bluuebunny/crossref_metadata_2025 huggingface dataset:
Investigating species co‐occurrence patterns when species are detected imperfectly
Authors: MacKenzie Darryl I. , Bailey Larissa L. , Nichols James. D.
Published: April 2004

Over the last 30 years there has been a great deal of interest in investigating patterns of species co‐occurrence across a number of locations, which has led to the development of numerous methods to determine whether there is evidence that a particular pattern may not have occurred by random chance.

A key aspect that seems to have been largely overlooked is the possibility that species may not always be detected at a location when present, which leads to ‘false absences’ in a species presence/absence matrix that may cause incorrect inferences to be made about co‐occurrence patterns. Furthermore, many of the published methods for investigating patterns of species co‐occurrence do not account for potential differences in the site characteristics that may partially (at least) explain non‐random patterns (e.g. due to species having similar/different habitat preferences).

Here we present a statistical method for modelling co‐occurrence patterns between species while accounting for imperfect detection and site characteristics. This method requires that multiple presence/absence surveys for the species be conducted over a reasonably short period of time at most sites. The method yields unbiased estimates of probabilities of occurrence, and is practical when the number of species is small (< 4).

To illustrate the method we consider data collected on two terrestrial salamander species, Plethodon jordani and members of the Plethodon glutinosus complex, collected in the Great Smoky Mountains National Park, USA. We find no evidence that the species do not occur independently at sites once site elevation has been allowed for, although we find some evidence of a statistical interaction between species in terms of detectability that we suggest may be due to changes in relative abundances.
Absence of costs of foraging excursions in relation to limpet aggregation
Authors: Coleman R. A. , Underwood A. J. , Chapman M. G.
Published: April 2004

Animal aggregation has been well studied, with many proximate and ultimate models proposed. Many of the proximate models have relied on cost–benefit arguments, but frequently aspects of cost have been inferred in relation to position in group. An expected cost to an animal that rests in aggregations, but departs to forage, is that being in the centre of a group may impede foraging opportunities, in that ‘inner’ animals cannot leave to forage until outer animals have done so.

Experiments with a limpetCellana tramoserica, on a rocky shore in New South Wales, Australia, showed that central limpets remain central more often than would be expected by chance. In respect of costs due to access to foraging, we show that there is no effect of position (central vs. outer) in timing of foraging excursions or of feeding‐rate. We also show that an aggregated distribution ofC. tramosericaat rest does not translate into an aggregated distribution of foraging animals.

We propose that aggregations ofC. tramosericaare probably a function of how the group reassembles after foraging and is much dependent on processes happening at a small spatial scale. It is highly probable that assumptions about the effects of limpet aggregation on rocky shore ecology (i.e. in influencing patchiness of algae) may be premature.
Scales and Sales: Changing Social and Spatial Fish Trading Networks in the Siiphandone Fishery, Lao PDR
Authors: Bush Simon R.
Published: April 2004

The Siiphandone wetland in Khong district, Champasak province, Lao PDR, is one of the most important fisheries in the Mekong River basin. The resource, situated along the Laos‐Cambodia border, supports the livelihoods of around 65,000 inhabitants, mainly semi‐subsistence rice farmers or fishers. In January 2000, the provincial authority was given a special dispensation by the Lao government to allow the importation of Cambodian fish through Khong district, for export to Thailand. Previously, in large part due to the government's policy of food self‐sufficiency, the export of Lao fish was illegal. This paper examines how the implementation of this law has influenced existing legal and illegal trade networks from the Siiphandone fishery by comparing the findings of two studies, one conducted before and the other after the change in the law. In doing so, the transition of the fishery from a local, food‐important resource to an increasingly regional, market‐oriented resource is examined. Conclusions are drawn as to the impact this change has had on the livelihoods of fishers and traders involved in the fishery.
Positionality and Praxis: Fieldwork Experiences in Rural India
Authors: Chacko Elizabeth
Published: April 2004

This paper provides a reflexive account of conducting fieldwork as a graduate student in the Sunderban area of West Bengal state, India, in the mid‐1990s. Reflecting on my personal experiences of research in a setting that was simultaneously familiar and foreign, I use frames of positionality to understand the impact of explicit and implied power structures on the research process, the relationships between the researcher and those researched, and the transfer of knowledge. This paper argues that the multiple subject positions and identities of both scholar and subjects as presented in the field vary with setting, and that these positionalities affect access to informants, the tenor and outcomes of encounters, and knowledge production. While self‐reflexivity is endorsed as a strategy for critically informed research, active measures such as openness about the agenda and activities undertaken, self‐disclosure, making conscious accommodations for the research subject's work schedule and time constraints, mutual sharing of information, and explicit recognition of the research subjects' expertise through lived experiences are proposed as strategies for equalising the power balance between scholar and subject.
Changes in the Indonesian Clothing Industry: Trade and Regulation
Authors: Hassler Markus
Published: April 2004

