Hop,Skip … No! Explaining Adolescent Girls’ Disinclination for Physical Activity

Purpose  

This study aimed to develop and validate the Girls’ Disinclination for Physical Activity Scale (G-DAS) and implement the scale along with an objective measure of physical activity (PA) in a longitudinal sample of adolescent girls.     

Histaminergic Activity in a Rodent Model of Parkinson’s Disease

Rats lesioned shortly after birth with 6-OHDA have been proposed to be a near-ideal model of severe Parkinson’s disease, because of non-lethality of the procedure, near-total destruction of nigrostriatal dopaminergic fibers, and near-total dopamine (DA) denervation of striatum. There are scarce data that in Parkinson’s disease, activity of the central histaminergic system is increased. Therefore, the aim of this study was to determine histamine content in the brain and the effect of histamine receptor antagonists on behavior of adult rats. At 3 days after birth, Wistar rats were pretreated with desipramine (20.0 mg/kg ip) 1 h before bilateral icv administration of the catecholaminergic neurotoxin 6-OHDA (67 μg base, on each side) or saline-ascorbic acid (0.1%) vehicle (control). At 8 weeks levels of DA and its metabolites l-3,4-dihydroxyphenylalanine (DOPAC) and homovanillic acid (HVA) were estimated in the striatum and frontal cortex by HPCL/ED technique. In the hypothalamus, hippocampus, frontal cortex, and medulla oblongata, the level of histamine was analyzed by immunoenzymatic method. Behavioral observations (locomotion, exploratory-, oral-, and stereotyped-activity) were additionally made on control and 6-OHDA neonatally lesioned rats. Effects of DA receptor agonists (SKF 38393, apomorphine) and histamine receptor antagonists (e.g., S(+)chlorpheniramine, H₁; cimetidine, H₂; thioperamide, H₃ agonist) were determined. We confirmed that 6-OHDA significantly reduced contents of DA and its metabolites in the brain in adulthood. Histamine content was significantly increased in the hypothalamus, hipocampus, and medulla oblongata. Moreover, in 6-OHDA-lesioned rats behavioral response was altered mainly by thioperamide (H₃ antagonist). These findings indicate that histamine and the central histaminergic system are altered in the brain of rats lesioned to model Parkinson’s disease, and that histaminergic neurons exert a modulating role in Parkinsonian 6-OHDA-lesioned rats.     

Biological Activity of sym-Triazines with Acetylcholine-like Substitutions as Multitarget Modulators of Alzheimer’s Disease

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Inhibitory Effect of IFN-��, on the Antitumor Activity of Celecoxib in U87 Glioma Model

Objective

Interferon-β, (IFN-β) has been used in the treatment of cancers. Inhibition of the enzyme cyclooxygenase (COX) with celecoxib had a significantly suppressive effect on tumor growth, angiogenesis, and metastasis in a variety of tumors. The aim of this study was to elucidate the antiglioma effect of combined treatment with IFN-β and celecoxib in U87 glioma model.

Methods

The in vitro effects of IFN-β (50-1,000 IU/mL) and celecoxib (50-250 µM) alone or combination of both on the proliferation and apoptosis of U87 cells were tested using MTT assay, FACS analysis and DNA condensation. To determine the in vivo effect, nude mice bearing intracerebral U87 xenograft inoculation were treated with IFN-β intraperitoneally (2×10⁵ IU/day for 15 days), celecoxib orally (5, 10 mg/kg) or their combination.

Results

IFN-β or celecoxib showed an inhibitory effect on the proliferation of U87 cells. When U87 cells were treated with IFN-β and celecoxib combination, it seemed that IFN-β interrupted the antiproliferative and apoptotic activity of celecoxib. No additive effect was observed on the survival of the tumor bearing mice by the combination of IFN-β and celecoxib.

Conclusion

These results suggest that IFN-β seems to inhibit the antiglioma effect of celecoxib, therefore combination of IFN-β and celecoxib may be undesirable in the treatment of glioma.     

