bluuebunny/crossref_metadata_2025_split huggingface dataset:
Trophic support delays but does not prevent cell‐intrinsic degeneration of neurons deficient for munc18‐1
Authors: Heeroma Joost H. , Roelandse Martijn , Wierda Keimpe , Van Aerde Karlijn I. , Toonen Ruud F. G. , Hensbroek Robert A. , Brussaard Arjen , Matus Andrew , Verhage Matthijs 
Published: July 2004

AbstractThe stability of neuronal networks is thought to depend on synaptic transmission which provides activity‐dependent maintenance signals for both synapses and neurons. Here, we tested the relationship between presynaptic secretion and neuronal maintenance using munc18‐1‐null mutant mice as a model. These mutants have a specific defect in secretion from synaptic and large dense‐cored vesicles [Verhage et al. (2000), Science, 287, 864–869; Voets et al. (2001), Neuron, 31, 581–591]. Neuronal networks in these mutants develop normally up to synapse formation but eventually degenerate. The proposed relationship between secretion and neuronal maintenance was tested in low‐density and organotypic cultures and, in vivo, by conditional cell‐specific inactivation of the munc18‐1 gene. Dissociated munc18‐1‐deficient neurons died within 4 days in vitro (DIV). Application of trophic factors, insulin or BDNF delayed degeneration up to 7 DIV. In organotypic cultures, munc18‐1‐deficient neurons survived until 9 DIV. On glial feeders, these neurons survived up to 10 DIV and 14 DIV when insulin was applied. Co‐culturing dissociated mutant neurons with wild‐type neurons did not prolong survival beyond 4 DIV, but coculturing mutant slices with wild‐type slices prolonged survival up to 19 DIV. Cell‐specific deletion of munc18‐1 expression in cerebellar Purkinje cells in vivo resulted in the specific loss of these neurons without affecting connected or surrounding neurons. Together, these data allow three conclusions. First, the lack of synaptic activity cannot explain the degeneration in munc18‐1‐null mutants. Second, trophic support delays but cannot prevent degeneration. Third, a cell‐intrinsic yet unknown function of munc18‐1 is essential for prolonged survival.
Stimulation of N‐methyl‐d‐aspartate receptors, AMPA receptors or metabotropic glutamate receptors leads to rapid internalization of AMPA receptors in cultured nucleus accumbens neurons
Authors: Mangiavacchi Simona , Wolf Marina E. 
Published: July 2004

AbstractIn hippocampus and other regions, α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptors are inserted into synapses during long‐term potentiation and removed during long‐term depression. However, little is known about regulation of AMPA receptor trafficking in the nucleus accumbens (NAc), despite growing evidence that glutamate‐dependent forms of plasticity in the NAc contribute to drug addiction. Using postnatal rat NAc cultures and an immunocytochemical method that selectively detects newly internalized GluR1, we studied the regulation of AMPA receptor internalization in NAc neurons by glutamate agonists. Newly internalized GluR1 was detected during 15 or 30 min of incubation at room temperature, indicating a basal rate of GluR1 turnover. The rate of GluR1 internalization was increased by glutamate (50 µm) within 5 min of its addition. Glutamate‐induced GluR1 internalization was partially blocked by either an AMPA receptor antagonist (CNQX; 20 µm) or an N‐methyl‐d‐aspartate (NMDA) receptor antagonist (APV; 50 µm). Both NMDA (50 µm) and AMPA (50 µm) increased GluR1 internalization in a Ca2+‐dependent manner. The NMDA effect was blocked by APV while the AMPA effect was blocked by APV or CNQX. We interpret these findings to suggest that NMDA and AMPA ultimately trigger GluR1 internalization through the same NMDA receptor‐dependent pathway. The effect of glutamate was also partially blocked by the group 1 metabotropic glutamate receptor antagonist N‐phenyl‐7‐(hydroxyimino)cyclopropa[b]chromen‐1a‐carboxamide (PHCCC; 50 µm), while the group 1 agonist 3,5‐dihydroxyphenylglycine (DHPG; 50 µm) stimulated GluR1 internalization. These data suggest that AMPA receptors on NAc neurons may be subject to rapid regulation of their surface expression in response to changes in the activity of glutamate inputs from cortical and limbic regions.
Anatomical and functional evidence for a role of arginine‐vasopressin (AVP) in rat olfactory epithelium cells
Authors: Levasseur Grégoire , Baly Christine , Grébert Denise , Durieux Didier , Salesse Roland , Caillol Monique 
Published: July 2004

