Synaptic reorganization in the hippocampal formation of alcohol-fed rats may compensate for functional deficits related to neuronal loss.

We have examined the behavioral and neuroanatomical effects of long-term alcohol intake in rats ingesting a 20% solution of ethanol for 30 weeks. Previous studies have shown that this treatment provokes neuronal degeneration in the hippocampal formation, which occurs in parallel with remodeling processes. Spatial reference and working memory of alcohol-fed rats were evaluated during last 4 weeks of treatment by comparison of their performance with age-matched controls on the Morris water maze. Alcohol consumption did not affect the performance of rats in the reference memory task as indicated by the measures derived from the acquisition trials and from the probe-trial, which were highly similar for alcohol-fed and control animals. Also, performance in the working memory task was not significantly altered in alcohol-treated animals. No treatment-related changes in swim speed or impairments of sensorimotor abilities, tested in the visible platform task, were detected. Stereological methods were applied to evaluate the damage inflicted by alcohol intake in the structure of the hippocampal formation. In the alcohol-treated animals, there was a noticeable cell loss in the granular layer of the dentate gyrus (10%), and in CA3 (18%) and CA1 (19%) hippocampal subdivisions. In spite of the neuronal loss, the total number of synapses between mossy fibers and CA3 pyramids was unaffected by alcohol treatment suggesting that new synaptic contacts were formed between the surviving neurons. We show that, regardless the marked hippocampal cell loss in rats exposed to chronic alcohol intake, the reorganization that takes place at the synaptic level may alleviate the expected functional deficits.     

Acute and chronic ethanol intake: Effects on spatial and non-spatial memory in rats

Abusive alcohol consumption produces neuronal damage and biochemical alterations in the mammal brain followed by cognitive disturbances. In this work rats receiving chronic and acute alcohol intake were evaluated in a spontaneous delayed non-matching to sample/position test. Chronic alcohol-treated rats had free access to an aqueous ethanol solution as the only available liquid source from the postnatal day 21 to the end of experiment (postnatal day 90). Acute alcoholic animals received an injection of 2 g/kg ethanol solution once per week. Subjects were evaluated in two tests (object recognition and spatial recognition) based on the spontaneous delayed non-matching to sample or to position paradigm using delays of 1 min, 15 min and 60 min. Results showed that chronic and acute alcohol intake impairs the rats' performance in both tests. Moreover, chronic alcohol-treated rats were more altered than acute treated animals in both tasks. Our results support the idea that chronic and acute alcohol administration during postnatal development caused widespread brain damage resulting in behavioral disturbances and learning disabilities.     

Intermittent binge alcohol exposure during the periadolescent period induces spatial working memory deficits in young adult rats

Human and animal studies suggest adolescence is a period of heightened sensitivity to adverse cognitive sequelae of alcohol exposure. The present study assessed the effects of intermittent binge ethanol intoxication during the periadolescent period of Wistar rats on subsequent performance in a Morris water maze spatial navigation task. On postnatal days 32-56, rats were exposed to ethanol or air 3 days/week via vapor inhalation chambers. Acquisition of spatial navigation was assessed beginning 5 days after the final day of exposure, with 3 days of training in the Morris Water maze (four trials per day spaced at 90-s intertrial intervals [ITIs]). Rats were placed into the water maze at one of four positions along the perimeter, with a different release position to begin each trial. A probe trial assessed retention of platform location on the day after the final set of training trials. Four days after this probe trial, rats entered a working memory phase in which the platform was in a new location each day and a variable ITI of 1, 2, or 4h was inserted between Trials 1 and 2; Trials 3 and 4 followed at 90-s intervals after Trial 2 on each day. The "savings" in latency to find the platform and distance traveled before finding it from Trial 1 to Trial 2 on each day served as an index of working memory. Ethanol-exposed rats showed similar acquisition of spatial navigation as control rats during training, as well as similar retention of platform location during the probe trial. However, rats exposed to average blood alcohol level (BAL) >200mg% showed accelerated forgetting, with decreased retention of platform location at the 2-h ITI (P<.05), compared to control rats. Therefore, a 4-week history of intermittent ethanol exposure at BAL in excess of 200mg% during periadolescence led to a working memory deficit in young adult rats, demonstrated by accelerated forgetting of novel information. These behavioral data are consistent with findings from adolescent human studies, indicating that binge-style alcohol exposure during the periadolescent stage of development is associated with deficits in retention of information.     

