Total sleep deprivation impairs fear memory retrieval by decreasing the basolateral amygdala activity.

It is well known that sleep deprivation impairs fear memory processes, but little is known about the underlying mechanisms or circuits. The aim of this study was to evaluate the effects of total sleep deprivation (24 h) on contextual fear memory acquisition, consolidation, and retrieval, as well as c-Fos activity in the hippocampus and amygdala. Fear memory recall was associated with an increase in the number of c-Fos-positive cells in the hippocampal CA1 and CA3 regions and the basolateral amygdala (BLA). Total sleep deprivation before to the acquisition and during consolidation of memory impaired retrieval and blocked the associated c-Fos activity in the hippocampus and amygdala. In contrast, total sleep deprivation before memory recall also impaired retrieval, but selectively prevented the increase of c-Fos activity in the amygdala (but not in the hippocampus). Our data indicate that sleep is essential not only for acquisition and consolidation but also for the retrieval of fear memories. They also suggest a differential susceptibility of specific memory-related neural circuits (hippocampus and BLA) to the absence of sleep.

[Synaptic plasticity as a substrate of resilience]. / Plasticidad sinaptica como sustrato de la resiliencia.

INTRODUCTION: Adverse life experiences promote the development of mental illness such as depression, anxiety or schizophrenia. However, some individuals are capable to overcome adversity, achieving a physical and psychological normal development; this process is known as resilience. AIM: To discuss the neuronal substrates of resilience. DEVELOPMENT: We propose that resilience at neuronal level needs systems for representing and evaluating the context (adverse situation) in order to display an adequate behavioural output, and for reorganizing memory associated to the adverse situation in order to tell a new story using the same elements of experience; this is, a system that allows to reorganize neuronal ensembles associated to the adverse memory. In this sense, it is not coincidence that neuronal substrates involving in resilience include the reward-guided behavior system (nucleus accumbens-ventral tegmental area), the emotional system (amygdala-hippocampus), the stress system (hypothalamus-pituitary-adrenal) and the system for context evaluation, representation and discrimination (prefrontal cortex-hippocampus). We emphasize that each adverse experience shapes both the activity of the resilience neuronal system and the behavioral output. CONCLUSIONS: We propose that synaptic plasticity in structures for representing and evaluating context is the neuronal substrate of resilience. Specifically, cortico-hippocampal interactions would allow to re-build adverse experiences through the reorganization of neuronal ensembles.

TITLE: Plasticidad sinaptica como sustrato de la resiliencia.Introduccion. Las experiencias adversas facilitan el desarrollo de enfermedades mentales como la depresion, la ansiedad o la esquizofrenia. Sin embargo, algunos individuos muestran capacidades para superar la adversidad logrando un desarrollo fisico y psicologico adecuado; este proceso se conoce como resiliencia. Objetivo. Discutir cual es el sustrato neuronal de la resiliencia. Desarrollo. Se plantea que la resiliencia, neuronalmente, necesita sistemas que representen y evaluen el contexto (la situacion adversa) para dar una salida conductual adecuada, y que reorganicen la memoria de la situacion adversa para poder contar otro relato a partir de los mismos elementos de la experiencia, es decir, un sistema que permita reorganizar los ensambles neuronales de dicha memoria. En este sentido, no es casualidad que los sustratos neuronales involucrados en la resiliencia incluyan al sistema de la motivacion-accion-recompensa (nucleo accumbens-area tegmental ventral), de las emociones (amigdala-hipocampo), del estres (eje hipotalamo-hipofiso-adrenal) y de la representacion, evaluacion y discriminacion del contexto (corteza prefrontal-hipocampo). Se hace enfasis en mostrar como las experiencias adversas especificas modulan tanto la actividad del sistema neuronal de la resiliencia como la salida conductual de cada individuo. Conclusiones. Se propone que la plasticidad sinaptica en estructuras que representan y evaluan el contexto son el sustrato neuronal de la resiliencia. Especificamente, las interacciones corticohipocampicas permitirian la reestructuracion de las experiencias adversas a traves de la reorganizacion de los ensambles neuronales.

Oleoylethanolamide affects food intake and sleep-waking cycle through a hypothalamic modulation.

Oleoylethanolamide (OEA) is an endogenous molecule related to endocannabinoids (eCBs) that induces satiety. It binds to the peroxisome-proliferator-activated receptor alpha (PPAR alpha). PPAR alpha is involved in feeding regulation and it has been proposed to play a role in sleep modulation. The objective of the present work is to show if this molecule modifies the sleep-waking cycle through central mechanisms. We have found that the peripheral administration of OEA reduces food intake and increases waking with a concomitant reduction of rapid eye movement sleep. Additionally, this treatment produces deactivation of the lateral hypothalamus, as inferred from the c-Fos expression evaluation. Finally, intra-lateral hypothalamus injection of OEA has mirrored the effects induced by this molecule when it is peripherally administered. In conclusion, we show for the very first time that OEA can modify the sleep-waking cycle and food intake, apparently mediated by the lateral hypothalamus.