Do Structural Properties Explain the Anticonvulsant Activity of Valproate Metabolites? A QSAR Analysis

Summary: Purpose: Differences in potency among valproate (VPA) metabolites could be explained by structural properties. Therefore, a quantitative structure–activity relation (QSAR) analysis was performed to study the relation between structural parameters and the effect of the following VPA metabolites: 4‐en‐VPA, 2‐en‐VPA, 3‐en‐VPA, 2,4'‐dien‐VPA, 4,4'‐dien‐VPA, 4‐hydroxy‐VPA, 3‐ceto‐VPA, 3‐hydroxy‐VPA, 5‐hydroxy‐VPA, and propylglutaric acid. Methods: By using the CAChe program package for biomolecules (Oxford Molecular, Ltd), we performed molecular modeling. The anticonvulsant activity determined on the threshold for maximal electroconvulsions in mice was obtained from a study of Löscher and Nau. Structural parameters were compared between metabolites with a double bond and metabolites with oxygen at either side chain (unpaired Student's t test). A single linear regression analysis between each structural parameter and the relative anticonvulsant potency was also performed. Results: Similar parameters were found between the cis and trans and R and S isomers. Biologic activity and most of the structural parameters were significantly different between metabolites with a double bond and metabolites with oxygen at either side chain. Activity was directly related to log P_oct (r² = 0.77) and to reactivity parameters and was inversely related to stability parameters and to molecular weight and surface. The most potent metabolites had a log P_oct value of higher than 2 units. Conclusions: Similar data were identified between cis and trans, and R and S isomers of VPA metabolites. Anticonvulsant activity was mainly related to log P_oct, probably reflecting the ability of VPA metabolites to cross the blood–brain barrier.     

Mothers’ and Fathers’ Attributions and Beliefs in Families of Girls and Boys with Attention-Deficit/Hyperactivity Disorder

This study examined parent and child gender effects on parents’ attributions and beliefs in regards to child symptoms of attention-deficit/hyperactivity disorder (ADHD). Participants included mothers and fathers of 19 girls and 17 boys with ADHD. Groups of boys and girls, aged 5–13 years, were equated on age and medication status, as well as ADHD symptom severity. These groups also were similar in the severity of comorbid oppositional behaviors and internalizing problems, as well as a variety of demographic characteristics. Parents’ attributions for child behavior were assessed in response to written scenarios describing either hyperactive/impulsive or inattentive symptoms of ADHD. Parents also completed a questionnaire assessing beliefs and knowledge about ADHD. There were no child gender effects for parents’ attributions or beliefs. All parents attributed inattentive symptoms to more internal, global and stable causes than impulsive symptoms. Mothers attributed both inattentive and impulsive child symptoms to more global and stable causes than did fathers. Fathers, but not mothers, reported more negative reactions to ADHD symptoms that were perceived as having an internal cause. Finally, mothers scored higher on beliefs in behavior management than did fathers, and fathers believed more in psychological causes and treatments for ADHD. Possible explanations for and implications of these results are explored.     

Comparison of Eating Attitudes between Adolescent Girls with and without Asperger Syndrome: Daughters’ and Mothers’ Reports

Despite the evidence that individuals with Asperger syndrome (AS) have a propensity for being underweight or having comorbid eating disorders, no previous research has compared the eating attitudes of adolescent girls with AS to typically developing peers. This study compared reports of eating problems provided by the adolescent girls themselves (56 with and 56 without AS) and their mothers on the EAT-26. Results indicated that adolescent girls with AS are at a higher risk for eating problems than their typically developing peers according to their reports and the reports of their mothers. Moreover, it was found that although the agreement between mothers’ and daughter’s reports is very satisfactory, mothers of girls with AS report statistically less eating-disordered behaviors than their daughters.     

Resting State Activity and the “Stream of Consciousness” in Schizophrenia—Neurophenomenal Hypotheses