AbstractThe olfactory epithelium (OE) is composed of olfactory sensory neurons (OSNs) and sustentacular cells; it lies in the nasal cavity where it is protected by a thin mucus layer. The finely regulated composition of this mucus provides OSN with a suitable ionic environment. To maintain the functional integrity of the epithelium despite permanent physical, chemical and microbial aggressions, both OSNs and surrounding sustentacular cells are continuously renewed from globose basal cells. Moreover, the sense of smell is involved in so numerous behaviours (feeding, reproduction, etc.) that it has to cross‐talk with the endocrine and neuroendocrine systems. Thus, besides its sensory function, the olfactory epithelium is thought to undergo a lot of complex regulatory processes. We therefore studied the effects of various neuropeptides on primary cultures of Sprague–Dawley rat olfactory epithelium cells. We found that arginine‐vasopressin (AVP) triggered a robust, dose‐dependent calcium increase in these cells. The cell response was essentially ascribed to the V1a AVP receptor, whose presence was confirmed by RT‐PCR and immunolabelling. In the culture, V1a but not V1b receptors were present, mainly localized in neurons. In the epithelium, both subtypes were found differentially distributed. V1a‐R were localized mainly in globose basal cells and at the apical side of the epithelium, in the area of the dendritic knobs of OSNs. V1b‐R were strongly associated with Bowman's gland cells and globose basal cells. These localizations suggested potential multifaceted roles of a hormone, AVP, in the olfactory epithelium.
Prolonged cannabinoid treatment results in spatial working memory deficits and impaired long‐term potentiation in the CA1 region of the hippocampus in vivo
Authors: Hill Matthew N. , Froc David J. , Fox Christopher J. , Gorzalka Boris B. , Christie Brian R. 
Published: July 2004

AbstractAdult male Long‐Evans rats were administered the potent cannabinoid 1 receptor agonist HU‐210 (100 µg/kg, i.p.) for 15 days continuously and their performance on a matching‐to‐place version of the Morris water maze was subsequently evaluated. Overall, experimental animals performed significantly worse initially on the reference memory component of this task, but their performance improved over 5 days until it was indistinguishable from that of control animals. Animals given HU‐210 did not exhibit working memory impairments at short intertrial delays (30 s); however, significant impairments were observed in learning performance with longer intertrial delays (300 s). In vivo electrophysiological analyses revealed that long‐term potentiation in the CA1 region of the hippocampus was significantly impaired following the administration of HU‐210 for 15 days. These results indicate that long‐term cannabinoid exposure can produce marked deficits in reference and working memory performance, and also impair hippocampal synaptic plasticity in vivo.
Brain‐derived neurotrophic factor acutely depresses excitatory synaptic transmission to GABAergic neurons in visual cortical slices
Authors: Jiang Bin , Kitamura Akihiko , Yasuda Hiroki , Sohya Kazuhiro , Maruyama Atsushi , Yanagawa Yuchio , Obata Kunihiko , Tsumoto Tadaharu 
Published: July 2004

AbstractBrain‐derived neurotrophic factor (BDNF) acutely modulates synaptic transmission to excitatory neurons in hippocampus and neocortex. The question of whether BDNF acts similarly on excitatory synaptic transmission to GABAergic neurons was eluded in previous studies using cortical slices. To address this question, we used transgenic mice in which expression of green fluorescence protein (GFP) is regulated by glutamic acid decarboxylase 67 (GAD67) promoter. In cortical slices prepared from these GAD67‐GFP knock‐in mice, we could detect GABAergic neurons under a fluorescent microscope. An application of BDNF rapidly depressed excitatory postsynaptic currents (EPSCs) evoked by layer IV stimulation in most GFP‐positive neurons in layer II/III of the cortex. This effect was seen at synapses activated during the BDNF application and blocked by anti‐TrkB IgG, indicating that the acute inhibitory action of BDNF is activity‐dependent and mediated through TrkB. Paired‐pulse ratios of the amplitude of EPSCs to paired stimulation at intervals of 10–100 ms were not significantly changed after BDNF application, suggesting that the site of depression may be postsynaptic. Responses to directly applied glutamate were also depressed by BDNF in most of neurons, being consistent with the interpretation of postsynaptic action of BDNF. The depressive action of BDNF was blocked by an intracellular injection of a Ca2+ chelator, suggesting that a rise in Ca2+ is involved in the acute depression of EPSCs. This action of BDNF was seen in 67% of parvalbumin (PV)‐positive neurons, but in only 19% of PV‐negative neurons, indicating that the depressive action is biased to PV‐positive GABAergic neurons.
In vivo31P NMR spectroscopy shows an increase in glycerophosphorylcholine concentration without alterations in mitochondrial function in the prefrontal cortex of medicated schizophrenic patients at rest
Authors: Shirayama Yukihiko , Yano Toshio , Takahashi Kiyohisa , Takahashi Seizo , Ogino Takashi 
Published: July 2004

