Alcohol and energy drinks: individual contribution of common ingredients on ethanol-induced behaviour

Since energy drinks (EDs) were sold to the general public as soft drinks and recreational beverages, mixing EDs with ethanol has grown in popularity, particularly among younger people. Given the research that links these drinks with higher risk behaviors and increased ethanol intake, ethanol combined with EDs (AmEDs) is a particularly worrying combination. EDs generally commonly include a variety of ingredients. Sugar, caffeine, taurine, and B-group vitamins are almost always present. Studies on the combined effect of ethanol and sugar and caffeine on ethanol-induced behaviors are extensive. Not so much in regards to taurine and vitamins. This review briefly summarises available information from research on the isolated compounds on EtOH-induced behaviors first, and secondly, the combination of AmEDs on EtOH effects. The conclusion is that additional research is needed to fully comprehend the characteristics and consequences of AmEDs on EtOH-induced behaviors

Bipolar disorder: a disorder of circadian regulation?

Dentro de los llamados trastornos del estado de ánimo, el trastorno bipolar ha sido poco estudiado, a pesar de su prevalencia y el grado de incapacidad que produce en la población. Para comprender adecuadamente los factores causales de un trastorno es necesaria la investigación básica. Sin embargo, la falta de un modelo animal satisfactorio en el caso del trastorno bipolar dificulta el progreso en el conocimiento de sus bases neurobiológicas. Esta revisión pretende aunar las recientes aportaciones realizadas en referencia al trastorno bipolar, y aportar así una visión de conjunto que ayude a esclarecer la línea causal, partiendo del nivel más básico: el componente genético subyacente. En concreto, este trabajo presenta evidencia sobre los avances obtenidos gracias a modelos animales de ratones mutantes de genes implicados en la regulación de los ritmos circadianos, foco actual de la hipótesis etiopatogénica del trastorno bipolar.Despite its prevalence and degree of disability, bipolar disorder has not received the attention it deserves within the so-called mood disorders. To properly understand the factors associated with its origin, basic research is needed. However, the lack of a satisfactory animal model hinders progress in understanding the neurobiological basis that gains importance in explaining this condition. This review, therefore, aims to combine the recent contributions about bipolar disorder, and thus provide an overview to help clarify the causal line, starting from the most basic level: the underlying genetic component. Specifically, this paper presents evidence on the progress achieved with animal models of mutant mice of genes involved in regulating circadian rhythms, current focus of etiopathogenic hypothesis of bipolar disorder

Cannabinoids, Chemical Senses, and Regulation of Feeding Behavior

The herb Cannabis sativa has been traditionally used in many cultures and all over the world for thousands of years as medicine and recreation. However, because it was brought to the Western world in the late 19th century, its use has been a source of controversy with respect to its physiological effects as well as the generation of specific behaviors. In this regard, the CB1 receptor represents the most relevant target molecule of cannabinoid components on nervous system and whole-body energy homeostasis. Thus, the promotion of CB1 signaling can increase appetite and stimulate feeding, whereas blockade of CB1 suppresses hunger and induces hypophagia. Taste and flavor are sensory experiences involving the oral perception of food-derived chemicals and drive a primal sense of acceptable or unacceptable for what is sampled. Therefore, research within the last decades focused on deciphering the effect of cannabinoids on the chemical senses involved in food perception and consequently in the pattern of feeding. In this review, we summarize the data on the effect of cannabinoids on chemical senses and their influences on food intake control and feeding behavior

Centrally formed acetaldehyde mediates ethanol-induced brain PKA activation

Centrally formed acetaldehyde has proven to be responsible for several psychopharmacological effects induced by ethanol. In addition, it has been suggested that the cAMP-PKA signaling transduction pathway plays an important role in the modulation of several ethanol-induced behaviors. Therefore, we hypothesized that acetaldehyde might be ultimately responsible for the activation of this intracellular pathway. We used three pharmacological agents that modify acetaldehyde activity (α-lipoic acid, aminotriazole, and d-penicillamine) to study the role of this metabolite on EtOH-induced PKA activation in mice. Our results show that the injection of α-lipoic acid, aminotriazole and d-penicillamine prior to acute EtOH administration effectively blocks the PKA-enhanced response to EtOH in the brain. These results strongly support the hypothesis of a selective release of acetaldehyde-dependent Ca2+ as the mechanism involved in the neurobehavioral effects elicited by EtOH.This research was supported by a grant from the Spanish Ministerio de Ciencia e Innovacion (PSI2011-28934/PSIC). Pablo Baliño was supported by a fellowship from the CICYT (BES-2009-024438). Ernesto Tarragon was supported at the time by Red de Trastornos Adictivos, Ministerio de Sanidad y Politica Social (RD06/0001/0028), Spain

