bluuebunny/crossref_metadata_2025 huggingface dataset:
Fish assemblage patterns in the littoral zone of a European reservoir
Authors: BROSSE SEBASTIEN , GROSSMAN GARY D. , LEK SOVAN
Published: January 2007

1. Although reservoirs are common aquatic habitats in Europe, there is little quantitative information on the spatial organisation of fish assemblages inhabiting their littoral zones. Consequently, we characterised fish assemblage structure in the littoral zone of a reservoir (Lake Pareloup) in SW France during late spring, summer and early autumn (the growing season).

2. We measured the relative abundance of fish weekly, from mid‐May to mid‐October, using point abundance sampling by electrofishing. We identified temporal patterns in assemblage structure using hierarchical cluster analysis, and then characterised the spatial distribution of 17 defined ecospecies using a Kohonen self‐organising map (SOM, an unsupervised Artificial Neural Network).

3. Our analyses revealed three distinct faunal structures within the littoral zone. From mid‐May to mid‐July, adults and young‐of‐the‐year (0+) occupied separate habitats, with most 0+ fish in vegetated habitats and adults in open water. From mid‐July to late August, some 0+ co‐occurred with adults, but most 0+ fishes remained in vegetated areas. Finally, from late August to mid‐October, most fish (both 0+ and adults) left the vegetation for unvegetated littoral habitats, the exception being fish species known to be dependent on macrophytes.

4. Contrary to patterns for adult fishes, the 0+ fish assemblage was dynamic. These dynamics were driven by ontogenetic species‐specific habitat changes. Consequently, there was little evidence of stable assemblages or strong assemblage–habitat relationships that would be expected of an ‘interactive’ assemblage. It is likely that the patterns observed are a result of species‐specific response to habitat availability in the lake.
Response of river metabolism to restoration of flow in the Kissimmee River, Florida, U.S.A.
Authors: COLANGELO DAVID J.
Published: January 2007

1. The single station diel oxygen curve method was used to determine the response of system metabolism to backfilling of a flood control canal and restoration of flow through the historic river channel of the Kissimmee River, a sub‐tropical, low gradient, blackwater river in central Florida, U.S.A. Gross primary productivity (GPP), community respiration (CR), the ratio of GPP/CR (P/R) and net daily metabolism (NDM) were estimated before and after canal backfilling and restoration of continuous flow through the river channel.

2. Restoration of flow through the river channel significantly increased reaeration rates and mean dissolved oxygen (DO) concentrations from <2 mg L−1 before restoration of flow to 4.70 mg L−1 after flow was restored.

3. Annual GPP and CR rates were 0.43 g O2 m−2 day−1 and 1.61 g O2 m−2 day−1 respectively, before restoration of flow. After restoration of flow, annual GPP and CR rates increased to 3.95 O2 m−2 day−1 and 9.44 g O2 m−2 day−1 respectively.

4. The ratio of P/R (mean of monthly values) increased from 0.29 during the prerestoration period to 0.51 after flow was restored, indicating an increase in autotrophic processes in the restored river channel. NDM values became more negative after flow was restored.

5. After flow was restored, metabolism parameters were generally similar to those reported for other blackwater river systems in the southeast U.S.A. Postrestoration DO concentrations met target values derived from free flowing, minimally impacted reference streams.
Nutrient availability and the carnivorous habit in Utricularia vulgaris
Authors: KIBRIYA SADIA , IWAN JONES J.
Published: January 2007

1. Carnivory in plants is thought to enhance growth through an increased supply of nutrients, although there are considerable costs involved. It has been assumed that the relative investment of biomass in traps is inversely proportional to the availability of nutrients from non‐carnivorous sources. Our aim was to test the effect of increasing nutrient concentration on investment in carnivory by Utricularia vulgaris.

2. Plants were grown under controlled conditions and nitrogen and phosphorus added at three loadings in a crossed design. Investment in carnivory was assessed as the proportion of (i) leaf biomass and (ii) leaf area comprising traps.

3. There was no effect of nutrient additions on plant growth or periphyton abundance. Investment in carnivory declined with increasing phosphorus loading. There was no effect of nitrogen, despite this being the nutrient commonly thought to be sought by carnivorous plants. Analysis of previously published data also indicated a decline in investment with increasing P availability.

4. Investment in carnivory in U. vulgaris is inversely proportional to the availability of phosphorus from non‐carnivorous sources.
Challenging the tragedy of the commons in root competition: confounding effects of neighbour presence and substrate volume
Authors: SEMCHENKO MARINA , HUTCHINGS MICHAEL J. , JOHN ELIZABETH A.
Published: January 2007

It has been claimed that, compared with plants grown without competition, plants competing for a common pool of soil‐based resources overproduce roots at the expense of reproduction (known as the tragedy of the commons). However, experiments on this phenomenon have manipulated not only the presence/absence of neighbours, but also substrate volume. Restricted substrate volume can itself affect plant growth, possibly through chemical self‐inhibition of root growth. We conducted an experiment with oats (Avena sativa) to examine whether the experimental design used in previous studies on the tragedy of the commons in root competition might have confounded the effects of detection of neighbours and substrate volume.

