bluuebunny/crossref_metadata_2025_split huggingface dataset:
The sense of smell: molecular basis of odorant recognition
Authors: Zarzo Manuel 
Published: September 2007

AbstractMost animal species rely on odorant compounds to locate food, predators, or toxins. The sense of smell is also involved in animal communication, and revealing the underlying mechanisms will therefore facilitate a deeper understanding of animal behaviour. Since the 1940s different theories have speculated on the fundamental basis of olfaction. It was assumed that odorant molecules were recognized by selective protein receptors in the nose, triggering a nervous signal processed by the brain. The discovery of these receptors in the early 1990s allowed great progress in understanding the physiological and biochemical principles of olfaction. An overview of the different mechanisms involved in the coding of odour character as well as odour intensity is presented here, focusing on the biochemical basis of odorant recognition. Despite the enormous progress achieved in recent years, details of odorant‐receptor interaction at the molecular level and the mechanisms of olfactory receptor activation are poorly understood. The likely role of metal ions in odorant recognition is discussed, and also the perireceptor events involved in odorant transport and biotransformation, with a view to providing a comprehensive overview of mammalian olfaction to guide future computational structural models and the design of functional experiments. Recent studies have analysed the olfactory genome of several species, providing information about the evolution of olfaction. The role of the olfactory system in animal communication is also described.
Leave it all behind: a taxonomic perspective of autotomy in invertebrates
Authors: Fleming Patricia A. , Muller Davina , Bateman Philip W. 
Published: September 2007

AbstractAutotomy is defined herein as the shedding of a body part, where (1) the loss of the body part is defensive (autotomy helps prevent the whole animal from being compromised and is in response to external stimuli); (2) shearing occurs by an intrinsic mechanism along a breakage plane (there has been selection for certain body parts to be pulled off easily); and (3) the loss is controlled ‐ the animal moves away from the trapped limb, the loss is under some form of central control (neural or hormonal), or the body part is detached quickly.Autotomy (under this defensive definition) has evolved independently for a diverse array of body parts in many taxa; we have summarised available information for over 200 invertebrate species. The advantages of autotomy include escape from entrapment, an effective form of attack, expulsion of an infected body part or in limiting wounding. We discuss how the incidence of autotomy may therefore be correlated with various traits such as limb function, sex differences, other defence mechanisms, habitat disturbance, and sociality. There are also costs associated with autotomy. Short‐term costs include loss of a specialised appendage or organ, reduced speed and stability, or even death. Long‐term costs include compromised foraging and feeding (often leading to reduced growth), altered anti‐predator, competitive or reproductive behaviour, and even defective development. Regenerating lost appendages may also incur significant costs for the individual. We examine the costs and benefits of autotomy, and discuss the evolutionary selective pressures that contribute to the prevalence and effectiveness of autotomy in invertebrates.
Exploring the role of vision in social foraging: What happens to group size, vigilance, spacing, aggression and habitat use in birds and mammals that forage at night?
Authors: Beauchamp Guy 
Published: September 2007

AbstractI examined the role of vision in social foraging by contrasting group size, vigilance, spacing, aggression and habitat use between day and night in many species of birds and mammals. The literature review revealed that the rate of predation/disturbance was often reduced at night while food was considered more available. Social foraging at night was prevalent in many species suggesting that low light levels at night are not sufficient to prevent the formation and cohesion of animal groups. Group sizes were similar or larger at night than during the day in more than half the bird populations and in the majority of mammal populations. Factors such as calls, feeding noises or smells may contribute to the formation and cohesion of groups at night. Larger numbers of foragers at night may also facilitate the aggregation of more foragers. Vigilance levels were usually lower at night perhaps as a response to the lower predation risk or to the decreased value of scanning for predators that are difficult to locate. Low light levels may also make visual cues that promote aggression less conspicuous, which may be a factor in the lower levels of aggression documented at night. Spacing varied as a function of time of day in response to changes in foraging mode or food availability. Habitats that are avoided during the day were often used at night. Foraging at night presents birds and mammals with a new set of constraints that influence group size, time budgeting and habitat use.
Mask‐ and distractor‐triggered inhibitory processes in the priming of motor responses: An EEG study
Authors: Jaśkowski Piotr , Białuńska Anita , Tomanek Monika , Verleger Rolf 
Published: September 2007