Policy frameworks at national and international levels have significant influence on the growth performance and industrialisation of developing economies. This paper aims to explore the influence of such regulatory policy frameworks on the development of the Indonesian clothing industry since the mid‐1980s based on an analysis of national clothing trade statistics provided by the Indonesian Central Bureau of Statistics. Although the Indonesian policy framework had a general export‐orientation, protectionist measures for the domestic market proved to be important in facilitating the growth of the Indonesian clothing industry. This paper also shows how the existing international clothing trade regulatory framework of the Multi‐Fibre Arrangement (MFA) influenced the integration of Indonesian clothing firms into global production and trade networks. Finally, the future policy changes and potential impacts for Indonesian clothing firms are discussed.
The Effects of Annual Harvesting on the Subsequent Phytomass and Species Composition of Grassland and Fernland: A Hong Kong Case
Authors: Hill R.D. , Peart M.R. , Dong‐Sheng Guan
Published: April 2004

Anthropogenic grasslands mixed with fern and shrubland, on scales from metres to kilometres, are widespread in tropical Southeast Asia, and especially in southern China and adjoining regions where harvesting for domestic fuel is a major factor in their maintenance. Baseline surveys in grassland and fernland in 1989–90 and resurveys in 2001 of three 6 × 20 m plots in Wong Chuk Yuen, Hong Kong, showed substantial change in species composition and total aboveground phytomass as a result of annual harvesting, with more pronounced change in the fernland.

Under harvesting pressure, the species composition of the grassland changed considerably, though the proportions of the various life‐forms did not. Ischaemum spp. and Miscanthus floridulus increased whereas Themeda gigantea died out while the proportion of other grass species remained much the same. Under the same regime the species composition and life‐forms of the fernland changed markedly. The proportion of Dicranopteris fern dropped substantially, though still comprising a third of the phytomass by 2001. The shrub Melastoma survived harvesting. A firebreak cut in the fernland became grassy under annual harvesting and remained grassy six years after cutting ceased. The annual harvests from the growth‐years 1991–2000 showed a substantial though variable increase in total phytomass. Analyses relating harvested phytomass with various climatic parameters showed no significant correlations. Some possible reasons for this are suggested. Although annual harvesting was clearly sustainable over the ten years of observation, the question of continued sustainability on sites harvested for centuries, the situation in much of southern China and parts of upland mainland Southeast Asia, remains unresolved.
Identifying Optimum Locations for Tropical Testing of United States Army Materiel and Systems
Authors: King W. Chris , Palka Eugene J. , Harmon Russell S.
Published: April 2004

This paper is an example of applied military geography focusing on a particular problem arising from the Panama Canal Treaty of 1977. One of the provisions of the treaty required the United States (US) military to completely withdraw from and relinquish its military and government facilities to the Republic of Panama prior to midnight on 31 December 1999. In so doing, the US army turned over to the Panama government all of its military bases, some of which had been used since World War I to test materiel, equipment and systems within a tropical environment. Given its global mission and responsibilities, the US army has a well‐established practice of testing its materiel, equipment and systems throughout the entire range of potential operating environments. The US experience in the Pacific in World War II and in Southeast Asia during the Vietnam War clearly demonstrated the need to test the performance of new equipment under the harsh conditions found in tropical jungles. Furthermore, since 1960, nearly 75 per cent of all international and internal armed conflicts have been in countries that are totally or partially in the tropics. This paper presents the findings of a scientific panel that was organised to propose a new location for testing US army materiel and systems within a tropical environment. Rather than simply choosing a location analogous to Panama, the panel sought to develop a methodology that could be employed for site selection based on any set of environmental criteria. This study is a classical locational analysis and reconfirms the integrative nature of geography and its utility for solving complex problems that cut across disciplinary boundaries.
Modulation of calcium/calmodulin kinase‐II provides partial neuroprotection against beta‐amyloid peptide toxicity
Authors: Lin Kim‐Fung , Chang Raymond Chuen‐Chung , Suen Ka‐Chun , So Kwok‐Fai , Hugon Jacques
Published: April 2004

Beta‐amyloid (Aβ) peptide‐induced neurotoxicity has been implicated in the pathogenesis of Alzheimer's disease (AD). The exact mechanism by which Aβ peptides trigger neuronal death is not well defined and may be related to an abrupt increase in intracellular calcium, leading to the activation of many pro‐apoptotic pathways. While modulation of intracellular calcium increase receives much attention for pharmaceutical intervention, Ca2+‐mediated pro‐apoptotic signalling pathways have not been systematically studied. We have reported our study on the roles of calcium/calmodulin‐dependent protein kinase II (CaMKII) in Aβ peptide neurotoxicity. By treating the primary cortical neurons exposed to Aβ peptides (Aβ25−35 and Aβ1−42) with two selective CaMKII inhibitors, autocamtide‐related inhibitory peptide (AIP) and KN93, Aβ peptide neurotoxicity was significantly reduced. Release of LDH and DNA fragmentation/condensation (by DAPI staining) in neurons exposed to Aβ peptides were significantly decreased in the presence of AIP and KN93. While these inhibitors significantly attenuated Aβ peptide‐triggered activation of caspase‐2 and caspase‐3, and AIP significantly decreased the degree of tau phosphorylation of the Aβ peptide‐treated neurons at early time, they could elicit partial neuroprotection only. Pharmacological inhibitor targeting calmodulin, W7, did not provide neuroprotection. Morphine, which activates CaMKII via µ receptors, augments Aβ‐induced LDH release, caspase‐2 and caspase‐3 activities and neuronal apoptosis. Taken together, although CaMKII plays a role in Aβ peptide neurotoxicity, pharmacological inhibition cannot afford complete neuroprotection.
Environmental enrichment reverses learning impairment in the Morris water maze after focal cerebral ischemia in rats
Authors: Dahlqvist Per , Rönnbäck Annica , Bergström Sven‐Anders , Söderström Ingegerd , Olsson Tommy
Published: April 2004