Six treatments combined two factors, namely the presence or absence of activated carbon, and either the presence of a plastic or a mesh partition, or the absence of a partition, between two plants in a pot. Activated carbon was used to adsorb root exudates and reduce their potential effects on root growth. In a seventh treatment, plants were grown alone in pots with half the substrate volume replaced by gravel, to fragment the distribution of available resources.

We observed no tragedy of the commons in a comparison of the performance of plants grown with and without partitions; plants performed equally well in the presence and absence of root competition.

In the treatment with gravel, plants displayed reduced tillering and shoot growth per unit root mass, and an earlier switch to reproduction.

Pot partitioning was associated with inhibition of root growth that was mediated by root exudates. When activated carbon was present, plants in partitioned pots performed better than plants growing with a root competitor.

We conclude that two processes could determine plant growth in the experimental design used in studies of the tragedy of the commons: (i) greater root self‐inhibition in the more limited space of partitioned pots, and (ii) inefficient root placement in larger substrate volumes in unpartitioned pots that are shared with roots of a competitor. These findings provide a new challenge for experimental designs attempting to demonstrate the role of self/non‐self discrimination in root competition.
The role of chemokines as inflammatory mediators in chronic hepatitis C virus infection
Authors: Zeremski M. , Petrovic L. M. , Talal A. H.
Published: January 2007

Summary. Hepatitis C virus (HCV) is a leading cause of chronic liver disease that can progress to cirrhosis and/or hepatocellular carcinoma. Intrahepatic inflammation and liver cell injury are defining features of chronic HCV infection. Chemokines, chemotactic cytokines that attract leucocytes to inflammatory sites, may be important in the development of intrahepatic inflammation. As T‐helper (Th)1 inflammatory cells, characterized by interferon (IFN)‐γand interleukin (IL)‐2 secretion, predominate in the liver during chronic HCV infection, chemokines that attract these cells might be particularly important in disease progression. In this review, we focus on the role of Th1 chemokines, which are all members of the CXC or CC subfamilies. Among the CXC chemokines, the non‐ELR group comprised of IFN‐γ‐inducible protein 10 (IP‐10), monokine induced by IFN‐γ(Mig) and IFN‐inducible T‐cell‐αchemoattractant (I‐TAC), attract Th1 cells through the interaction with their receptor, CXCR3. Among the CC subfamily, Th1‐associated chemokines include regulated upon activation, normal T‐cell expressed and secreted (RANTES) and macrophage inflammatory proteins (MIP)1αandβ. These chemokines attract cells through an interaction with their receptor, CCR5. While peripheral blood and intrahepatic levels of all of these chemokines are elevated in chronic hepatitis C patients, only select chemokines have been found to be correlated with hepatic inflammation. Among the six chemokines, IP‐10 has uniquely been shown to have prognostic utility as a marker of treatment outcome. In the future, chemokines might be used to monitor the natural course and progression of HCV‐associated liver disease, to identify patients with a high likelihood of achieving a therapeutic response, and they may even have potential as therapeutic targets.
Atypical skin graft‐vs.‐host disease following bone marrow transplantation in an infant
Authors: Kuskonmaz B. , Güçer S. , Boztepe G. , Cetin M. , Uckan D.
Published: January 2007

Abstract:  Herein, we describe an unusual presentation of acute graft versus host disease (GVHD) mimicking contact dermatitis in an infant who underwent 5/6 HLA‐matched bone marrow transplantation (BMT) from his mother for malignant infantile osteopetrosis. The initial rash on day +32 simulated diaper rash, which progressed to a belt‐shaped rash and then developed hyperkeratotic nodules on the hands. The acute GVHD was atypical and the course was progressive and fatal, with liver and gut involvement. This presentation of atypical initial skin involvement of acute GVHD may be useful for practicing clinicians in the BMT field who need to be aware of the early unusual signs of acute GVHD so that they can initiate prompt treatment.
Laparoscopic live donor nephrectomy: The pediatric recipient in a dual‐site program
Authors: Bergman Simon , Feifer Andrew , Feldman Liane S. , Bell Lorraine , Flageole Helene , Tchervenkov Jean , Anidjar Maurice , Stanbridge Donna , Fried Gerald M.
Published: January 2007