Deficits in trace fear conditioning in a rat model of fetal alcohol exposure: dose–response and timing effects

In humans, prenatal alcohol exposure can result in significant impairments in several types of learning and memory, including declarative and spatial memory. Animal models have been useful for confirming that many of the observed effects are the result of alcohol exposure, and not secondary to poor maternal nutrition or adverse home environments. Wagner and Hunt (2006) reported that rats exposed to ethanol during the neonatal period (postnatal days [PDs] 4–9) exhibited impaired trace fear conditioning when trained as adolescents, but were unaffected in delay fear conditioning. The present series of three experiments represent a more detailed analysis of ethanol-induced deficits in trace conditioning. In Experiment 1, the dose of ethanol given to neonates was varied (3.0, 4.0, or 5.0 g/kg/day). There was a dose-dependent reduction in trace conditioning, with the poorest performance observed in animals treated with the highest dose. In Experiment 2, it was found that the impairment in trace conditioning resulting from neonatal ethanol exposure was dependent on the duration of the trace interval used for training; less learning was evident in ethanol-exposed animals trained with longer trace interval durations. These results confirm other reports of delay-dependent memory deficits. Finally, Experiment 3 determined that ethanol exposure limited to the first half of the neonatal period (PDs 4–6) was more detrimental to later trace conditioning than exposure during the second half (PDs 7–9). These results support the hypothesis that trace-conditioning impairments resulting from early ethanol exposure are due to the drug's teratogenic effects on the developing hippocampus, as the findings parallel those observed in animals with discrete hippocampal lesions. Comparisons between delay and trace fear-conditioning performance in animals exposed to ethanol during the brain growth spurt provide a model system to study both selective learning impairments and possible treatment approaches for humans with fetal alcohol spectrum disorders.     

Neonatal alcohol impairs the context preexposure facilitation effect in juvenile rats: Dose-response and post-training consolidation effects

Alcohol exposure on postnatal days (PND) 4-9 in the rat adversely affects hippocampal anatomy and function and impairs performance on a variety of hippocampus-dependent tasks. Exposure during this developmental window reveals a linear relationship between alcohol dose and spatial learning impairment in the context preexposure facilitation effect (CPFE), a hippocampus-dependent variant of contextual fear conditioning. The purpose of the current report was to examine the effect of a range of alcohol doses administered during a narrower window, PND7-9, than previously reported (Experiment 1) and to begin to determine which memory processes involved in this task are impaired by developmental alcohol exposure (Experiment 2). In Experiment 1, rats pups received a single day binge alcohol dose of either 2.75, 4.00, 5.25 g/kg/day or were sham-intubated (SI) from PND7-9. Conditioned freezing during the test day was evident in all dosing groups, except for Group 5.25 g, indicating no graded dose-related behavioral deficits with alcohol exposure limited to PND7-9. In Experiment 2, rat pups were exposed to the highest effective dose from Experiment 1 (5.25 g/kg/day) or were sham intubated over PND7-9. During training, rats remained in the conditioning context for 5-min following immediate shock delivery. During this test of post-shock freezing, both SI and alcohol-exposed rats given prior exposure to the conditioning context showed comparable freezing levels. Since alcohol-exposed rats showed normal post-shock freezing, deficits by these rats on the test day likely reflect a failure to consolidate or retrieve a context-shock association, rather than a deficit in hippocampal conjunctive processes (consolidation, pattern completion) that occur prior to shock on the training day. These findings illustrate the value of the CPFE for characterizing the separable memory processes that are impaired by neonatal alcohol exposure in this task.     

