Situaciones problemáticas en el aprendizaje significativo de biología celular en la carrera de Odontología

Ponencia presentada en la II Muestra Nacional de Innovaciones en la Enseñanza de la Odontología y IV Muestra Institucional de Innovaciones en la Enseñanza de la Odontología. Córdoba, 13 y 14 de septiembre de 2012.En la formación de un odontólogo generalista, la Biología Celular comprende la adquisición de los conocimientos que son necesarios para el abordaje de la problemática de la tríada salud- enfermedad- atención en todos sus aspectos preventivos, terapéuticos y epidemiológicos.Fil: Zárate, A. M. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Cismondi, A. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Kohan, R. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Llanes, M. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Filiberti, A. M. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Scherma, M. E. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina.Fil: Brunotto, M. Universidad Nacional de Córdoba. Facultad de Odontología. Departamento de Biología Bucal. Cátedra A de Biología Celular; Argentina

Modeling Parkinson’s disease neuropathology and symptoms by intranigral inoculation of preformed human α-synuclein oligomers

The accumulation of aggregated α-synuclein (αSyn) is a hallmark of Parkinson’s disease (PD). Current evidence indicates that small soluble αSyn oligomers (αSynOs) are the most toxic species among the forms of αSyn aggregates, and that size and topological structural properties are crucial factors for αSynOs-mediated toxicity, involving the interaction with either neurons or glial cells. We previously characterized a human αSynO (H-αSynO) with specific structural properties promoting toxicity against neuronal membranes. Here, we tested the neurotoxic potential of these H-αSynOs in vivo, in relation to the neuropathological and symptomatic features of PD. The H-αSynOs were unilaterally infused into the rat substantia nigra pars compacta (SNpc). Phosphorylated αSyn (p129-αSyn), reactive microglia, and cytokine levels were measured at progressive time points. Additionally, a phagocytosis assay in vitro was performed after microglia pre-exposure to αsynOs. Dopaminergic loss, motor, and cognitive performances were assessed. H-αSynOs triggered p129-αSyn deposition in SNpc neurons and microglia and spread to the striatum. Early and persistent neuroinflammatory responses were induced in the SNpc. In vitro, H-αSynOs inhibited the phagocytic function of microglia. H-αsynOs-infused rats displayed early mitochondrial loss and abnormalities in SNpc neurons, followed by a gradual nigrostriatal dopaminergic loss, associated with motor and cognitive impairment. The intracerebral inoculation of structurally characterized H-αSynOs provides a model of progressive PD neuropathology in rats, which will be helpful for testing neuroprotective therapies

Alpha-Synuclein transgenic mice, h-α-SynL62, display α-Syn aggregation and a dopaminergic phenotype reminiscent of Parkinson's disease

Acknowledgments: The authors acknowledge Mandy Magbagbeolu and Heide Lueck for excellent technical assistance and Anna Thoma for assistance in behavioural testing and maintenance of animals. This work was funded by TauRx Therapeutics Ltd., Singapore. C.R.H. and C.M.W. declare that they are officers in TauRx Therapeutics Ltd.Peer reviewedPublisher PD

Identifying Neurobiological Markers in Obsessive–Compulsive Disorder: A Study Protocol for a Cross-Sectional Study in Subgroups of Differing Phenotype

Obsessive–compulsive disorder (OCD) represents a frequent and highly disabling mental disorder. Past attempts to characterize different disease subgroups focused on the time of onset (late vs. early onset), presence of insight (poor insight), and post-infectious forms (pediatric acuteonset neuropsychiatric syndrome, PANS). Each subgroup may be associated with a differing impact on cognition, functioning, sleep quality, and treatment response profile. Certain lines of evidence suggest brain-derived neurotrophic factor (BDNF) levels may differ between individuals living with OCD as compared with controls, but there is a lack of evidence on the variation of BDNF levels in OCD subgroups. Lastly, the potential of assessing inflammatory states, electroencephalogram, and polysomnography to characterize these subtypes has been hardly explored. Estimates of drugresistance rates indicate that 20% and up to 65% of affected adults and up to 35% of the pediatric population may not benefit from pharmacological treatments. At least part of the variability in treatment response could depend on the underlying biological heterogeneity. In the present project, we aim to increase the accuracy in characterizing the phenotypical and biological signature for the different OCD subtypes through clinical, cognitive, and sleep markers, along with other possible markers that may be biologically plausible