Abstract:  Background: At our institution, laparoscopic live donor nephrectomy (LLDN) is done at a different hospital site than pediatric recipient transplantation, whereas open donor nephrectomy (OLDN) is done in the adjacent operating room. The purpose of this study was to evalute the safety of a dual‐site renal transplantation program by comparing the outcomes of pediatric recipients of LLDN vs. OLDN. Methods: This is a retrospective study of consective pediatric recipients (n = 10) of LLDN (June 2002 to June 2005) compared to the 10 most recent pediatric recipients of OLDN (March 2001 to June 2005). Renal function was assessed with calculated creatinine clearance using the Schwartz formula and the following outcomes were assessed: delayed graft function, ureteral complications, acute rejection and patient and graft survival. Results are expressed as median (IQR). Results: When comparing the laparoscopic vs. open group, there were no significant differences in recipient age, height, weight, preoperative calculated creatinine clearance and warm ischemia time. Twelve month postoperative creatinine clearance was 88 ml/min/1.73 m2 (57–99) in the laparoscopic group (n = 8) and 66 ml/min/1.73 m2 (60–86) in the open group (n = 9), p = 0.2. In the LLDN group vs. the OLDN group, delayed graft function was 0% vs. 10% (p = 1.0), ureteral complications were 20% vs. 30% (p = 1.0), and acute rejection was 20% vs. 40% (p = 0.6). In the laparoscopic group, one‐yr patient and graft survival were both 100%, as compared to 100% and 89%, respectively, in the open group. Conclusion: A dual‐site laparoscopic donor nephrectomy program is not associated with adverse pediatric recipicent outcomes when compared to a same‐site open donor approach.
Unexpectedly high inter‐ and intrapatient variability of Ganciclovir levels in children
Authors: Vethamuthu Jennifer , Feber Janusz , Chretien Ann , Lampe Dagmar , Filler Guido
Published: January 2007

Abstract:  Few studies report Ganciclovir or Valganciclovir levels in children. Single‐center, retrospective study of all available Ganciclovir levels in transplanted children. Ganciclovir monitoring was performed as previously described [G. Filler (1998); Pediatric Nephrology, 12, 6]. For the normalization of dosing to GFR and target trough levels, we assumed first‐order kinetics. We analyzed 57 Ganciclovir levels in 20 children (mean age 8.6 ± 5.5 yr) treated with intravenous or oral Ganciclovir or oral Valganciclovir. Ganciclovir levels were drawn after IV therapy (n = 9), during oral Ganciclovir (n = 5), or during oral Valganciclovir (n = 15). Oral bioavailability of Valganciclovir was 42.0 ± 21.8%. The dose‐normalized intrapatient Valganciclovir variability was 83%. Mean GFR was 92 ± 22 mL/min/1.73 m2. Mean Ganciclovir concentration at last available measurement was 0.60 ± 0.09 mg/L. While target trough Ganciclovir levels have not been established, possibly subtherapeutic Ganciclovir levels <0.5 mg/L on recommended IV doses were found in eight patients. This subset of patients was significantly younger (4.5 ± 3.1 vs. 11.4 ± 5.0 yr). Levels <0.5 mg/L were found in 24/57 instances and 10 patients subsequently had their dose increased. The last Valganciclovir dose adjusted to a GFR of 100 mL/min/1.73 m2 was 842 ± 323 mg/m2/day. A high proportion of patients had low Ganciclovir levels both on intravenous and oral therapy. The oral bioavailability of Valganciclovir was 42%. Our data suggest substantial inter‐ and intrapatient variability of Ganciclovir levels after pediatric renal transplantation and may support the need for pharmacokinetic monitoring of Ganciclovir and Valganciclovir therapy for the prevention and treatment of CMV disease after pediatric transplantation. It is currently unclear what target trough level would be most suitable.
Sirolimus is not always responsible for new‐onset proteinuria after conversion for chronic allograft nephropathy
Authors: Abdurrahman Zainab , Sarwal Minnie , Millan Maria , Robertson Susan , Filler Guido
Published: January 2007

Abstract:  An eight‐yr‐old combined liver and kidney transplant recipient for hyperoxaluria type I developed significant proteinuria and hypertension after conversion of a Tacrolimus, MMF, and corticosteroids‐based immunosuppression to Sirolimus, low‐dose Tacrolimus, and corticosteroids six and a half yr after the transplant for chronic allograft nephropathy. There was only one class I HLA match and the recipient had multiple blood exposures prior to transplantation. The patient was treated with combined hemodialysis and peritoneal dialysis while awaiting transplantation to reduce the oxalate load. A renal biopsy revealed a de novo transplant glomerulopathy that was associated with specific HLA antibodies unrelated to the donor (HLA DR 17 and 18). After reintroduction of MMF, these antibodies became undetectable and the proteinuria completely resolved. We hypothesize that HLA antibodies may cause transplant glomerulopathy even if they are not donor‐specific. Their production appears more susceptible to MMF therapy. A thorough work‐up of new‐onset proteinuria after conversion to Sirolimus should be performed, including an immunological work‐up and a renal biopsy.
Cross‐sectional study of BK virus infection in pediatric kidney transplant recipients
Authors: Fogeda Marta , Muñoz Patricia , Luque Augusto , Morales Ma Dolores , Bouza Emilio ,   the BKV Study Group
Published: January 2007