Effects of postnatal protein malnutrition on learning and memory procedures

Protein malnutrition induces structural, neurochemical and functional changes in the central nervous system leading to alterations in cognitive and behavioral development of rats. The aim of this work was to investigate the effects of postnatal protein malnutrition on learning and memory tasks. Previously malnourished (6% protein) and well-nourished rats (16% protein) were tested in three experiments: working memory tasks in the Morris water maze (Experiment I), recognition memory of objects (Experiment II), and working memory in the water T-maze (Experiment III). The results showed higher escape latencies in malnourished animals in Experiment I, lower recognition indexes of malnourished animals in Experiment II, and no differences due to diet in Experiment III. It is suggested that protein malnutrition imposed on early life of rats can produce impairments on both working memory in the Morris maze and recognition memory in the open field tests.     

Effects of different exercise protocols on ethanol-induced spatial memory impairment in adult male rats

Chronic ethanol consumption is often accompanied by numerous cognitive deficits and may lead to long-lasting impairments in spatial learning and memory. The aim of the present study was to evaluate the therapeutic potential of regular treadmill exercise on hippocampal-dependent memory in ethanol-treated rats. Spatial memory was tested in a Morris Water Maze task. Adult male Wistar rats were exposed to ethanol (4 g/kg, 20% v/v for 4 weeks) and effects of three exercise protocols (pre-ethanol, post-ethanol and pre-to-post-ethanol treatment) were examined. Results showed that ethanol exposure resulted in longer escape latencies during the acquisition phase of the Morris Water Maze task. Moreover, all three exercise protocols significantly decreased the latency to locate the hidden platform. During the probe trial, ethanol led to decreased time spent in the target quadrant. In contrast, performance on the probe trial was significantly better in the rats that had done the post- and pre-to-post-ethanol, but not pre-ethanol, exercises. These findings suggest that treadmill running can attenuate the adverse effects of chronic ethanol exposure on spatial memory, and may serve as a non-pharmacological alcohol abuse treatment.     

Early protein malnutrition changes learning and memory in spaced but not in condensed trials in the Morris water-maze

Early protein malnutrition induces structural, neurochemical and functional changes in the central nervous system leading to alterations in cognitive and behavioral development of rats. The aim of the present study was to investigate the effects of protein malnutrition during lactation on acquisition and retention of spatial information using different training procedures (spaced x condensed trials). Rats treated with 16% (well-nourished) or 6% (malnourished) protein diets during the lactation phase and nutritionally recovered until 70 days of age were tested in the Morris water-maze in procedures of 1 trial/day (spaced trials), 4, 8, 12 trials/day (intermediate density) and 24 trials/day (condensed trials), completing 24 trials at the end of training. Seven and 28 days after the training the animals were tested again in just one trial to assess long-term memory. The results showed that protein malnutrition caused deficits on the spatial learning and memory in spaced but not in intermediate and condensed trials procedure. Seven and 28 days after the training there was an increase in the latency to find the platform but only malnourished animals submitted to 1 trial/day had significantly higher latency as compared with well-nourished controls. One of the possible hypotheses is that the effect protein malnutrition only in the procedure of spaced trials could be due to deficits in memory consolidation. It is suggested that these deficits can be the result of alterations produced by protein malnutrition in the hippocampal formation or in long-lasting emotional and/or motivational aspects of the rat's behavior.     

Effects of postnatal protein malnutrition on learning and memory procedures

Abstract

Protein malnutrition induces structural, neurochemical and functional changes in the central nervous system leading to alterations in cognitive and behavioral development of rats. The aim of this work was to investigate the effects of postnatal protein malnutrition on learning and memory tasks. Previously malnourished (6% protein) and well-nourished rats (16% protein) were tested in three experiments: working memory tasks in the Morris water maze (Experiment I), recognition memory of objects (Experiment II), and working memory in the water T-maze (Experiment III). The results showed higher escape latencies in malnourished animals in Experiment I, lower recognition indexes of malnourished animals in Experiment II, and no differences due to diet in Experiment III. It is suggested that protein malnutrition imposed on early life of rats can produce impairments on both working memory in the Morris maze and recognition memory in the open field tests.     