Cognitive impairment is common after ischemic stroke. In rodent stroke models using occlusion of the middle cerebral artery (MCA) this is reflected by impaired spatial memory associated with the size of the ischemic lesion. Housing in an enriched environment enhances brain plasticity and improves recovery of sensorimotor functions after experimental stroke in rats. In this study we report that postischemic housing in an enriched environment also attenuates the long‐term spatial memory impairment after MCA occlusion and extinguishes the association between spatial memory and infarct volume. An enriched environment did not significantly alter the expression of selected neuronal plasticity‐associated genes 1 month after MCA occlusion, indicating that most of the adaptive changes induced by an enriched environment have already occurred at this time point. We conclude that the attenuated memory impairment induced by environmental enrichment after MCA occlusion provides a useful model for further studies on the neurobiological mechanisms of recovery of cognitive functions after ischemic stroke.
Neuronal connexin36 association with zonula occludens‐1 protein (ZO‐1) in mouse brain and interaction with the first PDZ domain of ZO‐1
Authors: Li Xinbo , Olson Carl , Lu Shijun , Kamasawa Naomi , Yasumura Thomas , Rash John E. , Nagy James I.
Published: April 2004

Among the 20 members in the connexin family of gap junction proteins, only connexin36 (Cx36) is firmly established to be expressed in neurons and to form electrical synapses at widely distributed interneuronal gap junctions in mammalian brain. Several connexins have recently been reported to interact with the PDZ domain‐containing protein zonula occludens‐1 (ZO‐1), which was originally considered to be associated only with tight junctions, but has recently been reported to associate with other structures including gap junctions in various cell types. Based on the presence of sequence corresponding to a putative PDZ binding motif in Cx36, we investigated anatomical relationships and molecular association of Cx36 with ZO‐1. By immunofluorescence, punctate Cx36/ZO‐1 colocalization was observed throughout the central nervous system of wild‐type mice, whereas labelling for Cx36 was absent in Cx36 knockout mice, confirming the specificity of the anti‐Cx36 antibodies employed. By freeze‐fracture replica immunogold labelling, Cx36 and ZO‐1 in brain were found colocalized within individual ultrastructurally identified gap junction plaques, although some plaques contained only Cx36 whereas others contained only ZO‐1. Cx36 from mouse brain and Cx36‐transfected HeLa cells was found to coimmunoprecipitate with ZO‐1. Unlike other connexins that bind the second of the three PDZ domains in ZO‐1, glutathione S‐transferase‐PDZ pull‐down and mutational analyses indicated Cx36 interaction with the first PDZ domain of ZO‐1, which required at most the presence of the four c‐terminus amino acids of Cx36. These results demonstrating a Cx36/ZO‐1 association suggest a regulatory and/or scaffolding role of ZO‐1 at gap junctions that form electrical synapses between neurons in mammalian brain.
Glial cell line‐derived neurotrophic factor (GDNF) from adult rat tooth serves a distinct population of large‐sized trigeminal neurons
Authors: Kvinnsland Inger Hals , Luukko Keijo , Fristad Inge , Kettunen Päivi , Jackson Douglass L. , Fjeld Karianne , Von Bartheld Christopher S. , Byers Margaret R.
Published: April 2004

Glial cell line‐derived neurotrophic factor (GDNF) mediates trophic effects for specific classes of sensory neurons. The adult tooth pulp is a well‐defined target of sensory trigeminal innervation. Here we investigated potential roles of GDNF in the regulation of adult trigeminal neurons and the dental pulp nerve supply of the rat maxillary first molar. Western blot analysis and radioactive35S‐UTPin situhybridization revealed that GDNF in the dental pulp and its mRNAs were localized withNgfin the coronal pulp periphery, in particular in the highly innervated subodontoblast layer. Retrograde neuronal transport of iodinated GDNF and Fluorogold (FG) from the dental pulp indicated that GDNF was transported in about one third of all the trigeminal dental neurons. Of the GDNF‐labelled neurons, nearly all (97%) were large‐sized (≥35 µm in diameter). Analysis of FG‐labelled neurons revealed that, of the trigeminal neurons supporting the adult dental pulp, ≈ 20% were small‐sized, lacked isolectin B4 binding and did not transport GDNF. Of the large‐sized dental trigeminal neurons ≈ 40% transported GDNF. About 90% of the GDNF‐accumulating neurons were negative for the high‐temperature nociceptive marker VRL‐1. Our results show that a subclass of large adult trigeminal neurons are potentially dependent on dental pulp‐derived GDNF while small dental trigeminal neurons seems not to require GDNF. This suggests that GDNF may function as a neurotrophic factor for subsets of nerves in the tooth, which apparently mediate mechanosensitive stimuli. As in dorsal root ganglia both small‐ and large‐sized neurons are known to be GDNF‐dependent; these data provide molecular evidence that the sensory supply in the adult tooth differs, in some aspects, from the cutaneous sensory system.
Involvement of the sigma1 receptor in the modulation of dopaminergic transmission by amantadine
Authors: Peeters Magali , Romieu Pascal , Maurice Tangui , Su Tsung‐Ping , Maloteaux Jean‐Marie , Hermans Emmanuel
Published: April 2004