AbstractThe 31P NMR localised method was used to study the metabolism of phospholipid and high energy phosphate in the prefrontal cortex. The spectra were taken from patients with schizophrenia (11 males) receiving neuroleptic medication, and were compared to normal controls (15 males). Their spectral intensities were analysed using a non‐linear least‐squares method with a prior knowledge of the fixed chemical shifts and linewidths, leading to further resolution into resonances of glycerophosphorylethanolamine (GPE), glycerophosphorylcholine (GPC), phosphorylethanolamine (PE) and phosphorylcholine (PC). The metabolite concentrations were calculated referring to the spectral intensities of phosphate phantoms with known concentrations. T1 values of phantom and cerebrum were estimated from a series of localised inversion recovery spectra to correct for the signal saturation effects. The schizophrenic patients showed an increased concentration of GPC but not GPE, PE or PC. Furthermore, no difference was observed regarding the concentration of high‐energy phosphates such as phosphocreatine, inorganic phosphate and ATP. The patients did not show any differences in mitochondrial function such as phosphorylation potential and the ratio of the rate of ATP synthesis. Thus, an increase in GPC concentration in the prefrontal cortex could be characteristic of the pathophysiology of schizophrenia with mild negative symptoms.
The rewarding properties of MDMA are preserved in mice lacking µ‐opioid receptors
Authors: Robledo Patricia , Mendizabal Victoria , Ortuño Jordi , De La Torre Rafael , Kieffer Brigitte L. , Maldonado Rafael 
Published: July 2004

AbstractThe involvement of µ‐opioid receptors in the rewarding properties of MDMA was explored in µ‐opioid receptor knockout mice using the conditioning place preference paradigm. The associated release of dopamine in the nucleus accumbens was investigated by in vivo microdialysis. A significant rewarding effect of MDMA (10 mg/kg, i.p.) was observed in both wild‐type and µ‐opioid receptor knockout mice. MDMA (10 mg/kg, i.p.) also induced similar increases in dopamine and decreases in 3,4‐dihydroxyphenylacetic acid and homovanillic acid in the nucleus accumbens dialysates of both wild‐type and µ‐opioid receptor knockout mice. No significant differences in basal levels of dopamine, 3,4‐dihydroxyphenylacetic or homovanillic acids between wild‐type and µ‐opioid receptor knockout mice were observed. In summary, the present results suggest that, in contrast to what has been reported for other drugs of abuse such as opioids, ethanol, nicotine and Δ9‐tetrahydrocannabinol, µ‐opioid receptors do not play a major role in the rewarding properties of MDMA. These differences could be due to distinct mechanisms controlling dopamine release in the nucleus accumbens and suggest that the effects of MDMA on dopaminergic neurons are independent of µ‐opioid receptors.
Kv3 K+ channels enable burst output in rat cerebellar Purkinje cells
Authors: McKay B. E. , Turner R. W. 
Published: July 2004