The effects of Δ9-tetrahydrocannabinol on the dopamine system

Δ(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, is a pressing concern to global mental health. Patterns of use are changing drastically due to legalisation, availability of synthetic analogues (‘spice’), cannavaping and aggrandizements in the purported therapeutic effects of cannabis. Many of THC’s reinforcing effects are mediated by the dopamine system. Due to complex cannabinoid-dopamine interactions there is conflicting evidence from human and animal research fields. Acute THC causes increased dopamine release and neuron activity, whilst long-term use is associated with blunting of the dopamine system. Future research must examine the long-term and developmental dopaminergic effects of the drug

Endocannabinoid Regulation of Acute and Protracted Nicotine Withdrawal: Effect of FAAH Inhibition

Evidence shows that the endocannabinoid system modulates the addictive properties of nicotine. In the present study, we hypothesized that spontaneous withdrawal resulting from removal of chronically implanted transdermal nicotine patches is regulated by the endocannabinoid system. A 7-day nicotine dependence procedure (5.2 mg/rat/day) elicited occurrence of reliable nicotine abstinence symptoms in Wistar rats. Somatic and affective withdrawal signs were observed at 16 and 34 hours following removal of nicotine patches, respectively. Further behavioral manifestations including decrease in locomotor activity and increased weight gain also occurred during withdrawal. Expression of spontaneous nicotine withdrawal was accompanied by fluctuation in levels of the endocannabinoid anandamide (AEA) in several brain structures including the amygdala, the hippocampus, the hypothalamus and the prefrontal cortex. Conversely, levels of 2-arachidonoyl-sn-glycerol were not significantly altered. Pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for the intracellular degradation of AEA, by URB597 (0.1 and 0.3 mg/kg, i.p.), reduced withdrawal-induced anxiety as assessed by the elevated plus maze test and the shock-probe defensive burying paradigm, but did not prevent the occurrence of somatic signs. Together, the results indicate that pharmacological strategies aimed at enhancing endocannabinoid signaling may offer therapeutic advantages to treat the negative affective state produced by nicotine withdrawal, which is critical for the maintenance of tobacco use

Gene knockout animal models of depression, anxiety and obsessive compulsive disorders

In the past decades, the improving knowledge of genes implicated in the pathogenesis of psychiatric disorders together with the advancements in genetic engineering has led to the creation of mice in which one or more genes are inactivated or 'knocked out'. Knockout mice are extensively used to better investigate the molecular and cellular mechanisms underlying these diseases as well as the biological role of specific genes. Moreover, they are also useful tools for developing new therapeutic strategies. The success of using knockout mice is possible due to availability of several models used to mimic some clinical manifestations reported in psychiatric patients. In the present review, we will give an update of the most used gene knockout models in the field of psychiatric disorders including depression, anxiety, and obsessive-compulsive disorder

Emotional profile of female rats showing binge eating behavior

Binge eating disorder (BED) is characterized by uncontrolled consumption of a large amount of food in a brief period of time. A large body of evidence has shown that BED can be a chronic condition associated with elevated psychiatric comorbidity, including depression and anxiety, and compulsive behavior. In this study we used an animal model of BED in which binge eating behavior was induced in female rats by providing limited access to high fat diet (margarine) to investigate the emotional traits of bingeing animals before and after the binge-like consumption of margarine. Using the plus maze test to disclose a potential anxious phenotype, we found that bingeing rats are much more anxious before the access to margarine, and that this condition is significantly reduced after its consumption. Conversely, no difference was detected between bingeing rats in the marble burying test before and after access to margarine. Yet, the number of marbles buried by bingeing rats before margarine consumption was significantly higher than control groups thus suggesting a compulsive-like trait. In the forced swimming test, bingeing rats showed a decrease in depression-like behavior after the consumption of margarine. Altogether, our findings demonstrate the occurrence of an altered emotional state in female rats showing binge eating behavior