Effects of scopolamine on spontaneous alternation and shuttle avoidance in rats exposed to alcohol in utero

The behavioral effects of the anticholinergic scopolamine were examined in rats exposed to alcohol prenatally. Pregnant Long-Evans rats received isocaloric liquid diets containing either 35% or 0% ethanol-derived calories on Days 6-20 of gestation. A pair-feeding procedure was used, and a lab chow control group was also included. In Experiment 1, adult offspring were tested on a spontaneous alternation task following 1 mg/kg scopolamine or saline. Independent of prenatal treatment, scopolamine caused an increase in the number of trials to alternate. In Experiment 2, offspring were tested on a two-way shuttle avoidance learning task following a 1 mg/kg injection of scopolamine or methylscopolamine. Alcohol-exposed animals injected with methylscopolamine made fewer avoidances than controls on the second day of testing while treatment with scopolamine enhanced avoidance performance to control levels. These data suggest that prenatal exposure to alcohol does not interfere with scopolamine-induced changes in the behavior of adult rats.     

Effects of early protein malnutrition and scopolamine on learning and memory in the Morris water maze

The present study investigated the effects of early protein malnutrition on the spatial learning and memory processes. The consequences of malnutrition for the cholinergic system were evaluated by comparing the performance of malnourished and control animals in the Morris water maze after treatment with scopolamine. The learning test consisted of placing the animal in the maze to escape to a submerged platform with 12 trials per day for two consecutive days. After 24 trials, the platform was removed, the rats were placed in the maze and the time spent by them in each quadrant was recorded. After 28 days the animals were tested in a single trial to verify the retention of the spatial information. In the first Experiment, scopolamine (0.0, 0.2, 0.4 and 0.6 mg/kg per ml. i.p.) was administered 20 min before the experimental sessions. In the second experiment, a dose of 0.6 mg/kg was administered after the sessions, during the period in which learning consolidation occurs. In the first experiment, there was a significant effect of the drug, with scopolamine impairing, learning in both nutritional conditions. In the saline condition, control animals presented a better performance when compared with malnourished animals. However, 28 days later, both groups increased their latencies. With 0.2 and 0.4 mg/kg of scopolamine, the performance of both nutritional groups was similar and with 0.6 mg/kg malnourished animals performed better than controls. In the second experiment, malnourished animals were also less reactive to the effects of scopolamine, resulting in lower impairments as compared to control animals. These data suggest long-term changes in learning and memory as the result of changes produced by protein malnutrition in the cholinergic neurotransmitter system.     

Effects of early protein malnutrition and scopolamine on learning and memory in the Morris water maze

The present study investigated the effects of early protein malnutrition on the spatial learning and memory processes. The consequences of malnutrition for the cholinergic system were evaluated by comparing the performance of malnourished and control animals in the Morris water maze after treatment with scopolamine. The learning test consisted of placing the animal in the maze to escape to a submerged platform with 12 trials per day for two consecutive days. After 24 trials, the platform was removed, the rats were placed in the maze and the time spent by them in each quadrant was recorded. After 28 days the animals were tested in a single trial to verify the retention of the spatial information. In the first Experiment, scopolamine (0.0, 0.2, 0.4 and 0.6 mg/kg per ml. i.p.) was administered 20 min before the experimental sessions. In the second experiment, a dose of 0.6 mg/kg was administered after the sessions, during the period in which learning consolidation occurs. In the first experiment, there was a significant effect of the drug, with scopolamine impairing, learning in both nutritional conditions. In the saline condition, control animals presented a better performance when compared with malnourished animals. However, 28 days later, both groups increased their latencies. With 0.2 and 0.4 mg/kg of scopolamine, the performance of both nutritional groups was similar and with 0.6 mg/kg malnourished animals performed better than controls. In the second experiment, malnourished animals were also less reactive to the effects of scopolamine, resulting in lower impairments as compared to control animals. These data suggest long-term changes in learning and memory as the result of changes produced by protein malnutrition in the cholinergic neurotransmitter system.     