AbstractThe ability of cells to generate an appropriate spike output depends on a balance between membrane depolarizations and the repolarizing actions of K+ currents. The high‐voltage‐activated Kv3 class of K+ channels repolarizes Na+ spikes to maintain high frequencies of discharge. However, little is known of the ability for these K+ channels to shape Ca2+ spike discharge or their ability to regulate Ca2+ spike‐dependent burst output. Here we identify the role of Kv3 K+ channels in the regulation of Na+ and Ca2+ spike discharge, as well as burst output, using somatic and dendritic recordings in rat cerebellar Purkinje cells. Kv3 currents pharmacologically isolated in outside‐out somatic membrane patches accounted for ∼ 40% of the total K+ current, were very fast and high voltage activating, and required more than 1 s to fully inactivate. Kv3 currents were differentiated from other tetraethylammonium‐sensitive currents to establish their role in Purkinje cells under physiological conditions with current‐clamp recordings. Dual somatic‐dendritic recordings indicated that Kv3 channels repolarize Na+ and Ca2+ spikes, enabling high‐frequency discharge for both types of cell output. We further show that during burst output Kv3 channels act together with large‐conductance Ca2+‐activated K+ channels to ensure an effective coupling between Ca2+ and Na+ spike discharge by preventing Na+ spike inactivation. By contributing significantly to the repolarization of Na+ and especially Ca2+ spikes, our data reveal a novel function for Kv3 K+ channels in the maintenance of high‐frequency burst output for cerebellar Purkinje cells.
Decreased histamine H1 receptor binding in the brain of depressed patients
Authors: Kano Michiko , Fukudo Shin , Tashiro Atshushi , Utsumi Atshushi , Tamura Daisaku , Itoh Masatoshi , Iwata Ren , Tashiro Manabu , Mochizuki Hideki , Funaki Yoshihito , Kato Motohisa , Hongo Michio , Yanai Kazuhiko 
Published: July 2004

AbstractThe central histaminergic neuron system modulates the wakefulness, sleep–awake cycle, appetite control, learning and memory, and emotion. Previous studies have reported changes in neuronal histamine release and its metabolism under stress conditions in the mammalian brain. In this study, we examined, using positron emission tomography (PET) and [11C]‐doxepin, whether the histaminergic neuron system is involved in human depression. Cerebral histamine H1 receptor (H1R) binding was measured in 10 patients with major depression and in 10 normal age‐matched subjects using PET and [11C]‐doxepin. Data were calculated by a graphical analysis on voxel‐by‐voxel and ROI (region of interests) basis. Binding potential (BP) values for [11C]‐doxepin binding in the frontal and prefrontal cortices, and cingulate gyrus were significantly lower in the depressed patients than those in the normal control subjects. There was no area of the brain where [11C]‐doxepin binding was significantly higher in the depressed patients than in the controls. ROI‐based analysis also revealed that BP values for [11C]‐doxepin binding in the frontal cortex and cingulate gyrus decreased in proportion to self‐rating depressive scales scores. The results of this study demonstrate that depressed patients have decreased brain H1R binding and that this decrease correlates with the severity of depression symptoms. It is therefore suggested that the histaminergic neuron system plays an important role in the pathophysiology of depression and that its modulation may prove to be useful in the treatment of depression.
Is invasion success explained by the enemy release hypothesis?
Authors: Colautti Robert I. , Ricciardi Anthony , Grigorovich Igor A. , MacIsaac Hugh J. 
Published: July 2004

AbstractA recent trend in invasion ecology relates the success of non‐indigenous species (NIS) to reduced control by enemies such as pathogens, parasites and predators (i.e. the enemy release hypothesis, ERH). Despite the demonstrated importance of enemies to host population dynamics, studies of the ERH are split – biogeographical analyses primarily show a reduction in the diversity of enemies in the introduced range compared with the native range, while community studies imply that NIS are no less affected by enemies than native species in the invaded community. A broad review of the invasion literature implies at least eight non‐exclusive explanations for this enigma. In addition, we argue that the ERH has often been accepted uncritically wherever (i) NIS often appear larger, more fecund, or somehow ‘better’ than either congeners in the introduced region, or conspecifics in the native range; and (ii) known enemies are conspicuously absent from the introduced range. However, all NIS, regardless of their abundance or impact, will lose natural enemies at a biogeographical scale. Given the complexity of processes that underlie biological invasions, we argue against a simple relationship between enemy ‘release’ and the vigour, abundance or impact of NIS.
Adaptation in an insect host–plant pathogen interaction
Authors: Cory Jenny S. , Myers Judith H. 
Published: July 2004

AbstractSelection on parasites to adapt to local host populations may be direct or through other components of the system such as vectors or the food plant on which the parasite is ingested. To test for local adaptation of nucleopolyhedrovirus among island populations of western tent caterpillars, Malacosoma californicum pluviale, we compared virus isolates from three geographically distinct sites with different dominant host plants. Pathogenicity, speed of kill and virus production of each isolate were examined on the three food plants. Virus isolates from the two permanent host populations had the fastest speed of kill on the host plant from which they were isolated. This was not the case for a caterpillar population that goes extinct when populations are regionally low. Virus isolates on some plant species combined rapid speed of kill with high virus yield. Infection of hosts by mixed microparasite populations could facilitate local adaptation in response to differing food plant chemistry.
The behavioural ecology of personality: consistent individual differences from an adaptive perspective
Authors: Dall Sasha R. X. , Houston Alasdair I. , McNamara John M. 
Published: July 2004