Pharmacological effects of amantadine on dopaminergic transmission are proposed to result from an uncompetitive antagonism at glutamate N‐methyl‐d‐aspartate (NMDA) receptors. However, our previous studies examining amantadine‐mediated dopamine receptor regulation in the rat striatum revealed a discrepancy from a direct interference with glutamate transmission. Preliminary in vitro binding data from the literature suggested the interaction of amantadine with the sigma1 receptor. Therefore, we have now further characterized the pharmacological properties of amantadine and memantine at this receptor and investigated its involvement in the modulation of striatal dopaminergic transmission. Our binding studies using [3H]‐(+)SKF‐10,047 indicated that amantadine and memantine behave as ligands of the sigma1 receptor in rat forebrain homogenates (Ki values of 7.44 ± 0.82 and 2.60 ± 0.62 µm, respectively). In NG108‐15 neuroblastoma cells, both drugs (amantadine (100 µm) and memantine (10 µm)) potentiated the bradykinin‐induced mobilization of intracellular Ca2+, mimicking the effect of the sigma1 receptor agonist PRE‐084 (1 µm). Finally, we previously showed that in striatal membranes from amantadine‐treated rats, the functional coupling of dopamine receptors with G‐proteins was enhanced. Similarly, PRE‐084 dose‐dependently increased the [35S]GTPγS binding induced by dopamine (Emax 28 and 26% of basal, 0.3 and 1 mg/kg PRE‐084, respectively). By contrast, BD1047, which is without effect on its own, antagonized the effects of amantadine and PRE‐084. Together, these data demonstrate that aminoadamantanes behave as sigma1 receptor agonists, and confirm an involvement of this receptor in modulating dopamine receptors exerted by therapeutically relevant concentrations of amantadine.
Inhibition of auditory cortical responses to ipsilateral stimuli during dichotic listening: evidence from magnetoencephalography
Authors: Brancucci Alfredo , Babiloni Claudio , Babiloni Fabio , Galderisi Silvana , Mucci Armida , Tecchio Franca , Zappasodi Filippo , Pizzella Vittorio , Romani Gian Luca , Rossini Paolo Maria
Published: April 2004

The present magnetoencephalography (MEG) study on auditory evoked magnetic fields (AEFs) was aimed at verifying whether during dichotic listening the contralateral auditory pathway inhibits the ipsilateral one, as suggested by behavioural and patient studies. Ten healthy subjects were given a randomized series of three complex tones (261, 293 and 391 Hz, 500 ms duration), which were delivered monotically and dichotically with different intensities [60, 70 or 80 dBA (audio decibels)]. MEG data were recorded from the right auditory cortex. Results showed that the M100 amplitude over the right auditory cortex increased progressively when tones of increasing intensity were provided at the ipsilateral (right) ear. This effect on M100 was abolished when a concurrent tone of constant intensity was delivered dichotically at the contralateral (left) ear, suggesting that the contralateral pathway inhibited the ipsilateral one. The ipsilateral inhibition was present only when the contralateral tone fundamental frequency was similar to the ipsilateral tone. It was proposed that the occlusion mechanism would be exerted in cortical auditory areas as the dichotic effects were observed at M100 but not M50 component. This is the first evidence showing a neurophysiological inhibition driven by the contralateral auditory pathway over the ipsilateral one during dichotic listening.
Silicon chip with capacitors and transistors for interfacing organotypic brain slice of rat hippocampus
Authors: Hutzler Michael , Fromherz Peter
Published: April 2004

Probing projections between brain areas and their modulation by synaptic potentiation requires dense arrays of contacts for noninvasive electrical stimulation and recording. Semiconductor technology is able to provide planar arrays with high spatial resolution to be used with planar neuronal structures such as organotypic brain slices. To address basic methodical issues we developed a silicon chip with simple arrays of insulated capacitors and field‐effect transistors for stimulation of neuronal activity and recording of evoked field potentials. Brain slices from rat hippocampus were cultured on that substrate. We achieved local stimulation of the CA3 region by applying defined voltage pulses to the chip capacitors. Recording of resulting local field potentials in the CA1 region was accomplished with transistors. The relationship between stimulation and recording was rationalized by a sheet conductor model. By combining a row of capacitors with a row of transistors we determined a simple stimulus–response matrix from CA3 to CA1. Possible contributions of inhomogeneities of synaptic projection, of tissue structure and of neuroelectronic interfacing were considered. The study provides the basis for a development of semiconductor chips with high spatial resolution that are required for long‐term studies of topographic mapping.
Correspondence of AQP4 expression and hypoxic‐ischaemic brain oedema monitored by magnetic resonance imaging in the immature and juvenile rat
Authors: Meng Shuzhen , Qiao Min , Lin Lily , Del Bigio Marc R. , Tomanek Boguslaw , Tuor Ursula I.
Published: April 2004