Effects of one- and three-day binge alcohol exposure in neonatal C57BL/6 mice on spatial learning and memory in adolescence and adulthood

Binge-like alcohol exposure during the early postnatal period in rats and mice causes deficits in spatial learning and memory that persist into adulthood. Wozniak et al. (2004) reported that heavy binge alcohol exposure on postnatal day 7 (PD 7) in C57BL/6 (B6) mice produced profound spatial learning deficits in the Morris water maze when tested in adolescence (P30–39); when tested in adulthood, however, the deficits were greatly attenuated. Using a similar PD 7 binge alcohol exposure paradigm in B6 mice, we tested whether a single-day (PD 7 only) alcohol treatment produced place learning deficits in both adolescence and in adulthood, and further tested whether a more extended (3-day, PD 7–9) alcohol exposure would induce more severe and enduring deficits. B6 mice were given either 2 subcutaneous injections of alcohol (2.5 g/kg each) 2 h apart on PD 7 or on PD 7–9, and compared with controls that received saline vehicle injections and controls that received no injections. The alcohol injections on PD 7 produced average peak blood alcohol concentrations of 472 mg/dL and evoked typical patterns of activated caspase-3-positive neurons in the cortex, hippocampal formation, and striatum 6 h after the last injection. Mice were given standard place training or random location training in the Morris water maze either as adolescents (PD 30–39) or adults (PD 70–79). The adolescents acquired the place learning more slowly than adults, and the alcohol treatments produced only modest place acquisition deficits. In contrast, both the PD7 and the PD 7–9 alcohol treatments resulted in large and significant spatial learning impairments in adults. In contrast to the previous findings of Wozniak et al. (2004), these results indicate that binge alcohol exposure in the 3rd trimester equivalent produces significant and enduring deficits in spatial learning in B6 mice.     

Decrements in cognitive performance in metal inert gas welders exposed to aluminium

OBJECTIVES: Often little has been discovered of the cognitive functions affected by occupational toxins because many functions cooperate to produce the single performance scores typically reported from neuropsychological tests. To facilitate the interpretation of neuropsychological scores, the issue of occupational exposure to aluminium was examined with an approach intended to increase understanding of those cognitive processes that may be affected. METHODS: The investigation was a cross sectional study of asymptomatic aluminium welders and a reference group of mild steel welders. Based on urinary aluminium concentrations, welders were classified into a reference (n = 28), low (n = 27), and high (n = 24) exposure group. The mean urinary aluminium concentrations were 0.46, 2.25, and 9.98 mumol/l, respectively. A comprehensive neuropsychological examination was undertaken to assess psychomotor function, simple visual reaction time, attention related tasks, verbal and visual or visuospatial abilities as well as verbal and visual learning and memory. RESULTS: Aluminium welders showed no impairment on the finger tapping, Santa Ana dexterity, simple visual reaction times, any of the verbal memory tasks, the similarities subtest of Wechsler adult intelligence scale, or the Stroop task. However, the low exposed group performed poorer on the memory for designs and on more difficult block design items demanding preliminary visuospatial analysis. The time limited synonym task, embedded figures, digit symbol speed, and the backward counting component of the divided attention task showed exposure-response relations. CONCLUSIONS: The impairments found were circumscribed. When the neuropsychological tasks were scored to show some of the underlying theoretical cognitive structures, the results indicated that performance difficulties were mainly detected in tasks requiring working memory, particularly that relating to processing of visuospatial information. There was also evidence that such impairments are more readily found in time limited tasks involving visually presented material, in which effective visual scanning combined with control of working memory is demanded.       