Abstract:  BKV reactivation is associated with impaired graft function in adult kidney transplant patients. The clinical impact of BKV infection in the pediatric transplant population has not yet been fully evaluated. The objective of our study was to determine the prevalence of BKV infection in consecutive pediatric kidney transplant recipients in our center. Forty consecutive unselected pediatric kidney transplant recipients were studied. Mean age at screening was 15.6 ± 5.3 yr and samples were obtained a median of 60.5 months after transplantation (3–123). BKV‐DNA was analyzed in urine and plasma by qualitative nested‐PCR. A review of the literature was performed. Prevalence of viruria and viremia was 50% and 12.5%, respectively. Viremia was associated with the presence of hematuria (p = 0.02). The mean creatinine level in children without BKV replication was 1.6 mg/dL, BKV viruria was 0.9 mg/dL, and BKV viremia was 0.8 mg/dL. A literature review showed that viruria and viremia were found in 28.2% and 8.5% of cases, respectively; BKV nephropathy was found in 3.8% and graft loss in 11% of the patients with BKV nephropathy and in 0.4% of the children studied. Recipient serostatus was the most important risk factor. The rate of BKV replication and nephropathy among pediatric kidney recipients is similar to that of adults, but the incidence of graft loss is significantly lower.
Effect of resource availability on biparental care, and offspring neural and behavioral development in the California mouse (Peromyscus californicus)
Authors: Bredy Timothy W. , Brown Richard E. , Meaney Michael J.
Published: January 2007

Maternal care influences cognitive function in humans, primates and rodents; however, little is known about the effect of biparental care. Environmental factors such as resource availability play an important role in modulating parental investment strategies with subsequent effects on the offspring. Thus, we examined the interaction between foraging demand and biparental care on hippocampal development and novel object recognition in the monogamous, biparental California mouse. We characterized biparental behavior for 15 days in families exposed to either control (ad libitum feeding) or a high‐foraging demand across the weaning period. Adult male offspring were then tested in the open field, and for novel object and place recognition, as well as for hippocampal synaptic density and the expression of genes encoding for subunits of the N‐methyl‐d‐aspartate (NMDA) receptor complex, and the postsynaptic density (PSD)‐95 scaffolding protein. Under high‐foraging demand, the mothers' body weight was decreased at weaning and fathers spent significantly less time in contact with pups. Offspring reared under high‐foraging demand weighed less at weaning and, as adults, were more fearful in the open field and showed profound deficits in both novel object and place recognition. While synaptic density and NR1 mRNA expression were unaffected, offspring reared under high‐foraging demand showed increased NR2A and decreased NR2B mRNA expression. Further, PSD‐95 protein expression was decreased in mice reared under high‐foraging demand. Together, the results suggest that resource availability affects biparental investment strategies, with subsequent effects on hippocampal development and novel object recognition in the offspring.
The characteristics of neuronal injury in a static compression model of spinal cord injury in adult rats
Authors: Huang W. L. , George K. J. , Ibba V. , Liu M. C. , Averill S. , Quartu M. , Hamlyn P. J. , Priestley J. V.
Published: January 2007

Studies of spinal cord injury using contusion (impact) injury paradigms have shown that neuronal death is an acute event that is largely over within 24 h. However, much less is known about cell death following compression injury, despite compression being a key component of natural spinal injuries. We have therefore used neuronal nuclei (NeuN) immunostaining to examine the spatiotemporal pattern of neuronal loss after static compression injury in adult rats. 3D reconstruction was used to reveal the full effect of the injury. Neuronal loss at the injury epicentre, assessed by NeuN immunostaining, amounted to 44% at 1 day but increased to 73% at 3 days and 81% at 1 month. Neuronal loss was also seen 5 mm rostral and caudal to the epicentre, but was not significant until 3 days. NeuN loss was greatest in the ventral horns and in the intermediate grey matter, with the lateral dorsal horns relatively spared. Cystic cavities formed after injury, but were not evident until 4 weeks and were small in size. In contrast to the slow profile of neuronal loss, the compression injury also evoked a transient expression of activating transcription factor‐3 (ATF3) and activated c‐Jun in neurons. ATF3 expression peaked at 3 days and declined at 7 days. Our spatiotemporal analysis of compression injury shows that neuronal loss is much more protracted than in contusion injury, and highlights the potential for neuroprotective strategies. This study is also the first indication of ATF3 involvement in spinal cord injury.
Time‐course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations following intrastriatal injection of 6‐hydroxydopamine in the rat: new clues from an old model
Authors: Blandini Fabio , Levandis Giovanna , Bazzini Eleonora , Nappi Giuseppe , Armentero Marie‐Therese
Published: January 2007