Whether the water channel protein AQP4 is involved in the very early cell swelling and brain oedema observed with cerebral hypoxia–ischaemia (HI) and whether this response depends on the maturity of brain were investigated by comparing regional changes in AQP4 protein expression and signal intensity on magnetic resonance (MR) images in immature and juvenile brains. Maps of T2 and the apparent diffusion coefficient (ADC) of water were acquired in 1‐ and 4‐week‐old rats at times prior to HI, within the last 5 min of HI and 1 h or 24 h afterwards. AQP4 expression assessed with Western blotting was not significantly reduced until 24 h post‐HI irrespective of age. However, AQP4 immunostaining was decreased at the end of HI and at 1 h or 24 h after HI in the hemisphere ipsilateral to the occlusion with changes being similar in both age groups and coinciding well with regional reductions in ADC. IgG immunostaining to assess blood–brain barrier integrity and T2 were unchanged at early time points in 4‐week old rats despite decreases in AQP4 immunostaining. Thus, at early time points there were decreases in AQP4 detected with immunostaining but not Western blotting methods. However, the good correlation between alterations in ADC and AQP4 immunostaining suggests that changes in the AQP4 are involved in some of the early changes in brain water distribution observed in hypoxia‐ischemia, and supports the speculation that AQP4 is involved in the transport of water across the perivascular membranes into the vascular lumen.
In vivo effects of insulin‐like growth factor‐I (IGF‐I) on prenatal and early postnatal development of the central nervous system
Authors: Popken Gregory J. , Hodge Rebecca D. , Ye Ping , Zhang Jihui , Ng Winnie , O'Kusky John R. , D'Ercole A. Joseph
Published: April 2004

The in vivo actions of insulin‐like growth factor‐I (IGF‐I) on prenatal and early postnatal brain development were investigated in transgenic (Tg) mice that overexpress IGF‐I prenatally under the control of regulatory sequences from the nestin gene. Tg mice demonstrated increases in brain weight of 6% by embryonic day (E) 18 and 27% by postnatal day (P) 12. In Tg embryos at E16, the volume of the cortical plate was significantly increased by 52% and total cell number was increased by 54%. S‐phase labeling with 5‐bromo‐2′‐deoxyuridine revealed a 13–15% increase in the proportion of labeled neuroepithelial cells in Tg embryos at E14. In Tg mice at P12, significant increases in regional tissue volumes were detected in the cerebral cortex (29%), subcortical white matter (52%), caudate‐putamen (37%), hippocampus (49%), dentate gyrus (71%) and habenular complex (48%). Tg mice exhibited significant increases in the total number of neurons in the cerebral cortex (27%), caudate‐putamen (27%), dentate gyrus (69%), medial habenular nucleus (61%) and lateral habenular nucleus (36%). In the cerebral cortex and subcortical white matter of Tg mice, the total numbers of glial cells were significantly increased by 37% and 42%, respectively. The numerical density of apoptotic cells in the cerebral cortex, labeled by antibodies against active caspase‐3, was reduced by 26% in Tg mice at P7. Our results demonstrate that IGF‐I can both promote proliferation of neural cells in the embryonic central nervous system in vivo and inhibit their apoptosis during postnatal life.
Regulation of glutamate‐synthesizing enzymes by NMDA and potassium in cerebellar granule cells
Authors: Caballero‐Benítez Andrea , Alavez Silvestre , Uribe Rosa María , Morán Julio
Published: April 2004

The presence of 25 mm potassium (KCl) or N‐methyl‐d‐aspartate (NMDA) in cultured cerebellar granule neurons (CGN) induces a trophic effect, including a specific regulation of the enzymes involved in the glutamate neurotransmitter synthesis. In this study we explored the effect of these conditions on the cytosolic and mitochondrial isoenzymes of aspartate aminotransferase (AAT), and phosphate‐activated glutaminase (PAG) in CGN. We found that NMDA and KCl increased the AAT total activity by 40% and 70%, respectively. This effect was mediated by an augmentation in the protein levels (68% by NMDA, 58% by KCl). NMDA raised the Vmax and KCl raised both the maximol velocity (Vmax) and Michaelis constant (Km) of AAT. NMDA increased cytosolic AAT activity by 30% and mitochondrial activity by 70%; KCl increased cytosolic and mitochondrial AAT activity by 60% and 100%, respectively. This activation was also related to an increase in the protein levels. The effect of both conditions on the activity and protein levels were more pronounced in mitochondrial than cytosolic AAT and the increment elicited by KCl was higher in both isoforms than that produced by NMDA. The PAG and AAT mRNA levels were also regulated by incubation with NMDA and KCl similarly to the observed changes in the protein levels. These results suggest that NMDA receptor stimulation during CGN development differentially regulates the two AAT isoenzymes involved in the maturation of CGN and that the regulation of both AAT and PAG occurs also at the mRNA expression level, suggesting the involvement of a mechanism of gene expression regulation.
Effect of lithium on the circadian rhythms of locomotor activity and glycogen synthase kinase‐3 protein expression in the mouse suprachiasmatic nuclei
Authors: Iwahana Eiko , Akiyama Masashi , Miyakawa Kazuko , Uchida Ayumi , Kasahara Jiro , Fukunaga Kohji , Hamada Toshiyuki , Shibata Shigenobu
Published: April 2004

