This study provides a comprehensive review of the literature on memory impairment and the potential effective factors in patients with chronic pain.

A literature search of databases PubMed, EMBASE, SpringerLink, and PsycINFO until September 2012 was conducted using the keywords ‘memory’ and ‘chronic pain’. The study emphasises on publications over the past 20 years.

Memory impairment in chronic pain patients is substantial, but the aspects of memory (e.g. working memory, long-term memory, and autobiographical memory) in chronic pain patients and the potentially related factors (e.g. age, level of education, pain conditions, emotion, neural network, and use of analgesics) are modest. Memory impairment is interpreted with the attention-narrowing hypothesis and the capacity-reduction hypothesis.

The currently available data and theory have explained memory impairment in chronic pain patients, but many controversies remain. Future research should focus on the subclinical characteristics of chronic pain, enlarging the sample size, and emphasise on the experimental intervention method and the cognitive neuroscience method.

Alcohol dependence (AD) is one of the major elements that significantly influence drinking pattern that provoke the alcohol-induced organ damage. The structural and neurophysiologic abnormalities in the frontal lobes of chronic alcoholics were revealed by magnetic resonance imaging scans. It is well known that candidate genes involved in dopaminergic pathway are of immense interest to the researchers engaged in a wide range of addictive disorders. Dopaminergic pathway gene polymorphisms are being extensively studied with respect to addictive and behavioral disorders.

From the broad literature available, the current review summarizes the specific polymorphisms of dopaminergic genes that play a role in alcohol dependence.

No evidence indicating any strong association between AD and polymorphisms of dopamine pathway genes has emerged from the literature.

Further studies are warranted, considering a range of alcohol-related traits to determine the genes that influence alcohol dependence.

Some authors draw a connection between the dopaminergic pathways and emotional perception. The present study is based on that association and addresses the question whether methylphenidate and the resulting amelioration of the disturbed dopamine metabolism lead to an improvement of the facial affect recognition abilities in children with attention-deficit/hyperactivity disorder (ADHD).

A computer test was conducted on 21 participants, aged 7–14 years and with a diagnosis of ADHD – some with comorbid oppositional defiant disorder – conducted the FEFA (Frankfurt Test and Training of Facial Affect), a computer test to examine their facial affect recognition abilities. It consists of two subtests, one with faces and one with eye pairs. All participants were tested in a double-blind cross-over study, once under placebo and once under methylphenidate.

The collected data showed that methylphenidate leads to amelioration of facial affect recognition abilities, but not on a significant level. Reasons for missing significance may be the small sample size or the fact that there exists some overlapping in cerebral connections and metabolic pathways of the site of action of methylphenidate and the affected dopaminergic areas in ADHD. However, consistent with the endophenotype concept, certain gene locations of the dopaminergic metabolism as both an aetiological factor for ADHD and the deficient facial affect recognition abilities with these individuals were considered. Consulting current literature they were found to be not concordant. Therefore, we conclude that the lacking significance of the methylphenidate affect on facial affect recognition is based on this fact.

To give a review of the history of SCNP since the first meeting in 1960 with specific focus on UKU.

Consulting the appropriate minutes from the meetings.

One of the major goals of the SCNP was the standardization of clinical trials with psychotropic drugs. In 1969, the SCNP established a Committee for Clinical Investigations (UKU) with the representation of clinical investigators and the drug industry; moreover, during the 1970s and ’80s, the UKU initiated clinical trialsand contributed to the methodology of clinical investigations with psychotropic drugs. With the decrease in governmental funding and increasing influence of the US Food and Drug Administration on themethodology of clinical investigations around the world in the 1990s, the UKU was dissolved. The changes had a detrimental effect on the developments on the methodology of clinical investigations, and the lack of clinical feedback led to an impasse in psychotropic drug development with some pharmaceutical companies abandoning research in the central nervous system area.

It is suggested that a revival of UKU to provide a platform for dialogue among government, industry, and academia could help break the impasse.

Autism, a lifelong neuro-developmental disorder is a uniquely human condition. Animal models are not the perfect tools for the full understanding of human development and behavior, but they can be an important place to start. This review focused on the recent updates of animal model research in autism.

We have reviewed the publications over the last three decades, which are related to animal model study in autism.

Animal models are important because they allow researchers to study the underlying neurobiology in a way that is not possible in humans. Improving the availability of better animal models will help the field to increase the development of medicines that can relieve disabling symptoms. Results from the therapeutic approaches are encouraging remarkably, since some behavioral alterations could be reversed even when treatment was performed on adult mice. Finding an animal model system with similar behavioral tendencies as humans is thus vital for understanding the brain mechanisms, supporting social motivation and attention, and the manner in which these mechanisms break down in autism. The ongoing studies should therefore increase the understanding of the biological alterations associated with autism as well as the development of knowledge-based treatments therapy for those struggling with autism.

In this review, we have presented recent advances in research based on animal models of autism, raising hope for understanding the disease biology for potential therapeutic intervention to improve the quality of life of autism individuals.

Intrauterine growth restriction (IUGR) has been associated with metabolic disorders later in life such as obesity and diabetes as well as psychiatric disorders such as depression and schizophrenia. Therefore, we wanted to investigate whether behavioural, metabolic or neuroendocrine abnormalities could be provoked or exacerbated by a high-fat diet (HFD) in an experimental model of IUGR.

Pregnant dams were exposed to dexamethasone (DEX) in the third gestational week to induce IUGR. Late adolescent male offspring of DEX- and vehicle-treated dams were then fed a HFD or standard chow for 8 weeks and subjected to a variety of assessments.