Despite the progressive development of innovative animal models for Parkinson's disease, the intracerebral infusion of neurotoxin 6‐hydroxydopamine (6‐OHDA) remains the most widely used means to induce an experimental lesion of the nigrostriatal pathway in the animal, due to its relatively low complexity and cost, coupled with the high reproducibility of the lesion obtained. To gain new information from such a classic model, we studied the time‐course of the nigrostriatal damage, metabolic changes in the basal ganglia nuclei (cytochrome oxidase activity) and behavioural modifications (rotational response to apomorphine) following unilateral injection of 6‐OHDA into the corpus striatum of rat, over a 4‐week period. Striatal infusion of 6‐OHDA caused early damage of dopaminergic terminals, followed by a slowly evolving loss of dopaminergic cell bodies in the substantia nigra pars compacta, which became apparent during the second week post‐injection and peaked at the 28th day post‐infusion; the rotational response to apomorphine was already present at the first time point considered (Day 1), and remained substantially stable throughout the 4‐week period of observation. The evolution of the nigrostriatal lesion was accompanied by complex changes in the metabolic activity of the other basal ganglia nuclei investigated (substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and subthalamic nucleus), which led, ultimately, to a generalized, metabolic hyperactivity, ipsilaterally to the lesion. However, peculiar patterns of metabolic activation, or inhibition, characterized the post‐lesional responses of each nucleus, in the early and intermediate phases, with peculiar response profiles that varied closely related to the functional position occupied within the basal ganglia circuitry.
Dissociation of sustained attention from central executive functions: local activity and interregional connectivity in the theta range
Authors: Sauseng P. , Hoppe J. , Klimesch W. , Gerloff C. , Hummel F. C.
Published: January 2007

Human brain oscillatory activity was analysed in the electroencephalographic theta frequency range (4–7 Hz) while subjects executed complex sequential finger movements with varying task difficulty and memory load. Local frontal‐midline theta activity was associated with the general level of cognitive demand, with the highest amplitudes in the most demanding condition. Using low‐resolution electromagnetic tomography analysis (LORETA), this theta activity was localized in the anterior cingulate gyrus including the cingulate motor area. These results suggest that local theta activity in the anterior cingulate gyrus represents correlates of an attentional system that allocate cognitive resources. In addition, interregional connectivity in the theta frequency range was modulated by memory‐related executive functions independently of task difficulty. Connectivity analyses revealed a more distributed long‐range network including frontal and parietal cortices during execution of novel compared with well‐trained finger movement sequences. Thus, these results are compatible with a model in which theta long‐range coupling indicates integration of sensory information into executive control components of complex motor behaviour.
Prenatal exposure to polybrominated diphenylether 99 enhances the function of the glutamate–nitric oxide–cGMP pathway in brain in vivo and in cultured neurons
Authors: Llansola Marta , Erceg Slaven , Monfort Pilar , Montoliu Carmina , Felipo Vicente
Published: January 2007

Polybrominated diphenylethers (PBDEs) are widely used as flame retardants. Significant amounts of PBDEs are present in the milk of lactating women. The possible neurotoxic effects of PBDEs are not well known. Perinatal exposure to PBDEs affects both motor and cognitive functions by mechanisms that remain unclear. Some types of learning depend on N‐methyl‐d‐aspartate receptor activation, which increases intracellular calcium that binds to calmodulin and activates nitric oxide synthase, increasing nitric oxide formation that activates guanylate cyclase, increasing cGMP formation. Part of this cGMP is released to the extracellular fluid. We studied whether prenatal exposure of rats to PBDE99 alters the function of this glutamate–nitric oxide–cGMP pathway in rat brain in vivo. At 10 weeks of age, rats treated with PBDE99 showed increased function of the glutamate–nitric oxide–cGMP pathway in brain in vivo, as assessed by microdialysis in freely moving rats. The increased function of the pathway was reproduced in primary cultures of cerebellar neurons prepared from rats prenatally exposed to PBDE99 as well as in neurons cultured from normal rats and treated in vitro with PBDE99. Increased calmodulin content and activation of soluble guanylate cyclase by nitric oxide contributed to the increased function of the pathway.
Early functional development of interneurons in the zebrafish olfactory bulb
Authors: Mack‐Bucher Julia A. , Li Jun , Friedrich Rainer W.
Published: January 2007

In the adult olfactory bulb (OB) of vertebrates, local GABAergic interneurons (INs) mediate recurrent and lateral inhibition between the principal neurons of the OB, the mitral cells (MCs), and play pivotal roles in the processing of odor‐evoked activity patterns. The properties and functions of INs in the developing OB are, however, not well understood. We studied the functional development of INs in the OB of living zebrafish larvae 3–6 days postfertilization using anatomical techniques and in‐vivo two‐photon Ca2+ imaging. We identified MCs and INs by cell‐type‐specific expression of transgenic fluorescent markers and found that the IN : MC ratio was lower than in the adult fish. Moreover, the fraction of INs responding with Ca2+ signals to a set of natural odors was substantially lower than in adults. Odors of different chemical classes evoked overlapping patterns of Ca2+ signals that were concentrated in the center of the IN layer. The GABAA receptor agonists GABA and muscimol strongly suppressed odor responses, whereas a GABAA receptor antagonist enhanced responses and altered the spatial distribution of odor‐evoked activity. These results indicate that IN odor responses at early developmental stages are sparse and exhibit no obvious chemotopic organization. Nevertheless, GABAergic signaling is already inhibitory at early stages of OB development and strongly influences odor‐evoked activity patterns. Hence, INs already participate in the processing of odor information at very early stages of OB development even though the majority of INs emerge only at later stages.
Melatonin induces gene‐specific effects on rhythmic mRNA expression in the pars tuberalis of the Siberian hamster (Phodopus sungorus)
Authors: Wagner Gabriela C. , Johnston Jonathan D. , Tournier Benjamin B. , Ebling Francis J. P. , Hazlerigg David G.
Published: January 2007