A circadian clock located in the suprachiasmatic nucleus (SCN) regulates the period of physiological and behavioural rhythms to approximately 24 h. Lithium can lengthen the period of circadian rhythms in most organisms although little is known about the underlying mechanism. In the present study, we examined Drosophila shaggy ortholog glycogen synthase kinase‐3 (GSK‐3) protein expression in the SCN after lithium treatment. When locomotor activity was assessed, we found an association between the effect of lithium and the period of circadian oscillation as well as the level of GSK‐3 protein expression. The decreased expression of GSK‐3 and increased expression of phosphorylated GSK‐3 (pGSK‐3) resulted in an antiphasic circadian rhythm between the two in the SCN of lithium‐treated mice housed under both light–dark and constant dark conditions. The enzyme activity of GSK‐3 in the SCN was low when the level of pGSK‐3 protein was high, as examined by immunoblotting analysis. Thus, GSK‐3 enzyme activity has a correlation with the expression of GSK‐3 protein in the SCN. Although both GSK‐3 and pGSK‐3 proteins are also expressed in the arcuate nucleus, lithium did not affect their expression. Based on the association that we found between lengthened circadian period and GSK‐3 protein and GSK‐3 activity in the SCN, we suggest that GSK‐3 plays a role in regulating the period of the mammalian circadian pacemaker.
Loss of GLUR2 α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazoleproprionic acid receptor subunit differentially affects remaining synaptic glutamate receptors in cerebellum and cochlear nuclei
Authors: Petralia Ronald S. , Sans Nathalie , Wang Ya‐Xian , Vissel Bryce , Chang Kai , Noben‐Trauth Konrad , Heinemann Stephen F. , Wenthold Robert J.
Published: April 2004

The α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazoleproprionic acid (AMPA) type of ionotropic glutamate receptor is the major mediator of fast neurotransmission in the brain and spinal cord. Most AMPA receptors are impermeable to calcium because they contain the GluR2 subunit. However, some AMPA receptors lack GluR2 and pass calcium which can mediate synaptic plasticity and, in excess, neurotoxicity. Previously, we showed a decrease in the density of synaptic AMPA receptors in the hippocampus of mice lacking GluR2. In this study, using these GluR2‐lacking mice, we examined other areas of the brain that differ in the amount of GluR2 normally present. Like hippocampal spines, cerebellar Purkinje spines normally express AMPA receptors with high GluR2 and showed a decrease in synaptic AMPA receptors in mutant mice. In contrast, neurons that normally express AMPA receptors with little or no GluR2, such as in the anteroventral cochlear nucleus, showed no decrease in AMPA receptors and even showed an increase in one AMPA receptor subunit. These two different patterns may relate to preadaptations to prevent calcium neurotoxicity; such mechanisms might be absent in Purkinje and hippocampal spines so that these neurons must decrease their total expression of synaptic AMPA receptors (calcium permeable in mutant mice) to prevent calcium neurotoxicity. In addition, we found that another glutamate receptor, GluRδ2, which is abundant only in parallel fibre synapses on Purkinje cells and in the dorsal cochlear nucleus, is up‐regulated at these synapses in mutant mice; this probably reflects some change in GluRδ2 targeting to these synapses.
Bidirectional modulation of windup by NMDA receptors in the rat spinal trigeminal nucleus
Authors: Woda Alain , Blanc Olivier , Voisin Daniel L. , Coste Jérôme , Molat Jean‐Louis , Luccarini Philippe
Published: April 2004

Activation of afferent nociceptive pathways is subject to activity‐dependent plasticity, which may manifest as windup, a progressive increase in the response of dorsal horn nociceptive neurons to repeated stimuli. At the cellular level, N‐methyl‐d‐aspartate (NMDA) receptor activation by glutamate released from nociceptive C‐afferent terminals is currently thought to generate windup. Most of the wide dynamic range nociceptive neurons that display windup, however, do not receive direct C‐fibre input. It is thus unknown where the NMDA mechanisms for windup operate. Here, using the Sprague–Dawley rat trigeminal system as a model, we anatomically identify a subpopulation of interneurons that relay nociceptive information from the superficial dorsal horn where C‐fibres terminate, to downstream wide dynamic range nociceptive neurons. Using in vivo electrophysiological recordings, we show that at the end of this pathway, windup was reduced (24 ± 6%, n = 7) by the NMDA receptor antagonist AP‐5 (2.0 fmol) and enhanced (62 ± 19%, n = 12) by NMDA (1 nmol). In contrast, microinjections of AP‐5 (1.0 fmol) within the superficial laminae increased windup (83 ± 44%, n = 9), whereas NMDA dose dependently decreased windup (n = 19).These results indicate that NMDA receptor function at the segmental level depends on their precise location in nociceptive neural networks. While some NMDA receptors actually amplify pain information, the new evidence for NMDA dependent inhibition of windup we show here indicates that, simultaneously, others act in the opposite direction. Working together, the two mechanisms may provide a fine tuning of gain in pain.
Dopamine receptor‐mediated regulation of RGS2 and RGS4 mRNA differentially depends on ascending dopamine projections and time
Authors: Taymans Jean‐Marc , Kia Hossein Kami , Claes Robby , Cruz Catarina , Leysen Josée ,   Xavier Langlois
Published: April 2004