Only diet affected the hypothalamus-pituitary-adrenal (HPA) axis stress response, as HFD doubled the observed corticosterone levels following acute restraint. HFD and prenatal DEX exposure concomitantly exacerbated depressive-like behaviour in the forced swim test, even though no interaction was seen. Prenatal DEX treatment tended to increase the basal acoustic startle response (ASR), while an interaction between HFD and DEX was present in the ASR pre-pulse inhibition suggestive of fundamental changes in neuronal gating mechanisms. Metabolic parameters were only affected by diet, as HFD increased fasting glucose and insulin levels.

We conclude that chronic HFD may be more important in programming of the HPA axis stress responsiveness than an adverse foetal environment and therefore potentially implies an increased risk for developing psychiatric and metabolic disease.

Psychological factors contribute to bipolar disorder illness course, representing targets for psychological intervention. Research to date has focused on bipolar I disorder, extrapolating results to bipolar II disorder. The current study addresses this discrepancy by exploring cognitive and coping styles in patients diagnosed with bipolar I or II disorder.

Participants were recruited from the Sydney-based Black Dog Institute. Diagnoses were derived via the MINI International Neuropsychiatric Interview. Baseline cognitive and coping style measures were completed, and mood symptoms assessed over a 6-month period. Clinician-rated mood status was assessed at follow-up to determine the predictive utility of cognitive and coping styles.

The follow-up sample comprised 151 participants. Differential relationships between cognitive style, coping styles and mood symptoms emerged across the bipolar sub-types. Some key differences were that a broader set of negative cognitive styles were associated with bipolar II depression symptoms; while few relationships were observed between coping styles and bipolar II symptoms.

Differences in cognitive and coping style relationships with symptom expression across bipolar I and II disorder may provide clinicians with fruitful guides for directing treatment interventions when relevant maladaptive styles are observed. Further exploration of differences in cognitive and coping styles in bipolar I and II disorder is warranted.

Mazindol is a sympathomimetic amine, widely used as an anorectic agent in the treatment of obesity. This drug causes psychostimulant effects because of its pharmacological profile similar to amphetamine, acting like a monoamine reuptake inhibitor. However, the mechanisms underlying the action of mazindol are still not clearly understood.

Swiss mice received a single acute administration of mazindol (0.25, 1.25 and 2.5 mg/kg, ip) or saline. After 2 h, the animals were killed by decapitation; the brain was removed and used for the evaluation of activities of mitochondrial respiratory chain complexes, Krebs cycle enzymes and creatine kinase.

Acute administration of mazindol decreased complex I activity only in the hippocampus. Complex IV activity was increased in the cerebellum (2.5 mg/kg) and cerebral cortex (0.25 mg/kg). Citrate synthase activity was increased in the cerebellum (1.25 mg/kg) and cerebral cortex (1.25 mg/kg), and creatine kinase activity was increased in the cerebellum (1.25 mg/kg).

We suggest that the inhibition of complex I in the hippocampus only and activation of complex IV, citrate synthase and creatine kinase occurs because of a stimulus effect of mazindol in the central nervous system, which causes a direct impairment on energy metabolism.

Several studies have reported that vegetarian diets are associated with a higher prevalence of major depression. Therefore, we hypothesised that the consumption of animal products, especially eggs, may have positive effects on mental health, especially on major depression, because a previous study reported that egg consumption produces numerous beneficial effects in humans. The purpose of the present study was to evaluate the effects of chronic whole-egg treatment on depression-like behaviours in Wistar rats, a control strain, and Wistar Kyoto rats, an animal model of depression.

In both the rats, either whole-egg solution (5 ml/kg) or distilled water (5 ml/kg) was orally administrated for 35 days. During these periods, the open-field test (OFT) was conducted on the 21st day, and a forced swimming test (FST) was enforced on the 27th and 28th days. On the 36th day, the plasma and brain were collected.

Chronic whole-egg treatment did not affect line crossing in the OFT, whereas it reduced the total duration of immobility in the FST on both strains. Furthermore, interestingly, the results indicated the possibility that whole-egg treatment elevated the incorporation of tryptophan into the brain, and the tryptophan concentration in the prefrontal cortex was actually increased by the treatment.

This study demonstrated that whole-egg treatment exerts an antidepressant-like effect in the FST. It is suggested that whole egg may be an excellent food for preventing and alleviating the conditions of major depression.

Substance dependence disorder is a chronically relapsing condition characterised by neurobiological changes leading to loss of control in restricting a substance intake, compulsion and withdrawal syndrome. In the past few years, (endo)cannabinoids have been raised as a possible target in the aetiology of drug addiction. On the other hand, although the exact mechanisms of the genesis of addiction remain poorly understood, it is possible that neuroinflammation might also play a role in the pathophysiology of this condition. Studies demonstrated that (endo)cannabinoids act as immunomodulators by inhibiting cytokines production and microglial cell activation. Thus, in the present review, we explore the possible role of neuroinflammation on the therapeutic effects of cannabinoids on drug addiction.

We conducted an evidence-based review of the literature in order to assess the role of cannabinoids on the neuroinflammatory hypothesis of addiction (terms: addiction, cannabinoids and inflammation). We searched PubMed and BioMedCentral databases up to April 2014 with no date restrictions.

In all, 165 eligible articles were included in the present review. Existing evidence suggests that disruption in cannabinoid signalling during the drug addiction process leads to microglial activation and neuroinflammation.

The literature showed that inflammation and changes in endocannabinod signalling occur in drug abuse; however, it remains uncertain whether these changes are causally or coincidentally associated with addiction. Additional studies, therefore, are needed to elucidate the contribution of neuroinflammation on the behavioural and neuroprotective effects of cannabinoids on drug addiction.