Schizophrenia is a multifaceted disorder with various symptoms including auditory hallucinations, egodisturbances, passivity phenomena, and delusions. Recent neurobiological approaches have focused on, especially, the abnormal contents of consciousness, the “substantive parts” as James said, to associate them with the neural mechanisms related to sensory, motor, and cognitive functions, and the brain’s underlying stimulus-induced or task-evoked activity. This leaves open, however, the neural mechanisms that provide the temporal linkage or glue between the various contents, the transitive parts that makes possible the “stream of consciousness.” Interestingly, schizophrenic patients seem to suffer from abnormalities specifically in the “transitive parts” when they experience contents as temporally disconnected or fragmented which in phenomenological psychiatry has been described as “temporal fragmentation.” The aim of this article is to develop so-called neurophenomenal hypothesis about the direct relationship between phenomenal features of the “stream of consciousness,” the “transitive parts,” and the specific neuronal mechanisms in schizophrenia as based on healthy subjects. Rather than emphasizing stimulus-induced and task-evoked activity and sensory and lateral prefrontal cortical regions as in neurocognitive approaches with their focus on the “substantive parts,” the focus shifts here to the brain’s intrinsic activity, its resting state activity, which may account for the temporal linkage or glue between the contents of consciousness, the transitive parts.Key words: schizophrenia, stream of consciousness, James, cortical midline structures, auditory hallucinations, thought disturbances, frequency fluctuations, functional connectivity     

Atypical Antipsychotics Mediate Dynamics of Intrinsic Brain Activity in Early-Stage Schizophrenia? A Preliminary Study

ObjectiveAbnormalities of static brain activity have been reported in schizophrenia, but it remains to be clarified the temporal variability of intrinsic brain activities in schizophrenia and how atypical antipsychotics affect it. MethodsWe employed a resting-state functional magnetic resonance imaging (rs-fMRI) and a sliding-window analysis of dynamic amplitude of low-frequency fluctuation (dALFF) to evaluate the dynamic brain activities in schizophrenia (SZ) patients before and after 8-week antipsychotic treatment. Twenty-six schizophrenia individuals and 26 matched healthy controls (HC) were included in this study. ResultsCompared with HC, SZ showed stronger dALFF in the right inferior temporal gyrus (ITG.R) at baseline. After medication, the SZ group exhibited reduced dALFF in the right middle occipital gyrus (MOG.R) and increased dALFF in the left superior frontal gyrus (SFG.L), right middle frontal gyrus (MFG.R), and right inferior parietal lobule (IPL.R). Dynamic ALFF in IPL.R was found to significant negative correlate with the Scale for the Assessment of Negative Symptoms (SANS) scores at baseline. ConclusionOur results showed dynamic intrinsic brain activities altered in schizophrenia after short term antipsychotic treatment. The findings of this study support and expand the application of dALFF method in the study of the pathological mechanism in psychosis in the future.     

Glutamatergic Ventral Pallidal Neurons Modulate Activity of the Habenula–Tegmental Circuitry and Constrain Reward Seeking

Background

The ability to appropriately integrate and respond to rewarding and aversive stimuli is essential for survival. The ventral pallidum (VP) plays a critical role in processing both rewarding and aversive stimuli. However, the VP is a heterogeneous structure, and how VP subpopulations integrate into larger reward networks to ultimately modulate these behaviors is not known. We identify a noncanonical population of glutamatergic VP neurons that play a unique role in responding to aversive stimuli and constraining inappropriate reward seeking.

Does Neighbourhood Walkability Moderate the Effects of Mass Media Communication Strategies to Promote Regular Physical Activity?

Background

Mass media campaigns are widely used in Australia and elsewhere to promote physical activity among adults. Neighbourhood walkability is consistently shown to be associated with walking and total activity. Campaigns may have different effects on individuals living in high and low walkable neighbourhoods.

Purpose

The purpose of this study is to compare pre- and post-campaign cognitive and behavioural impacts of the Heart Foundation’s Find Thirty every day® campaign, in respondents living in high and lower walkable neighbourhoods.

Methods

Pre- and post-campaign cross-sectional survey data were linked with objectively measured neighbourhood walkability. Cognitive and behavioural impacts were assessed using logistic regression stratified by walkability.

Results

Cognitive impacts were significantly higher post-campaign and consistently higher in respondents in high compared with lower walkable neighbourhoods. Post campaign sufficient activity was significantly higher and transport walking significantly lower, but only in residents of lower walkable areas.

Conclusions

Cognitive impacts of mass media physical activity campaigns may be enhanced by living in a more walkable neighbourhood.

     

Cerebral Cortical Activity Following Non-invasive Cerebellar Stimulation—a Systematic Review of Combined TMS and EEG Studies

The Cerebellum - The cerebellum sends dense projections to both motor and non-motor regions of the cerebral cortex via the cerebellarthalamocortical tract. The integrity of this tract is crucial...     