RGS2 and RGS4 mRNAs are regulated in the rat striatum by dopaminergic agents. The present study further characterizes this regulation in three experiments. First, dopamine type 1 (receptor) (D1)‐ and dopamine type 2 (receptor) (D2)‐mediated regulator of G‐protein signalling (RGS) gene regulation was investigated in animals with deleted ascending dopaminergic pathways. We showed that RGS2 expression is controlled by D1 receptors either by direct action on D1 receptors or indirectly by presynaptic D2 receptors. Conversely, RGS4 gene expression is independent of presynaptic D2 receptors. Second, the study of colocalization between RGS2 or RGS4 and D1 or D2 by double labelling in situ hybridization histochemistry revealed broad expression of RGS2 and RGS4 mRNA in striatal subpopulations with colocalization of RGS2 and RGS4 with both D1 and D2 receptors. Finally, to test how far their gene regulation is temporally concerted, changes in RGS2 and RGS4 mRNA levels were measured in parallel with receptor occupancy by specific dopaminergic drugs at different time‐points. RGS2 was rapidly/transiently up‐regulated by the D1 agonist SKF82958 and the D2 antagonist haloperidol (peak at 0.5 h) and down‐regulated by the D1 antagonist SCH23390 and the D2 agonist quinpirole (trough at 1 and 2 h). RGS4 showed a delayed/transient up‐regulation with SCH23390 and quinpirole (peak at 4 and 2 h) and down‐regulation with haloperidol (trough at 8 h). Depending on the drug used, the degree of receptor occupancy did (D1 agonist and RGS2) or did not (D2 antagonist and RGS2) run parallel to RGS gene expression changes, indicating that certain drug effects are direct and others indirect. The precise control of RGS2 and RGS4 expression by dopamine receptors pleads in favour of their potential contribution to the fine‐tuning of D1 and D2 receptor signalling cascades.
Localized expression of amphiphysin Ir, a retina‐specific variant of amphiphysin I, in the ribbon synapse and its functional implication
Authors: Hosoya Osamu , Tsutsui Ken , Tsutsui Kimiko
Published: April 2004

In the vertebrate retina, presynaptic terminals of photoreceptors and bipolar cells form ribbon synapses and release neurotransmitter continuously. Endocytic machinery in the ribbon synapse is likely to differ from that in conventional synapses because of the much higher rate of synaptic vesicle recycling. However, protein components of the ribbon synapse identified so far are quite similar to those of the conventional synapses. Recently we identified amphiphysin I splice variants, termed amphiphysin Ir, that are transcribed specifically in retina from the authentic amphiphysin I gene [Y. Terada et al. (2002) FEBS Lett., 519, 185–190]. Amphiphysin I is a nerve terminal‐enriched protein, and involved in synaptic vesicle endocytosis as heterodimer with amphiphysin II, an isoform of amphiphysin I. We report here that the retina‐specific amphiphysin Ir is expressed exclusively in the ribbon synapse and not in conventional synapses. This is the first endocytosis‐related, ribbon synapse‐specific protein identified in the retina. By immunoprecipitation and double‐immunolabelling, amphiphysin Ir was shown to be associated not only with amphiphysin II, but also with dynamin, clathrin and α‐adaptin that are involved in synaptic vesicle recycling. The results suggest that endocytosis of the synaptic vesicle membrane in retinal ribbon synapses proceeds through a pathway similar to the one that is used in conventional synapses, although amphiphysin Ir is substituted for amphiphysin I. Amphiphysin Ir may play an essential role in the avid endocytic activity of ribbon synapses by associating with yet unknown protein partner(s) through its large insertional domain, which is absent from the conventional amphiphysin I.
Putative Physiological Significance of Vasopressin V1a Receptor Activation in Rat Pituicytes
Authors: Rosso L. , Peteri‐Brunbäck B. , Mienville J.‐M.
Published: April 2004

Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat pituicytes. During stimulation with adenosine, pituicytes become stellate, which is characterized by a round, phase‐bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate pituicytes revert to a flat shape. The effects of both hormones are mediated by V1a receptor activation, which also induces biphasic Ca2+i signals in pituicytes. Stellation reversal requires Ca2+‐dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V1a receptor activation by vasopressin or oxytocin also stimulates [3H]taurine efflux from cultured pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative‐feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in pituicytes. These results support the concept that, during specific physiological states, pituicyte V1a receptor activation modulates the release of neurohypophysial hormones.
The Role of Vasopressin in the Genetic and Neural Regulation of Monogamy
Authors: Lim M. M. , Hammock E. A. D. , Young L. J.
Published: April 2004

Arginine vasopressin modulates pairbond formation in the monogamous prairie vole (Microtus ochrogaster). Our laboratory has investigated the genetic and neural mechanisms by which vasopressin and its V1a receptor (V1aR) regulate social attachment between mates. Non‐monogamous vole species show strikingly different distribution patterns of brain V1aR expression compared to monogamous species, and these patterns are thought to arise from species differences in the respective promoter sequences of the V1aR gene. Individual differences in prairie vole V1aR patterns may also reflect individual differences in promoter sequences. Pharmacological and genetic manipulation of the specific brain regions that express V1aR in the ‘monogamous pattern’ allows multilevel examination of the neural circuits that underlie pairbond formation in monogamous species. For example, V1aR are expressed in brain regions involved in reward circuitry in monogamous vole species and have been implicated in pairbonding. V1aR are also highly expressed in regions implicated in the olfactory processing of sociosexual behaviour. We hypothesize that both circuits of reward and olfactory memory underlie the cognitive mechanisms that control pairbonding. When used in conjuction, genetic and cellular analyses of a complex social behaviour can provide a coherent framework with which to examine the role of the vasopressin system in species evolution and neural control of behaviour.
Steroid‐Independent Regulation of Uterine Oxytocin Receptors
Authors: Siebel A. L. , Gehring H. M. , Parry L. J.
Published: April 2004