Hesperidin Reduces Memory Impairment Associated with Adult Rat Hippocampal Neurogenesis Triggered by Valproic Acid

Treatment with valproic acid (VPA) deteriorates hippocampal neurogenesis, which leads to memory impairment. Hesperidin (Hsd) is a plant-based bioflavonoid that can augment learning and memory. This study aimed to understand the effect of Hsd on the impairment of hippocampal neurogenesis and memory caused by VPA. The VPA (300 mg/kg) was administered by intraperitoneal injection twice daily for 14 days, and Hsd (100 mg/kg/day) was administered by oral gavage once a day for 21 days. All rats underwent memory evaluation using the novel object location (NOL) and novel object recognition (NOR) tests. Immunofluorescent staining of Ki-67, BrdU/NeuN, and doublecortin (DCX) was applied to determine hippocampal neurogenesis in cell proliferation, neuronal survival, and population of the immature neurons, respectively. VPA-treated rats showed memory impairments in both memory tests. These impairments resulted from VPA-induced decreases in the number of Ki-67-, BrdU/NeuN-, and DCX-positive cells in the hippocampus, leading to memory loss. Nevertheless, the behavioral expression in the co-administration group was improved. After receiving co-administration with VPA and Hsd, the numbers of Ki-67-, BrdU/NeuN-, and DCX-positive cells were improved to the normal levels. These findings suggest that Hsd can reduce the VPA-induced hippocampal neurogenesis down-regulation that results in memory impairments.     

Aging-Related Behavioral,Adiposity, and Glucose Impairments and Their Association following Prenatal Alcohol Exposure in the C57BL/6J Mouse

People that experience prenatal alcohol exposure (PAE) may have behavioral and metabolic impairments, and it is unclear whether these remain stable or change with age. We assessed behavioral and metabolic endpoints across the lifespan in a mouse model of fetal alcohol spectrum disorder (FASD). Pregnant C57BL/6J mice received alcohol (ALC; 3 g/kg) or maltose-dextrin (control, CON) daily from embryonic day 8.5 to 17.5. Offspring were tested on accelerating rotarod, Y-maze, novel object recognition, and fear conditioning at 6 weeks and 10 and 17 months; females were also tested at 24 months. Body composition, fasting glucose, and glucose clearance were assessed at 18 months. Female but not male ALC mice had greater adiposity than age-matched CON from 7 months onward. At 18 months, male but not female ALC mice had reduced glucose clearance and ALC mice were more likely to have elevated fasting glucose. In the rotarod training session, ALC females performed worse than CON. In the Y-maze, significant exposure-age interactions affected ALC performance in both sexes versus age-match CON. For fear conditioning, all animals acquired the task and froze more at older ages. In both the context and cued tasks, there were exposure-age interactions and ALC animals frozen less than CON at 10 months. Correlation analysis revealed that fasting glucose and glucose clearance correlated with % of body fat in ALC but not in CON mice. Additionally, glucose intolerance and % body fat negatively correlated with performance in the rotarod, context learning, and novel object recognition tasks in ALC but not CON mice. All mice exhibit worsening of behavioral performance as they age, and PAE did not further exacerbate this. ALC but not CON mice displayed adiposity and glucose intolerance that correlate with their cognitive impairments, suggesting that these may be mechanistically related in PAE. Findings emphasize that FASD should be considered a whole-body disorder.     

Age-independent and dose-response effects of ethanol on spatial memory in rats.