Implications of glial nitric oxide in neurodegenerative diseases

Nitric oxide (NO) is a pleiotropic janus-faced molecule synthesized by nitric oxide synthases (NOS) which plays a critical role in a number of physiological and pathological processes in humans. The physiological roles of NO depend on its local concentrations, as well as its availability and the nature of downstream target molecules. Its double-edged sword action has been linked to neurodegenerative disorders. Excessive NO production, as the evoked by inflammatory signals, has been identified as one of the major causative reasons for the pathogenesis of several neurodegenerative diseases. Moreover, excessive NO synthesis under neuroinflammation leads to the formation of reactive nitrogen species and neuronal cell death. There is an intimate relation between microglial activation, NO and neuroinflammation in the human brain. The role of NO in neuroinflammation has been defined in animal models where this neurotransmitter can modulate the inflammatory process acting on key regulatory pathways, such as those associated with excitotoxicity processes induced by glutamate accumulation and microglial activation. Activated glia express inducible NOS and produce NO that triggers calcium mobilization from the endoplasmic reticulum, activating the release of vesicular glutamate from astroglial cells resulting in neuronal death. This change in microglia potentially contributes to the increased age-associated susceptibility and neurodegeneration. In the current review, information is provided about the role of NO, glial activation and age-related processes in the central nervous system (CNS) that may be helpful in the isolation of new therapeutic targets for aging and neurodegenerative diseases

Effects of α-synuclein levels on cerebral synaptic function: Validation of a novel PET radioligand for the early diagnosis of Parkinson’s disease

Background In Parkinson’s disease, converging evidence supports a pathogenic role for excessive α–synuclein accumulation in synaptic terminals that may propagate back to the soma of vulnerable nerve cells such as neurons in the substantia nigra pars compacta. The resulting loss of dopaminergic terminals in the striatum can be demonstrated in vivo using 18F-Dopa-PET (positron emission tomography). However, there’s currently no validated biomarker of the progressive synaptic dysfunction in other vulnerable areas such as the cerebral cortex. Goal In this longitudinal study, we will test the hypothesis that the loss of synaptic terminals in a mouse model of excessive α–synuclein accumulation can be demonstrated in vivo before the occurrence of behavioural disturbances using 18F-UCB-H, a new PET biomarker developed at CRC. We will also test if this new imaging modality is sensitive enough to study the effect of a disease modifying therapy such as chronic physical exercise. Methods We will use microPET for the in vivo quantification of 18F-UCB-H brain uptake in 16 wild type animals and 16 transgenic (Tg) mice overexpressing human α–syn under the mThy1 promotor every 2 months. Data will be validated against post-mortem analyses after the last PET study. Predictions We predict decreased tracer uptake over time in the basal ganglia and cerebral cortex in Tg mice as compared with WT animals. Also, we predict a relationship between 18F-UCB-H uptake levels in basal ganglia and cerebral cortex and progressive alterations in both motor and cognitive functions, respectively. Further, we also expect that chronic exercise will slow down both motor and cognitive disturbances, as well as the rate of 18F-UCB-H brain uptake decreases. Conclusion If 18F-UCB-H PET proves to be a valid biomarker for the early detection of α–synuclein accumulation in the pre-clinical model of PD, the methods will tested on human clinical populations

Octodon degus: A Model for the Cognitive Impairment Associated with Alzheimer's Disease

Octodon degus (O. degus) is a diurnal rodent that spontaneously develops several physiopathological conditions, analogous in many cases to those experienced by humans. In light of this, O. degus has recently been identified as a very valuable animal model for research in several medical fields, especially those concerned with neurodegenerative diseases in which risk is associated with ageing. O. degus spontaneously develops β-amyloid deposits analogous to those observed in some cases of Alzheimer’s disease (AD). Moreover, these deposits are thought to be the key feature for AD diagnosis, and one of the suggested causes of cell loss and cognitive deficit. This review aims to bring together information to support O. degus as a valuable model for the study of cerebral aging

L’École biblique, l’archéologie et le développement de la photographie en Palestine

Dans les environs d’Hébron, Assomptionistes se tenant sur le mur entourantle chêne de Mambré (Ramat-el Khalil), l’endroit où, selon la légende, Abraham a rencontré les Saints visiteurs. Notre présentation concerne les deux facettes du fonds photographique ancien de l’École biblique. Nous le faisons de manière assez informelle : l’École est heureuse de faire part de ce trésor d’archives photographiques, ouvert aux chercheurs. Pour avoir une idée de l’éventuel intérêt de ce fonds pour la recher..