Cigarette smoking is associated with a wide variety of adverse reproductive outcomes, including increased infant mortality and decreased birth weight. Prenatal exposure to tobacco smoke, of which nicotine is a major teratogenic component, has also been linked to the acceleration of the risk for different psychiatric disorders, including conduct disorder and attention deficit hyperactivity disorder (ADHD). Whether this increased risk is influenced by the direct effects of gestational nicotine exposure on the developing fetus remains uncertain. In this study we provide experimental evidence for the effects of prenatal nicotine exposure on measures of attention and impulsivity in adult male rats. Offspring of females exposed during pregnancy to 0.06 mg/ml nicotine solution as the only source of water (daily consumption: 69.6±1.4 ml/kg; nicotine blood level: 96.0±31.9 ng/ml) had lower birth weight and delayed sensorimotor development measured by negative geotaxis, righting reflex, and grip strength. In the 5-choice serial reaction time test, adult rats showed increased numbers of anticipatory responses and omissions errors, more variable response times, and lower accuracy with evidence of delayed learning of the task demands when the 1 s stimulus duration was introduced. In contrast, prenatal nicotine exposure had no effect on exploratory locomotion or delay-discounting test. Prenatal nicotine exposure increased expression of the D5 dopamine receptor gene in the striatum, but did not change expression of other dopamine-related genes (DRD4, DAT1, NR4A2, and TH) in either the striatum or the prefrontal cortex. These data suggest a direct effect of prenatal nicotine exposure on important aspects of attention, inhibitory control, or learning later in life.
These results provide evidence of a cognitive impairment resulting from nicotine deprivation in rodents. Specifically, blockade of D(1) receptors by SCH23390 produced decrements in performance that were qualitatively similar but greater in magnitude to the alterations observed following nicotine withdrawal. Overall, assessing nicotine withdrawal in the 5-CSRTT presents an animal model that exhibits robust construct and face validity.
Delay discounting, one element which underlies decision-making, can be defined as the depreciation of the value of a reward related to the time that it takes to be released. High rates of delay discounting are found in subjects who are willing to forgo greater rewards available only after some length of time and who show a preference for smaller rewards that are available immediately. Widely used as a measure of impulsiveness, delay discounting can be evaluated using experimental tasks. The present review evaluated tasks of delay discounting, their features, measures of evaluation and anomalies, and some variables that can affect delay discounting results and applications in the study of individual and intra-individual differences.
Individual differences in nicotine effects lead to questions about appropriate experimental procedures for prenatal nicotine exposure in rodent models. The objective of this study was to develop a method for gestational studies in rats based on oral nicotine exposure, and to evaluate the neurodevelopmental effects. Female Lister hooded rats were exposed to nicotine solutions both before and during pregnancy. These females were divided into groups consuming solutions of different concentrations such that animals that initially consumed the solutions most readily were exposed to progressively higher concentrations. Offspring of these females were evaluated in a test battery measuring maturational and developmental milestones. Female rats ingested nicotine solutions at levels that provided blood nicotine concentrations of 10-60 ng/ml, at daily dose levels of 2.9-6.2 mg/kg. Solutions with concentrations below 0.06 mg/ml were well tolerated with some moderate adverse effects at the highest dose. Concentrations above 0.08 mg/ml led to a large drop in fluid consumption and body weight. Strong teratogenic effects of prenatal nicotine exposure were observed at concentrations above 0.04 mg/ml, including developmental and maturational delays shown by measures of pinnae detachment, fur appearance, incisor eruption, eye opening and righting reflex. Negative geotaxis, grip strength and weight gain were impaired and postnatal mortality was increased. This study design provides a model for the impact of prenatal exposure to nicotine at blood levels comparable with those in medium and heavy smokers. There were marked developmental and behavioural deficits induced in the offspring of nicotine-exposed female rats.
Attention-deficit hyperactivity disorder (ADHD) may be caused by genetic or environmental factors. Among environmental factors, perinatal complications are related, such as neonatal hypoxia-ischemia (HI). Thus, the aim of this study was to investigate whether HI contributes to the development of characteristics related to ADHD in adult rats, and to correlate the behavioral results with brain damage volume. Male Wistar rats were divided into 2 groups: HI and control. The HI procedure consisted of a permanent occlusion of the right common carotid artery followed by a period of hypoxia (90 min; 8% O₂ and 92% N₂) on the 7th postnatal day. Two months later, animals were evaluated in the open field test during a single 5-min session, and in the 5-choice serial reaction time task (5-CSRTT), over 25 weeks. Our results demonstrated that animals submitted to HI manifest cognitive impairments in task acquisition, deficits in sustained attention, and increases in impulsivity and compulsivity in response to task manipulation in the 5-CSRTT. Locomotor activity observed in open field did not differ between groups. Moreover, brain volume loss in the total hemisphere, cerebral cortex, white matter, hippocampus, and striatum were observed in HI animals, especially on the side ipsilateral to the lesion. From these results, we can infer that neonatal HI is an environmental factor that could contribute to the development of behavioral characteristics observed in ADHD that are associated with general brain atrophy.
The improvements in performance produced by nicotine did not resemble the effect of increased motivation, but some effects of amphetamine resembled those of reducing the level of motivation for food. Motivational levels did not confound assessments of the attentional effects of the drugs in terms of response accuracy.
Lisiane Bizarro Araujo ae RESUMO. A avaliação em psicoterapia constitui um desafio para pesquisadores e clínicos. Esta revisão crítica sobre possibilidades de avaliação de processo e resultado em psicoterapia estimula o debate sobre a incorporação da prática clínica baseada em evidências como meio de obter informação científica quanto à adequação da intervenção terapêutica. Através de estudos sobre a avaliação do processo psicoterápico é possível elucidar conexões entre o tratamento psicológico e seus efeitos. Desta forma, torna-se possível identificar mecanismos de ação terapêutica e estratégias que podem potencializar o processo de mudança. Este debate poderá favorecer a aproximação entre pesquisa e prática clínica. Identificar variáveis das quais pode depender a eficácia/efetividade do tratamento psicoterápico repercute no aprimoramento do treinamento de psicólogos em formação e no delineamento de intervenções custo-efetivas. Palavras-chave: Tratamento psicoterápico, eficácia e efetividade, prática baseada em evidência.
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