AbstractMasked stimuli presented near the threshold of conscious awareness may act as primes, affecting responses to subsequent targets. With arrows as primes and targets, the prime–mask–target sequence has been shown to evoke triphasic lateralized readiness potentials (LRP) with two phases of imbalance between hemispheres preceding the target‐related contralateral preponderance of negativity: first a negative, then a positive preponderance contralateral to prime direction. The present article provides evidence that the second wave is related to mask presentation and reflects inhibitory processing independent of reductions in prime visibility, even being evoked by nonmasking distractors that leave the prime fully accessible for consciousness. Of all hypotheses put forward to account for inverse effects in masked priming, this finding is most compatible with the mask‐triggered inhibition hypothesis suggested byP. Jaśkowski (2007).
Peripheral inflammation increases Scya2 expression in sensory ganglia and cytokine and endothelial related gene expression in inflamed tissue
Authors: Yang Hsiu‐Ying T. , Mitchell Kendall , Keller Jason M. , Iadarola Michael J. 
Published: September 2007

AbstractThe sensation of pain (nociception) is a critical factor in host defense during tissue injury and inflammation and is initiated at the site of injury by activation of primary afferent C‐fiber and A‐∂ nerve endings. Inflammation induces tissue alterations that sensitize these nociceptive nerve terminals, contributing to persistent pain. To understand this ‘algesic tissue environment’ and peripheral nervous signaling to the CNS and immune system, we examined cytokine and endothelial‐related gene expression profiles in inflamed rat tissues and corresponding dorsal root ganglia (DRG) by microarray and RT‐PCR following hind paw injection of carrageenan. In inflamed tissue, forty‐two cytokine and endothelial‐related genes exhibited elevated expression. In contrast, in DRG, only Scya2 (chemokine C‐C motif ligand 2) mRNA was up‐regulated, leading to an increase in its gene product monocyte chemoattractant protein‐1. Scya2 mRNA was localized byin situhybridization‐immunocytochemical double‐labeling to a subpopulation of vanilloid receptor‐1 (transient receptor potential vanilloid subtype 1) containing neurons, and its expression was increased by direct transient receptor potential vanilloid subtype 1 stimulation with the vanilloid agonist resiniferatoxin, indicating sensitivity to nociceptive afferent activity. Our results are consistent with the idea that monocyte chemoattractant protein‐1 at the site of peripheral injury and/or in DRG is involved in inflammatory hyperalgesia.
Expression of functional Kir6.1 channels regulates glutamate release at CA3 synapses in generation of epileptic form of seizures
Authors: Soundarapandian Mangala M. , Wu Di , Zhong Xiaofen , Petralia Ronald S. , Peng Lisheng , Tu Weihong , Lu Youming 
Published: September 2007

AbstractThe Kir6.1 channels are a subtype of ATP‐sensitive inwardly rectifying potassium (KATP) channels that play an essential role in coupling the cell’s metabolic events to electrical activity. In this study, we show that functional Kir6.1 channels are located at excitatory pre‐synaptic terminals as a complex with type‐1 Sulfonylurea receptors (SUR1) in the hippocampus. The mutant mice with deficiencies in expressing the Kir6.1 or the SUR1 gene are more vulnerable to generation of epileptic form of seizures, compared to wild‐type controls. Whole‐cell patch clamp recordings demonstrate that genetic deletion of the Kir6.1/SUR1 channels enhances glutamate release at CA3 synapses. Hence, expression of functional Kir6.1/SUR1 channels inhibits seizure responses and possibly acts via limiting excitatory glutamate release.
Developmental changes of glycosphingolipids and expression of glycogenes in mouse brains
Authors: Ngamukote Sathaporn , Yanagisawa Makoto , Ariga Toshio , Ando Susumu , Yu Robert K. 
Published: September 2007