The oxytocin receptor is an important contractile‐associated protein, up‐regulated at term in the myometrium in many mammalian species. We conducted studies in a novel animal model to challenge the general view that gonadal steroids are a major regulatory factor of uterine oxytocin receptors. Female marsupials have separate uteri and, in monovular species such as the tammar wallaby, the conceptus is present in one uterus whereas the contralateral uterus is empty. A marked increase in myometrial oxytocin receptors occurs only in the gravid uterus. Fetectomy experiments demonstrated that local embryo‐derived factors stimulate this gravid uterus‐specific increase in oxytocin receptors, and that uterine distension is probably not a key component in this regulatory pathway. Unilateral ovariectomy has no significant effect on uterine oxytocin receptors, emphasizing the impact of the conceptus on oxytocin receptor regulation and the minimal influence of gonadal steroids on parturition in this species. Our data highlight that regulation of uterine oxytocin receptor expression is multifactorial, and does not necessarily rely on gonadal steroids.
Functional Genomics of Social Recognition
Authors: Choleris E. , Kavaliers M. , Pfaff D. W.
Published: April 2004

Although various types of group living are widespread in mammals, including humans, the study of the hormonal and genetic underpinnings of nonsexual social behaviour, is in its infancy compared to the analysis of sexual behaviour mechanisms. Oxytocin, vasopressin and gonadal hormones certainly play an important role. Social recognition, where animals identify and recognize other individual conspecifics, is a crucial prerequisite for the occurrence of a wide range of social behaviours. Social recognition is also important for coping with one major cost of life in a group: the increased risk of exposure to parasites and infection. We review recent functional genomic studies on the involvement of oxytocin and oestrogen‐receptor genes in the regulation of social recognition in mice and in the ecologically relevant context of parasite recognition and avoidance. Based on quantitative studies of social recognition with gene‐knockout mice and with antisense DNA, we propose a four‐gene micronet contributing to social recognition. This micronet involves the genes coding for oestrogen receptors alpha (ER‐α), beta (ER‐β), oxytocin and the oxytocin receptor. In this model, circulating oestrogens promote transcription of (i) oxytocin in the paraventricular nucleus of the hypothalamus through ER‐β and (ii) oxytocin receptor in the amygdala through ER‐α. This model forms the core around which increasingly complex genetic, hormonal and neural interactions associated with social behaviours and recognition can be organized.
Magnocellular Dendrites: Prototypic Receiver/Transmitters
Authors: Morris J. F. , Ludwig M.
Published: April 2004

The hypothalamic magnocellular neurones of the supraoptic and paraventricular nuclei of mammals are among the best understood of all peptidergic neurones, and therefore serve as a model for understanding the functions of other peptidergic neurones. The release of vasopressin‐ and oxytocin‐containing neurosecretory vesicles from their dendrites was first established 15 years ago. This local release is now known to have many functions, including controlling the interactions between oxytocin neurones and their surrounding glia, and facilitating and inhibiting the electrical activation of the neurones. Technical advances now permit dynamic analysis of dendritic release. Here, we review recent studies that focus on the conditional priming of dendritic peptide release by peptide‐induced liberation of intracellular calcium, and the role of dendritic protein synthesis in the dendritic peptide release and the control of receptive properties of the neurones.
Magnetic Resonance Imaging of the Hypothalamic‐Neurohypophyseal System
Authors: Fujisawa I.
Published: April 2004

Magnetic resonance imaging (MRI) is a revolutionary advance in diagnostic imaging of the hypothalamic‐neurohypophyseal system (HNS). The detailed anatomy of the sellar and parasellar region is clearly visible using MRI, because it has no bony artifacts and multidirectional capability. The posterior lobe of the pituitary gland displays a characteristic bright signal on the MR T1‐weighted image (T1WI), and is distinctly separated from the anterior lobe. The bright signal is absent in patients with central diabetes insipidus, and is thought to reflect normal vasopressin storage in the posterior lobe. The signal intensity ratio of the posterior lobe to the pons on T1WI is strongly correlated with vasopressin content in the posterior lobe. In addition to the morphological evaluation, MRI provides unique information concerning the function of the HNS. The MRI findings of the HNS (normal condition, central diabetes insipidus, a depleted posterior lobe, an ectopic posterior lobe, and a damming‐up phenomenon of the neurosecretory vesicles in the pituitary stalk) are demonstrated in this article.
Neural Pathways Controlling Central and Peripheral Oxytocin Release During Stress
Authors: Onaka T.
Published: April 2004

Oxytocin is released from the pituitary gland in response to a variety of stressful stimuli, including noxious stimuli, conditioned fear and exposure to novel environments. These responses are believed to be mediated, at least in part, by noradrenergic projections from the medulla oblongata, and some of these noradrenergic neurones also contain prolactin‐releasing peptide (PrRP). Central administration of either PrRP or noradrenaline stimulates oxytocin secretion into the circulation. Stressful stimuli activate PrRP‐containing noradrenergic neurones in the medulla oblongata, and it is thus possible that PrRP/noradrenergic projections to the hypothalamus mediate oxytocin responses to stressful stimuli. Here, the roles of brainstem PrRP/noradrenergic projections to the hypothalamus in oxytocin responses to different kinds of stressful stimuli are reviewed, with a particular emphasis on conditioned fear. Roles of dendritic oxytocin release during stress and metabolic factors affecting stress pathways are also discussed.