In mammals, circadian and photoperiodic information is encoded in the pineal melatonin signal. The pars tuberalis (PT) of the pituitary is a melatonin target tissue, which transduces photoperiodic changes and drives seasonal changes in prolactin secretion from distal lactotroph cells. Measurement of photoperiodic time in the PT is believed to occur through melatonin dependent changes in clock gene expression, although it is unclear whether the PT should be considered a melatonin sensitive peripheral oscillator. We tested this hypothesis in the Siberian hamster (Phodopus sungorus) firstly by investigating the effects of melatonin injection, and secondly by determining whether temporal variation in gene expression within the PT persists in the absence of a rhythmic melatonin signal. Hamsters preconditioned to long days were treated with melatonin during the late light phase, to advance the timing of the nocturnal melatonin peak, or placed in constant light for one 24 h cycle, thereby suppressing endogenous melatonin secretion. Gene expression in the PT was measured by in situ hybridization. We show that melatonin rapidly induces cry1 mRNA expression without the need for a prolonged melatonin‐free interval, acutely inhibits mt1 expression, advances the timing of peak rev‐erbα expression and modulates per1 expression. With the exception of cry1, these genes continue to show temporal changes in expression over a first cycle in the absence of a melatonin signal. Our data are consistent with the hypothesis that the hamster PT contains a damped endogenous circadian oscillator, which requires a rhythmic melatonin signal for long‐term synchronization.
Developmental divergence of sleep‐wake patterns in orexin knockout and wild‐type mice
Authors: Blumberg Mark S. , Coleman Cassandra M. , Johnson Eric D. , Shaw Cynthia
Published: January 2007

Narcolepsy, a disorder characterized by fragmented bouts of sleep and wakefulness during the day and night as well as cataplexy, has been linked in humans and nonhuman animals to the functional integrity of the orexinergic system. Adult orexin knockout mice and dogs with a mutation of the orexin receptor exhibit symptoms that mirror those seen in narcoleptic humans. As with narcolepsy, infant sleep‐wake cycles in humans and rats are highly fragmented, with consolidated bouts of sleep and wakefulness developing gradually. Based on these common features of narcoleptics and infants, we hypothesized that the development of sleep‐wake fragmentation in orexin knockout mice would be expressed as a developmental divergence between knockouts and wild‐types, with the knockouts lagging behind the wild‐types. We tested this hypothesis by recording the sleep‐wake patterns of infant orexin knockout and wild‐type mice across the first three postnatal weeks. Both knockouts and wild‐types exhibited age‐dependent, and therefore orexin‐independent, quantitative and qualitative changes in sleep‐wake patterning. At 3 weeks of age, however, by which time the sleep and wake bouts of the wild‐types had consolidated further, the knockouts lagged behind the wild‐types and exhibited significantly more bout fragmentation. These findings suggest the possibility that the fragmentation of behavioural states that characterizes narcolepsy in adults reflects reversion back toward the more fragmented sleep‐wake patterns that characterize infancy.
Prokineticin 2 depolarizes paraventricular nucleus magnocellular and parvocellular neurons
Authors: Yuill Erik A. , Hoyda Ted D. , Ferri Catharine C. , Zhou Qun‐Yong , Ferguson Alastair V.
Published: January 2007

Blind whole‐cell patch‐clamp techniques were used to examine the effects of prokineticin 2 (PK2) on the excitability of magnocellular (MNC), parvocellular preautonomic (PA), and parvocellular neuroendocrine (NE) neurons within the hypothalamic paraventricular nucleus (PVN) of the rat. The majority of MNC neurons (76%) depolarized in response to 10 nm PK2, effects that were eliminated in the presence of tetrodotoxin (TTX). PK2 also caused an increase in excitatory postsynaptic potential (EPSP) frequency, a finding that was confirmed by voltage clamp recordings demonstrating increases in excitatory postsynaptic current (EPSC) frequency. The depolarizing effects of PK2 on MNC neurons were also abolished by kynurenic acid (KA), supporting the conclusion that the effects of PK2 are mediated by the activation of glutamate interneurons within the hypothalamic slice. PA (68%) and NE (67%) parvocellular neurons also depolarized in response to 10 nm PK2. However, in contrast to MNC neurons, these effects were maintained in TTX, indicating that PK2 directly affects PA and NE neurons. PK2‐induced depolarizations observed in PA and NE neurons were found to be concentration‐related and receptor mediated, as experiments performed in the presence of A1MPK1 (a PK2 receptor antagonist) abolished the effects of PK2 on these subpopulations of neurons. The depolarizing effects of PK2 on PA and NE neurons were also shown to be abolished by PD 98059 (a mitogen activated protein kinase (MAPK) inhibitor) suggesting that PK2 depolarizes PVN parvocellular neurons through a MAPK signalling mechanism. In combination, these studies have identified separate cellular mechanisms through which PK2 influences the excitability of different subpopulations of PVN neurons.
Inactivation of the prelimbic, but not infralimbic, prefrontal cortex impairs the contextual control of response conflict in rats
Authors: Marquis Jean‐Philippe , Killcross Simon , Haddon Josephine E.
Published: January 2007