AbstractGlycosphingolipids (GSLs) and their sialic acid‐containing derivatives, gangliosides, are important cellular components and are abundant in the nervous system. They are known to undergo dramatic changes during brain development. However, knowledge on the mechanisms underlying their qualitative and qualitative changes is still fragmentary. In this investigation, we have provided a detailed study on the developmental changes of the expression patterns of GSLs, GM3, GM1, GD3, GD1a, GD2, GD1b, GT1b, GQ1b, A2B5 antigens (c‐series gangliosides such as GT3 and GQ1c), Chol‐1α (GT1aα and GQ1bα), glucosylceramide, galactosylceramide (O1 antigen), sulfatide (O4 antigen), stage‐specific embryonic antigen‐1 (Lewis x) glycolipids, and human natural killer‐1 glycolipid (sulfoglucuronosyl paragloboside) in developing mouse brains [embryonic day 12 (E12) to adult]. In E12–E14 brains, GD3 was a predominant ganglioside. After E16, the concentrations of GD3 and GM3 markedly decreased, and the concentrations of a‐series gangliosides, such as GD1a, increased. GT3, glucosylceramide, and stage‐specific embryonic antigen‐1 were expressed in embryonic brains. Human natural killer‐1 glycolipid was expressed transiently in embryonic brains. On the other hand, Chol‐1α, galactosylceramide, and sulfatide were exclusively found after birth. To provide a better understanding of the metabolic basis for these changes, we analyzed glycogene expression patterns in the developing brains and found that GSL expression is regulated primarily by glycosyltransferases, and not by glycosidases. In parallel studies using primary neural precursor cells in culture as a tool for studying developmental events, dramatic changes in ganglioside and glycosyltransferase gene expression were also detected in neurons induced to differentiate from neural precursor cells, including the expression of GD3, followed by up‐regulation of complex a‐ and b‐series gangliosides. These changes in cell culture systems resemble that occurring in brain. We conclude that the dramatic changes in GSL pattern and content can serve as useful markers in neural development and that these changes are regulated primarily at the level of glycosyltransferase gene expression.
The effects of oxidative stress on parkin and other E3 ligases
Authors: LaVoie Matthew J. , Cortese Giuseppe P. , Ostaszewski Beth L. , Schlossmacher Michael G. 
Published: September 2007

AbstractAutosomal recessive mutations within the Parkin gene are associated with degeneration of the substantia nigra and locus coeruleus and an inherited form of Parkinson’s disease (PD). As loss‐of‐function mutations in parkin are responsible for a familial variant of PD, conditions that affect wild‐type parkin are likely to be associated with increased risk of idiopathic disease. Previous studies uncovered a unique vulnerability of the parkin protein to dopamine (DA)‐induced aggregation and inactivation. In this study, we compared several proteins that share structural elements or ubiquitinating activity with parkin. We report that oxidative stress in several cell lines and primary neurons induces the aggregation of parkin into high molecular weight species, at least a portion of which are self‐associated homo‐multimers. While parkin was preferentially affected by excess DA, each of the E3 proteins tested were made more insoluble by oxidative stress, and they varied in degree of susceptibility (e.g. parkin > HHARI ≅ CHIP > c‐Cbl > E6AP). These conditions of oxidative stress were also associated with decreased parkin E3 ligase activity. Similar to recently conducted studies on α‐synuclein processing, both macroautophagy and the proteasome participate in parkin degradation, with the proteasome playing the predominant role for normal parkin turnover and macroautophagy being more important in the degradation of aggregated parkin. These data further highlight the selective vulnerability of parkin to DA‐induced modifications, demonstrating for the first time the ability of both endogenous and ectopically expressed parkin to transition into an insoluble state in part through self‐association and oligomer formation.
Monoamine oxidase‐A modulates apoptotic cell death induced by staurosporine in human neuroblastoma cells
Authors: Fitzgerald Julia C. , Ufer Christoph , De Girolamo Luigi A. , Kuhn Hartmut , Billett E. Ellen 
Published: September 2007

AbstractMonoamine oxidases (MAOs) are mitochondrial enzymes which control the levels of neurotransmitters in the brain and dietary amines in peripheral tissues via oxidative deamination. MAO has also been implicated in cell signalling. In this study, we describe the MAO‐A isoform as functional in apoptosis induced by staurosporine (STS) in human dopaminergic neuroblastoma cells (SH‐SY5Y). Increased levels of MAO‐A activity were induced by STS, accompanied by increased MAO‐A protein and activation of the initiator of the intrinsic pathway, caspase 9, and the executioner caspase 3. MAO‐A mRNA levels were unaffected by STS, suggesting that changes in MAO‐A protein are due to post‐transcriptional events. Two unrelated MAO‐A inhibitors reduced caspase activation. STS treatment resulted in sustained activation of the mitogen‐activated protein kinase pathway enzymes extracellular regulated kinase, c‐jun terminal kinase and p38, and depletion of the anti‐apoptotic protein Bcl‐2. These changes were significantly reversed by MAO inhibition. Production of reactive oxygen species was increased following STS exposure, which was blocked by both MAO inhibition and the antioxidant N‐acetylcysteine. Therefore our data provide evidence that MAO‐A, through its production of reactive oxygen species as a by‐product of its catalytic activity on the mitochondrial surface, is recruited by the cell to enhance apoptotic signalling.
Metabotropic actions of kainate receptors in the CNS
Authors: Rodríguez‐Moreno Antonio , Sihra Talvinder S. 
Published: September 2007