Results of previous studies have shown that ethanol impairs the acquisition of spatial memory in adolescent rats at doses below those required to impair the acquisition in adults. However, the previous work did not identify doses of ethanol that failed to impair acquisition in adolescents or that impaired acquisition in both adolescent and adult animals. This was our aim in the present study. Male, Long-Evans hooded rats (adolescent and adult) were treated intraperitoneally with 0.0, 0.5, or 2.5 g/kg of ethanol 30 min before daily training on a spatial or nonspatial version of the Morris water maze task. Twenty-four hours after training on the spatial task the animals were given a 1-min probe trial. The low dose of ethanol (0.5 g/kg) failed to impair the performance of animals from either age group on any tasks. It did, however, enhance the initial rate of acquisition on the spatial task. The 2.5-g/kg dose eliminated acquisition of spatial learning in animals of both ages and significantly attenuated performance on a nonspatial task in both age groups. However, the treatment effect in the nonspatial task was eliminated with controlling for baseline performance. These results establish a low dose of ethanol (0.5 g/kg) that does not impair acquisition of spatial memory in adolescent or adult rats. Moreover, the study findings show that 2.5 g/kg of ethanol markedly impairs acquisition of spatial memory in both adolescent and adult animals.     

Functional magnetic resonance imaging in studies of neurocognitive effects of alcohol use on adolescents and young adults

Alcohol use disorders (defined as alcohol abuse or dependence) are prevalent and serious problems among adolescents and young adults. Adolescence is a time of trying new experiences and activities that emphasize socializing with peers, and conforming to peer-group standards. These new activities may place young people at particular risk for initiating and continuing alcohol consumption. Exposing the brain to alcohol during adolescence may interrupt key processes of brain development, leading to cognitive impairment as well as to further escalation of alcohol use. Alcohol-induced adolescent learning impairments could affect academic and occupational achievements. Functional magnetic resonance imaging (fMRI) is a relatively new imaging technique that allows studying neurocognitive function. fMRI aims to determine the neurobiological correlate of behavior by identifying the brain regions that become active during the performance of specific tasks in vivo. The technique is non-invasive and relatively safe. This allows repeated studies to be carried out within a given subject. Several fMRI studies have been performed to evaluate neurocognitive function in adolescents and young adults with alcohol use disorders. Adolescents and young adults with alcohol use disorders had abnormalities in brain response to a working memory task. The results of the studies of cue reactivity and craving responses in young people suggest that the elevated physiological response and altered cognitive reactions to alcohol are involved in the pathogenesis of alcohol dependence in adolescents and young adults. Future fMRI studies may help ascertain the adverse affects of alcohol on brain function during early neurodevelopmental stages. fMRI may be uniquely powerful in the delineation of the underlying pathophysiology of alcohol use disorders in adolescents and young adults.     

儿童行为抑制测验及行为训练

行为抑制是执行功能的核心内容,是为完成任务而对无关信息或行为的抑制。其早期缺陷易导致社会性交流障碍,工作记忆、情绪调节、注意力等执行功能问题。随着对行为抑制认识的逐渐深入,出现了一系列成熟的测验方法,包括Stroop任务、侧抑制、Navon任务、Simon任务以及多源冲突任务等,这些行为抑制测验方法在行为障碍的诊断中发挥了重要作用。对正在发育的儿童实施行为抑制训练可促进执行功能发展。行为抑制的早期健康发展可有效提高儿童的自控力和注意力,从而改善学习能力。了解有关行为抑制的测验方法及行为训练,对促进儿童执行功能发展有重要作用。     

EFFECTS OF ACUTE ALCOHOL ADMINISTRATION ON VERBAL AND SPATIAL LEARNING

The effects of alcohol and placebo on cognitive functioningin male, Asian-American college students were evaluated witha double-blind, placebo-controlled cross-over design using amulti-trial learning test in which verbal and spatial learningwere simultaneously assessed. Verbal recall was impaired consistentlyacross learning trials, while impairment of spatial recall wasevident only on later learning trials. Recall of spatial informationwas influenced by order of presentation and amount of exposuretime of items. Results do not support a theory that spatiallearning is more impaired by alcohol than verbal learning, andthus do not lend support for the hypothesis that alcohol hasa greater effect on right than left hemisphere functioning.Results provide evidence that alcohol increases susceptibilityto interference effects.