One fundamental function of the prefrontal cortex (PFC) is to guide context‐appropriate behaviour in situations of response conflict. Haddon and Killcross recently developed a task in rats which mimics some aspects of response conflict seen in human cognitive paradigms such as the Stroop task. Using this paradigm they demonstrated that large PFC lesions including the prelimbic (PL), infralimbic (IL) and anterior cingulate cortices (ACC) selectively impaired performance on incongruent trials which required the use of task‐setting contextual cues to control responding in the face of ambiguous response information. The current experiment was conducted to determine whether specific PFC regions were responsible for the deficit in incongruent performance. Rats were trained on two instrumental biconditional discriminations, one auditory and one visual, in two different contexts. Following acquisition, rats were implanted with guide cannulae aimed at the PL or the IL cortices of the rat prefrontal cortex. Following retraining, rats received microinfusions of the GABAA agonist muscimol or artificial cerebrospinal fluid (aCSF) into either the PL or the IL prior to presentations of novel congruent and incongruent audiovisual compounds of the training stimuli in extinction. Results showed that temporary inactivation of the PL cortex led to a selective deficit on incongruent compound trials, but left congruent, and hence biconditional task performance intact. By contrast, IL inactivation had no effect on the accuracy of responding during either congruent or incongruent trials. These results suggest that the PL cortex is necessary for the use of task‐setting contextual cues to control responding to conflicting information.
Enhanced synaptic excitation–inhibition ratio in hippocampal interneurons of rats with temporal lobe epilepsy
Authors: Stief F. , Zuschratter W. , Hartmann K. , Schmitz D. , Draguhn A.
Published: January 2007

A common feature of all epileptic syndromes is the repetitive occurrence of pathological patterns of synchronous neuronal activity, usually combined with increased neuronal discharge rates. Inhibitory interneurons of the hippocampal formation control both neuronal synchronization as well as the global level of activity and are therefore of crucial importance for epilepsy. Recent evidence suggests that changes in synaptic inhibition during temporal lobe epilepsy are rather specific, resulting from selective death or alteration of interneurons in specific hippocampal layers. Hence, epilepsy‐induced changes have to be analysed separately for different types of interneurons. Here, we focused on GABAergic neurons located at the border between stratum radiatum and stratum lacunosum‐moleculare of hippocampal area CA1 (SRL interneurons), which are included in feedforward inhibitory circuits. In chronically epileptic rats at 6–8 months after pilocarpine‐induced status epilepticus, frequencies of spontaneous and miniature inhibitory postsynaptic currents were reduced, yielding an almost three‐fold increase in excitation–inhibition ratio. Consistently, action potential frequency of SRL interneurons was about two‐fold enhanced. Morphological alterations of the interneurons indicate that these functional changes were accompanied by remodelling of the local network, probably resulting in a loss of functional inhibitory synapses without conceivable cell death. Our data indicate a strong increase in activity of interneurons in dendritic layers of the chronically epileptic CA1 region. This alteration may enhance feedforward inhibition and rhythmogenesis and – together with specific changes in other interneurons – contribute to seizure susceptibility and pathological synchronization.
Intermittent ethanol exposure induces inflammatory brain damage and causes long‐term behavioural alterations in adolescent rats
Authors: Pascual Maria , Blanco Ana M. , Cauli Omar , Miñarro Jose , Guerri Consuelo
Published: January 2007

Adolescent brain development seems to be important for the maturation of brain structures and behaviour. Intermittent binge ethanol drinking is common among adolescents, and this type of drinking can induce brain damage. Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol intoxication enhances cyclooxygenase‐2 (COX‐2) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions. Adolescent rats were exposed to ethanol (3.0 g/kg) for two consecutive days at 48‐h intervals over 14 days. Levels of COX‐2, iNOS and cell death were assessed in the neocortex, hippocampus and cerebellum 24 h after the final ethanol administration. The following day or 20 days after the final injection (adult stage), animals were tested for different behavioural tests (conditional discrimination learning, rotarod, object recognition, beam‐walking performance) to assess cognitive and motor functions. Our results show that intermittent ethanol intoxication upregulates COX‐2 and iNOS levels, and increases cell death in the neocortex, hippocampus and cerebellum. Furthermore, animals treated with ethanol during adolescence exhibited behavioural deficits that were evident at the end of ethanol treatments and at the adult stage. Administration of indomethacin, a COX‐2 inhibitor, abolishes the induction of COX‐2 and iNOS expression and cell death, preventing ethanol‐induced behavioural deficits. These findings indicate that binge pattern exposure to ethanol during adolescence induces brain damage by inflammatory processes and causes long‐lasting neurobehavioural consequences. Accordingly, administering indomethacin protects against ethanol‐induced brain damage and prevents detrimental ethanol effects on cognitive and motor processes.
ω‐Conotoxin CVIB differentially inhibits native and recombinant N‐ and P/Q‐type calcium channels
Authors: Motin Leonid , Yasuda Takahiro , Schroeder Christina I. , Lewis Richard J. , Adams David J.
Published: January 2007