AbstractKainate receptors (KARs), together with NMDA and α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate receptors (AMPA), are typically described as ionotropic glutamate receptors. Although ionotropic functions for KARs are beginning to be characterized in multiple brain regions, both, in the pre‐ and post‐synaptic compartments of the synapse, there is accumulating evidence that KARs mediate some of their effects without invoking ion‐fluxes. Thus, since 1998, when the first metabotropic action of KARs was described in the modulation of GABA release in hippocampal interneurons, there have been increasing reports that some of the functions of KARs involve the participation of intracellular signalling cascades and depend on G protein activation. These surprising observations, attesting metabotropic actions of KARs, akin to those usually attributed to seven transmembrane region G protein‐coupled receptors, make the physiological classification and description of glutamate receptors more complex. In the present review, we describe the metabotropic roles of KARs in the CNS and discuss the intriguing properties of this receptor which, structurally shows all the facets of a typical ionotropic receptor, but appears to express a metabotropic remit at some key synapses.
Which clinical and experimental data link temporal lobe epilepsy with depression?
Authors: Kondziella Daniel , Alvestad Silje , Vaaler Arne , Sonnewald Ursula 
Published: September 2007

AbstractThe association of temporal lobe epilepsy with depression and other neuropsychiatric disorders has been known since the early beginnings of neurology and psychiatry. However, only recently havein vivoandex vivotechniques such as Positron Emission Tomography, Magnetic Resonance Imaging and Magnetic Resonance Spectroscopy in combination with refined animal models and behavioral tests made it possible to identify an emerging pattern of common pathophysiological mechanisms. We now have growing evidence that in both disorders altered interaction of serotonergic and noradrenergic neurons with glutamatergic systems is associated with abnormal neuronal circuits and hyperexcitability. Neuronal hyperexcitability can possibly evoke seizure activity as well as disturbed emotions. Moreover, decreased synaptic levels of neurotransmitters and high glucocorticoid levels influence intracellular signaling pathways such as cAMP, causing disturbances of brain‐derived and other neurotrophic factors. These may be associated with hippocampal atrophy seen on Magnetic Resonance Imaging and memory impairment as well as altered fear processing and transient hypertrophy of the amygdala. Positron Emission Tomography studies additionally suggest hypometabolism of glucose in temporal and frontal lobes. Last, but not least, in temporal lobe epilepsy and depression astrocytes play a role that reaches far beyond their involvement in hippocampal sclerosis and ultimately, therapeutic regulation of glial‐neuronal interactions may be a target for future research. All these mechanisms are strongly intertwined and probably bidirectional such that the structural and functional alterations from one disease increase the risk for developing the other. This review provides an integrative update of the most relevant experimental and clinical data on temporal lobe epilepsy and its association with depression.
Immunomodulatory effects of etanercept in a model of brain injury act through attenuation of the acute‐phase response
Authors: Campbell Sandra J. , Jiang Yanyan , Davis Andrew E. M. , Farrands Rebecca , Holbrook Joanna , Leppert David , Anthony Daniel C. 
Published: September 2007

AbstractTNF‐α has proved to be a successful target in the treatment of many peripheral inflammatory diseases, but the same interventions worsen immune‐mediated CNS disease. However, anti‐TNF‐α strategies may offer promise as therapy for non‐immune CNS injury. In this study, we have microinjected IL‐1β or lipopolysaccharide (LPS) into the rat brain as a simple model of brain injury and have systemically administered the TNF‐α antagonist etanercept to discover whether hepatic TNF‐α, produced as part of the acute‐phase response to CNS injury, modulates the inflammatory response in the brain. We report a significant reduction in neutrophil numbers recruited to the IL‐1β‐ or LPS‐challenged brain as a result of TNF‐α inhibition. We also show an attenuation in the levels of hepatic mRNA including TNF‐α mRNA and of TNF‐α‐induced genes, such as the chemokines CCL‐2, CXCL‐5, and CXCL‐10, although other chemokines elevated by the injury were not significantly changed. The reduction in hepatic chemokine synthesis results in reduced numbers of circulating neutrophils, and also a reduction in the numbers recruited to the liver as a consequence of brain injury. These findings suggest that TNF‐α inhibitors may reduce CNS inflammatory responses by targeting the hepatic acute‐phase response, and thus therapies for brain injury need not cross the blood–brain barrier to be effective.
Glycogen synthase kinase‐3β: homologous regulation of cell surface insulin receptor level via controlling insulin receptor mRNA stability in adrenal chromaffin cells
Authors: Yokoo Hiroki , Nemoto Takayuki , Yanagita Toshihiko , Satoh Shinya , Yoshikawa Norie , Maruta Toyoaki , Wada Akihiko 
Published: September 2007

