares essas hipotéticas relações do que alguns especialistas pensam e mais complexa a problemática abordada.

The aim of the present work was to study the time course effects in levels of mRNA encoding N‐methyl‐d‐aspartate receptor subunit 1 (NMDAR1) after long‐term cocaine self‐administration (1 mg/kg/ injection) and its extinction using a yoked‐box procedure. NMDAR1 content was measured by quantitative in situ hybridization histochemistry in prefrontal cortex, caudate‐putamen, nucleus accumbens, olfactory tubercle, and piriform cortex immediately after cessation of the last session of cocaine self‐administration (Day 0) and 1, 5, and 10 days after the extinction period. The results show that long‐term cocaine self‐administration and its extinction alter NMDAR1 gene expression in these forebrain regions, and that the changes depend upon the brain region examined and the type of cocaine administration (contingent, noncontingent, and saline). Compared to saline and noncontingent cocaine administration, contingent cocaine produced an up‐regulation in NMDAR1 gene expression on Day 0 in all the brain regions analyzed. NMDAR1 levels of contingent animals decreased progressively in the absence of cocaine, and the decrement persisted 10 days after the extinction of cocaine self‐administration behavior in all the forebrain areas, with the exception of olfactory tubercle. In contrast, noncontingent cocaine administration did not produce any change in NMDAR1 gene expression on Day 0, and extinction resulted in an increase of NMDAR1 mRNA content on Days 1 and 5 and returned to control (saline) values on Day 10. These results suggest that an interaction between environmental stimuli and the pharmacological action of cocaine during drug self‐administration and its extinction may represent an important factor in the regulation of cocaine effects on NMDAR1 gene expression.