Activity deprivation leads to seizures in hippocampal slice cultures: is epilepsy the consequence of homeostatic plasticity?

SUMMARY: Neural networks operate robustly despite destabilizing factors, ranging from gene product turnover to circuit refinement, throughout life. Maintaining functional robustness of neuronal networks critically depends upon forms of homeostatic plasticity including synaptic scaling. Synaptic strength and intrinsic excitability have been shown to "scale" (up or down) in response to altered ambient activity levels, and this has led to the general idea that homeostatic plasticity operates along a continuum. After 48 hours of activity deprivation, cultured hippocampal networks exhibited a homeostatic-type reconfiguration that was discrete: a switch from spontaneous spiking to oscillatory bursting. Blockade of fast glutamatergic and GABAergic transmission abolished spontaneous network bursting, but the majority of neurons exhibited intrinsic bursting in response to current injection, which was not the case in control tissue. This de novo intrinsic bursting could be blocked by cadmium chloride, suggesting that this bursting involves calcium mechanisms. Immunohistochemistry confirmed that activity-deprived slice cultures exhibited a widespread upregulation of voltage-dependent calcium channels compared with controls. Calcium imaging studies from activity-deprived slices demonstrated that spontaneous bursting was not a local behavior, but rather a global, synchronous phenomenon, reminiscent of seizure activity. These data suggest that the input/output transformation of individual neurons undergoing homeostatic remodeling is more complex than simple scaling. Network consequences of this transformation include network destabilization of epileptic proportions. Spontaneous activity plays a critical role in actively maintaining homeostatic balance in networks, which is lost after activity deprivation.     

Cerebrospinal Fluid Microglial Markers in Alzheimer’s Disease: Elevated Chitotriosidase Activity but Lack of Diagnostic Utility

Activated microglial cells, which are the resident macrophages of the central nervous system, surround amyloid β-plaques in Alzheimer's disease (AD) brains. Inflammation including microglial activation may contribute in AD pathogenesis, and biomarkers for this process may thus be of value to study AD pathogenesis and might facilitate development of therapies targeting these cells. We therefore examined cerebrospinal fluid (CSF) biomarkers in patients with AD, other dementias, mild cognitive impairment and in healthy controls. Samples were analyzed for markers with known association to macrophage activity, including chitotriosidase, YKL-40 (CHI3L1, HC gp-39) and chemokine CC motif ligand 2 (CCL2, MCP1). Patients with AD had higher chitotriosidase activity than controls and patients with stable mild cognitive impairment, consistent with the presence of activated microglial cells in AD brains, but with large overlaps between groups. CCL2 and YKL-40 concentrations did not differ among groups. Microglial markers are unlikely to be useful for AD diagnosis, but might be useful for identification of distinct subgroups of patients, and for the development and implementation of drugs targeting microglial pathology.     

Mutant α-Synuclein Overexpression Mediates Early Proinflammatory Activity

Microglia provide immune surveillance for the brain through both the removal of cellular debris and protection against infection by microorganisms and “foreign” molecules. Upon activation, microglia display an altered morphology and increased expression of proinflammatory molecules. Increased numbers of activated microglia have been identified in a number of neurodegenerative diseases including Parkinson’s disease (PD). What remains to be determined is whether activated microglia result from ongoing cell death or are involved in disease initiation and progression. To address this question we utilized a transgenic mouse model that expresses a mutated form of a key protein involved in Parkinson’s disease, α-synuclein. Herein, we report an increase in activated microglia and proinflammatory molecules in 1-month-old transgenic mice well before cell death occurs in this model. Frank microglial activation is resolved by 6 months of age while a subset of proinflammatory molecules remain elevated for 12 months. Both tyrosine hydroxylase mRNA expression and α-synuclein protein are decreased in the striatum of older animals evidence of dystrophic neuritic projections. To determine whether mutated α-synuclein could directly activate microglia primary microglia-enriched cell cultures were treated with exogenous mutated α-synuclein. The data reveal an increase in activated microglia and proinflammatory molecules due to direct interaction with mutated α-synuclein. Together, these data demonstrate that mutated α-synuclein mediates a proinflammatory response in microglia and this activity may participate in PD pathogenesis.