AbstractIndividual humans, and members of diverse other species, show consistent differences in aggressiveness, shyness, sociability and activity. Such intraspecific differences in behaviour have been widely assumed to be non‐adaptive variation surrounding (possibly) adaptive population‐average behaviour. Nevertheless, in keeping with recent calls to apply Darwinian reasoning to ever‐finer scales of biological variation, we sketch the fundamentals of an adaptive theory of consistent individual differences in behaviour. Our thesis is based on the notion that such ‘personality differences’ can be selected for if fitness payoffs are dependent on both the frequencies with which competing strategies are played and an individual's behavioural history. To this end, we review existing models that illustrate this and propose a game theoretic approach to analyzing personality differences that is both dynamic and state‐dependent. Our motivation is to provide insights into the evolution and maintenance of an apparently common animal trait: personality, which has far reaching ecological and evolutionary implications.
Using the angle frequency method to detect signals of competition and predation in experimental time series
Authors: Sandvik Gunnar , Jessup Christine M. , Seip Knut L. , Bohannan Brendan J. M. 
Published: July 2004

AbstractIdentifying interactions among organisms is central to the study of ecology. The Angle Frequency Method (AFM) allows the detection of interactions in time series data. The AFM takes pairwise data plotted in phase diagrams and identifies signals (vector directions in phase diagrams) associated with particular interactions. Using microbial experimental systems consisting of predators (bacteriophage T4) and prey/competitors (strains of Escherichia coli), we demonstrate that the AFM can identify predator–prey and competitive interactions. The level of control afforded by such microbial experimental systems allows direct tests of the utility and robustness of the AFM. Signals of predation were distinct from signals of competition, with the strongest signal of predation corresponding to the collapse of the predator population at low prey densities. Signals of competition reflected the difference in competitive strength between the superior and the inferior competitors. In addition, the effects of invasion and resource enrichment on interactions in the laboratory communities were detectable using the AFM. Our analyses support results from model simulations and analyses of lake time series by identifying similar sets of signals characteristic of predation and competition, and demonstrate that the AFM is an effective tool in rigorous studies of time series.
Markov chain models predict the consequences of experimental extinctions
Authors: Timothy Wootton J. 
Published: July 2004

AbstractPredicting the effects of species extinction is challenging because of ecosystem complexity. Using novel long‐term experimental deletions of two mussel species, I found that a multi‐species Markov chain model, which was parameterized under non‐experimental conditions, accurately predicted the effects of local extinction in an intertidal community. Systematically deleting species from the model predicted declining ecosystem biomass with reduced biodiversity, but relatively constant ecosystem resilience following disturbance. The effects of reduced biodiversity on these variables ranged widely, illustrating the need for species‐specific predictions of extinction effects. The results show that Markov chain models can be useful tools for predicting consequences of local species extinction without extensive experimentation.
Connectivity, scale‐dependence, and the productivity–diversity relationship
Authors: Chase Jonathan M. , Ryberg Wade A. 
Published: July 2004

AbstractWe surveyed freshwater ponds (localities) nested within watersheds (regions) to evaluate the relationship between productivity and animal species richness at different spatial scales. In watersheds where the ponds were relatively distant from one another (likely reducing the level of interpond dispersal of many organisms), we found a scale‐dependent productivity–diversity relationship; at local scales (among ponds), diversity was a hump‐shaped function of productivity, whereas at regional scales (among watersheds), diversity monotonically increased with productivity. Furthermore, this relationship emerged because there was a strong relationship between productivity and pond‐to‐pond species compositional differences. Alternatively, in watersheds where ponds were relatively close together (likely leading to higher rates of dispersal of many organisms), we found no scale‐dependence; diversity was a hump‐shaped function of productivity at both local and regional scales. Here, the relationship between species compositional dissimilarity and productivity was much weaker. We conclude that whether or not scale‐dependence is observed in productivity–diversity relationships will depend, at least in part, on the degree of connectivity among localities within regions.