De la restauración neuronal a la reorganización de los circuitos neuronales: una aproximación a las funciones del sueño / From neuronal recovery to the reorganisation of neuronal circuits: a review of the functions of sleep

Objetivo. Analizar datos y conceptos que se han generadoen torno a una de las funciones propuestas para el sueño: la restauraciónneuronal. Desarrollo. El sueño es un estado de concienciadiferente de la vigilia. Los mamíferos invierten una buena partede su vida en dormir; por ejemplo, los humanos dormimos una terceraparte de nuestra vida, pero ¿para qué invertir tanto tiempo enun estado donde perdemos contacto con el entorno?, ¿qué pasaríasi no durmiéramos? La privación de sueño total altera procesoscognitivos, como la memoria o la atención; si esta privación seprolonga, el sujeto se deteriora y muere. Se ha propuesto que elsueño sirve para restaurar a los organismos del desgaste ocurridodurante la vigilia y, dado que los primeros efectos de la ausenciade sueño se observan en procesos que dependen directamente delcerebro, se ha sugerido que la restauración neuronal es su principalobjetivo. En este trabajo se analizan algunos estudios sobre losefectos de la privación de sueño total en humanos y ratas, así comola relación entre el sueño y el sistema de las neurotrofinas, el cualpromueve la supervivencia y la restauración neuronal. Finalmente,se discuten teorías recientes sobre la función del sueño. Conclusiones.La restauración de las neuronas no es el fin último del sueño,sino mantener y reorganizar los circuitos neuronales, incluyendo laneoformación de sinapsis, que permiten modificar redes neuronalesexistentes, por efecto de la experiencia, y todo esto para el adecuadofuncionamiento del cerebro y su adaptación al ambiente

Aim. To analyse the data and concepts that have been produced in relation to one of the functions that have beensuggested for sleep, namely, neuronal recovery. Development. Sleep is a state of consciousness that is different to that ofarousal. Mammals devote an important part of their lives to sleeping; for example, as humans, we sleep for a third of our lives,but why do we spend so much time in a state where we lose contact with our surroundings? What would happen if we didn’tsleep? Total sleep deprivation alters cognitive processes such as memory or attention, and if this deprivation is prolonged, theindividual deteriorates and dies. It has been suggested that sleep provides the organism with time to recover from the wear andtear that occurs during the waking state and, given that the first effects of the absence of sleep are seen to affect processes thatare directly dependent on the brain, it has been claimed that its main purpose is to allow neuronal recovery. In this work weanalyse some of the studies on the effects of total sleep deprivation in humans and rats, as well as the relationship betweensleep and the neurotrophin system, which promotes neuronal survival and recovery. Finally, the latest theories about thefunction of sleep are discussed. Conclusions. Neuron recovery is not the ultimate purpose of sleep; rather it is to allow formaintenance and reorganisation of neuronal circuits, including new synapse formation, which enables existing neuronalnetworks to be modified by the effect of experience, and all this makes it possible for the brain to work properly and to adaptitself to the environment

[From neuronal recovery to the reorganisation of neuronal circuits: a review of the functions of sleep]. / De la restauración neuronal a la reorganización de los circuitos neuronales: una aproximación a las funciones del sueño.

AIM: To analyse the data and concepts that have been produced in relation to one of the functions that have been suggested for sleep, namely, neuronal recovery. DEVELOPMENT: Sleep is a state of consciousness that is different to that of arousal. Mammals devote an important part of their lives to sleeping; for example, as humans, we sleep for a third of our lives, but why do we spend so much time in a state where we lose contact with our surroundings? What would happen if we didn't sleep? Total sleep deprivation alters cognitive processes such as memory or attention, and if this deprivation is prolonged, the individual deteriorates and dies. It has been suggested that sleep provides the organism with time to recover from the wear and tear that occurs during the waking state and, given that the first effects of the absence of sleep are seen to affect processes that are directly dependent on the brain, it has been claimed that its main purpose is to allow neuronal recovery. In this work we analyse some of the studies on the effects of total sleep deprivation in humans and rats, as well as the relationship between sleep and the neurotrophin system, which promotes neuronal survival and recovery. Finally, the latest theories about the function of sleep are discussed. CONCLUSIONS: Neuron recovery is not the ultimate purpose of sleep; rather it is to allow for maintenance and reorganisation of neuronal circuits, including new synapse formation, which enables existing neuronal networks to be modified by the effect of experience, and all this makes it possible for the brain to work properly and to adapt itself to the environment.