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We examined how the experience of a threatening stimulus alters subsequent behavior in a situation where the immediate threat is absent. A small huddle of 12-day-old rats was exposed to a potentially infanticidal adult male rat for 5 min. During male exposure, pups were significantly more immobile than control pups. Thirty, 60, and 180 min after male exposure, the pups were isolated for 5 min from litter and dam in an unfamiliar environment. When isolated, pups that had been previously exposed to the male emitted significantly fewer ultrasonic vocalizations than controls, but did not differ in immobility. Low levels of vocalization were apparent 30 and 60 min after male exposure and were not evident at 180 min. The pups seemed to have adjusted their behavior to a potential male threat in a different context for a limited period of time. (C) 2003 Wiley Periodicals, Inc

2-week-old rats. --- Adult. --- Alters. --- Anxiety-like behavior. --- Behavior. --- Behavioral-inhibition. --- Cat odor. --- Control. --- Defensive behaviors. --- Environment. --- Experience. --- Exposure. --- Immobility. --- Infant rats. --- Infanticide. --- Level. --- Male rat. --- Male. --- Neural plasticity. --- Ontogeny. --- Periaqueductal gray. --- Preweanling rats. --- Pups. --- Rat. --- Rats. --- Responses. --- Stimulus. --- Time. --- Ultrasonic vocalization. --- Vocalization.

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The present study assessed alterations in mesolimbic enkephalin (ENK) mRNA levels after predator [2,5-dihydro-2,4,5-trimethylethiazoline (TMT)] and non-predator (butyric acid) odor encounter and/or light-dark (LD) testing in CD-1 mice immediately, 24, 48 and 168 h after the initial odor encounter and/or LD testing. The nucleus accumbens, ventral tegmental area, basolateral (BLA), central (CEA) and medial amygdaloid nuclei, prelimbic and infralimbic cortex were assessed for fos-related antigen (FRA) and/or ENK mRNA as well as neuronal activation of ENK neurons (FRA/ENK). Mice exposed to TMT displayed enhanced freezing and spent less time in the light of the immediate LD test relative to saline- or butyric acid-treated mice. Among mice exposed to TMT, LD anxiety-like behavior was associated with increased FRA in the prelimbic cortex and accumbal shell and decreased ENK-positive neurons in the accumbal core. Mice displaying high TMT-induced LD anxiety exhibited increased ENK-positive neurons in the BLA, CEA and medial amygdaloid nuclei relative to mice that displayed low anxiety-like behavior in the LD test after TMT exposure. In the BLA and CEA, 'high-anxiety' mice also displayed increased FRA/ENK after TMT exposure and LD testing. In contrast to neural cell counts, the level of ENK transcript was decreased in the BLA and CEA of 'high-anxiety' mice after TMT exposure and LD testing. These data suggest that increased FRA may regulate stressor-responsive genes and mediate long-term behavioral changes. Indeed, increased ENK availability in mesolimbic sites may promote behavioral responses that detract from the aversiveness of the stressor experience

Accumbens. --- Activation. --- Activity. --- Amygdala. --- Anxiety-like behavior. --- Anxiety. --- Area. --- Behavior. --- Behavioral-responses. --- Butyric acid. --- Cortex. --- Defensive behavior. --- Double dissociation. --- Emotional responses. --- Enkephalin. --- Experience. --- Exposure. --- Expression. --- Extended amygdala. --- Fos-related antigen. --- Freezing. --- Gene. --- Genes. --- Individual-differences. --- Infralimbic cortex. --- Infralimbic. --- Level. --- Light. --- Long-term. --- Male-rats. --- Mice. --- Neuronal. --- Neurons. --- Nucleus accumbens. --- Nucleus-accumbens. --- Nucleus. --- Odor. --- Posttraumatic-stress-disorder. --- Predator odor. --- Predator. --- Prelimbic. --- Response. --- Responses. --- Self-stimulation. --- Stressor. --- Test. --- Time. --- Unconditioned fear. --- Ventral tegmental area.

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Although sphingolipids are ubiquitous components of cellular membranes, their abundance in cells is generally lower than glycerolipids or cholesterol, representing less than 20% of total lipid mass. Following their discovery in the brain—which contains the largest amounts of sphingolipids in the body—and first description in 1884 by J.L.W. Thudichum, sphingolipids have been overlooked for almost a century, perhaps due to their complexity and enigmatic nature. When sphingolipidoses were discovered, a series of inherited diseases caused by enzyme mutations involved in sphingolipid degradation returned to the limelight. The essential breakthrough came decades later, in the 1990s, with the discovery that sphingolipids were not just structural elements of cellular membranes but intra- and extracellular signaling molecules. It turned out that their lipid backbones, including ceramide and sphingosine-1-phosphate, had selective physiological functions. Thus, sphingolipids emerged as essential players in several pathologies including cancer, diabetes, neurodegenerative disorders, and autoimmune diseases. The present volume reflects upon the unexpectedly eclectic functions of sphingolipids in health, disease, and therapy. This fascinating lipid class will continue to be the subject of up-and-coming future discoveries, especially with regard to new therapeutic strategies.

Research & information: general --- Biology, life sciences --- S1P receptor --- inflammation --- S1P transporter --- spinster homolog 2 --- barrier dysfunction --- anxiety --- depression --- sphingolipids --- sphingomyelinase --- ceramidase --- Smpd1 --- acid sphingomyelinase --- forebrain --- depressive-like behavior --- anxiety-like behavior --- ceramide --- ceramides --- ceramidases --- neurodegenerative diseases --- infectious diseases --- sphingosine 1-phoshate --- sphingosine 1-phosphate receptor --- S1P1-5 --- sphingosine 1-phosphate metabolism --- sphingosine 1-phosphate antagonistst/inhibitors --- sphingosine 1-phosphate signaling --- stroke --- multiple sclerosis --- neurodegeneration --- fingolimod --- Sphingosine-1-phosphate --- obesity --- type 2 diabetes --- insulin resistance --- pancreatic β cell fate --- hypothalamus --- sphingosine-1-phosphate --- ischemia/reperfusion --- cardioprotection --- vasoconstriction --- coronary flow --- myocardial function --- myocardial infarct --- albumin --- type 1 diabetes --- beta-cells --- islets --- insulin --- cytokines --- S1P --- animal models --- cystic fibrosis --- autophagy --- myriocin --- Aspergillus fumigatus --- CLN3 disease --- Cln3Δex7/8 mice --- flupirtine --- allyl carbamate derivative --- apoptosis --- cancer --- gangliosides --- immunotherapy --- metastasis --- phenotype switching --- sphingosine 1-phosphate --- Sphingosine 1-phosphate (S1P) --- S1P-lyase (SGPL1) --- tau --- calcium --- histone acetylation --- hippocampus --- cortex --- astrocytes --- neurons --- sphingosine kinase --- G-protein-coupled receptors --- Gαq/11 --- sphingosine kinase 1 --- SK1 --- microRNA --- transcription factor --- hypoxia --- long non-coding RNA