AbstractIn cultured bovine adrenal chromaffin cells, 48 h‐treatment with 20 mmol/L LiCl, 1 mmol/L valproic acid, 30 μmol/L SB216763, 30 μmol/L SB415286, or 100 nmol/L insulin, a condition that inhibits constitutive active glycogen synthase kinase‐3 (GSK‐3), decreased cell surface 125I‐insulin binding capacity by ∼39%, without altering the Kd value; LiCl, SB216763 or insulin decreased insulin receptor (IR) and IR precursor levels, attenuating insulin‐induced Tyr‐autophosphorylation of IR. LiCl increased inhibitory Ser9‐phosphorylation of GSK‐3β at 6 h, decreasing 125I‐insulin binding at 24 h. SB216763‐induced 125I‐insulin binding reduction (IC50 = 3 μmol/L) was preceded by β‐catenin level increase by SB216763 (EC50 = 11 μmol/L), a hallmark of GSK‐3 inhibition. Insulin‐induced rapid (> 1 min) Ser9‐phosphorylation of GSK‐3β (Nemoto et al. 2006) was followed by ∼48% decrease of IR level. LiCl did not stimulate endocytosis, nor proteolysis of IR. LiCl destabilized IR mRNA (t1/2 = 9.3 vs. 6.5 h), decreasing IR mRNA level by ∼47%, without altering IR gene transcription. Decreases of 125I‐insulin binding and IR level, as well as increased Ser9‐phosphorylation of GSK‐3β were restored to the control levels by washing the test compound‐treated cells. Thus, GSK‐3β regulates IR level via controlling IR mRNA stability.
Key role of the nicotinic receptor in neurotransmitter exocytosis in human chromaffin cells
Authors: Pérez‐Alvarez Alberto , Albillos Almudena 
Published: September 2007

AbstractThe whole‐cell secretory response evoked by acetylcholine (ACh) in human chromaffin cells was examined using a new protocol based on quickly switching from the voltage‐clamp to the current‐clamp (CC) configuration of the patch‐clamp technique. Our experiments revealed that Ca2+ entry through the nicotinic receptor at hyperpolarized membrane potentials contributed as much to the exocytosis (100.4 ± 27.3 fF) evoked by 200 ms pulses of ACh, as Ca2+ flux through voltage‐dependent Ca2+ channels at depolarized membrane potentials. The nicotinic current triggered a depolarization event with a peak at +49.3 mV and a ‘plateau’ phase that ended at −23.9 mV, which was blocked by 10 μmol/L mecamylamine. When a long ACh stimulus (15 s) was applied, the nicotinic current at the end of the pulse reached a value of 15.45 ± 3.6 pA, but the membrane potential depolarization still remained at the ‘plateau’ stage until withdrawal of the agonist. Perfusion with 200 μmol/L Cd2+ during the 15 s ACh pulse completely abolished the plasma membrane depolarization at the end of the pulse, indicating that Ca2+ entry through Ca2+ channels contributed to the membrane potential depolarization provoked by prolonged ACh pulses. These findings also reflect that voltage‐dependent Ca2+ channels were recruited by the small current flowing through the desensitized nicotinic receptor to maintain the depolarization. Finally, muscarinic receptor activation triggered a delayed exocytotic process after prolonged ACh stimulation, dependent on Ca2+ mobilization from the endoplasmic reticulum. In summary, we show here that nicotinic and muscarinic receptors contribute to the exocytosis of neurotransmitters in human chromaffin cells, and that the nicotinic receptor plays a key role in several stages of the stimulus–secretion coupling process in these cells.