ω‐Conotoxins are routinely used as selective inhibitors of different classes of voltage‐gated calcium channels (VGCCs) in excitable cells. In the present study, we examined the potent N‐type VGCC antagonist ω‐conotoxin CVID and non‐selective N‐ and P/Q‐type antagonist CVIB for their ability to block native VGCCs in rat dorsal root ganglion (DRG) neurons and recombinant VGCCs expressed in Xenopus oocytes. ω‐Conotoxins CVID and CVIB inhibited depolarization‐activated whole‐cell VGCC currents in DRG neurons with pIC50 values of 8.12 ± 0.05 and 7.64 ± 0.08, respectively. Inhibition of Ba2+ currents in DRG neurons by CVID (∼ 66% of total) appeared to be irreversible for > 30 min washout, whereas Ba2+ currents exhibited rapid recovery from block by CVIB (≥ 80% within 3 min). The recoverable component of the Ba2+ current inhibited by CVIB was mediated by the N‐type VGCC, whereas the irreversibly blocked current (∼ 22% of total) was attributable to P/Q‐type VGCCs. ω‐Conotoxin CVIB reversibly inhibited Ba2+ currents mediated by N‐ (CaV2.2) and P/Q‐ (CaV2.1), but not R‐ (CaV2.3) type VGCCs expressed in Xenopus oocytes. The α2δ1 auxiliary subunit co‐expressed with CaV2.2 and CaV2.1 reduced the sensitivity of VGCCs to CVIB but had no effect on reversibility of block. Determination of the NMR structure of CVIB identified structural differences to CVID that may underlie differences in selectivity of these closely related conotoxins. ω‐Conotoxins CVIB and CVID may be useful as antagonists of N‐ and P/Q‐type VGCCs, particularly in sensory neurons involved in processing primary nociceptive information.
JNK1 contributes to metabotropic glutamate receptor‐dependent long‐term depression and short‐term synaptic plasticity in the mice area hippocampal CA1
Authors: Li Xin‐Mei , Li Chen‐Chen , Yu Shan‐Shan , Chen Ju‐Tao , Sabapathy Kanaga , Ruan Di‐Yun
Published: January 2007

Several recent reports implicate an important role played by c‐Jun N‐terminal kinases (JNKs) in long‐term potentiation (LTP). However, little is known about how the isoforms of JNKs participate in synaptic plasticity. Here we showed that short‐term synaptic plasticity was impaired in the hippocampal area CA1 of JNK1‐deficient (JNK1–/–) mice; these mice showed normal LTP in response to a strong tetanus and no alteration of N‐methyl‐d‐aspartate receptor‐dependent long‐term depression (LTD) in the hippocampus. However, LTD induced either by group I metabotropic glutamate receptors (mGluRs) agonist dihydroxyphenylglycine or by paired‐pulse low‐frequency stimulation was absent in both the JNK1–/– slices and in JNK inhibitor anthrax [1, 9‐cd] pyrazol‐6(2H)‐1 (SP600125)‐pretreated slices. Induction of mGluR‐dependent LTD resulted in an increase in phosphorylation of JNK1 substrates, including p‐c‐Jun and p‐ATF2 in wild‐type (WT) mice, and these increases failed to occur in the JNK1–/– or SP600125‐pretreated mice. These results demonstrated that JNK1 played a crucial role in the short‐term synaptic plasticity and mGluR‐dependent LTD, whereas hippocampus LTP was not affected by JNK1 deficiency.
Differential effects of NT‐4, NGF and BDNF on development of neurochemical architecture and cell size regulation in rat visual cortex during the critical period
Authors: Engelhardt Maren , Di Cristo Graziella , Berardi Nicoletta , Maffei Lamberto , Wahle Petra
Published: January 2007

Development of inhibition is a crucial determinant of the time course of visual cortical plasticity. BDNF strongly affects interneuron development and the onset and closure of the critical period for ocular dominance plasticity. Less is known on the effects of NT‐4 despite a clear involvement in ocular dominance plasticity. We have investigated the effects of NT‐4 on interneuron development by supplying NT‐4 with osmotic minipumps during two time windows overlapping the onset (P12–20) and the peak (P20–28) of the critical period. We assessed the expression of interneuronal markers and soma size maturation either after the end of the infusion periods or at the end of the critical period (P45). We found that NT‐4 was very effective in regulating interneuron development. NPY, SOM and PARV neuron somata grew faster during both infusion periods whereas CR neurons only responded during the early infusion period. The effects of soma size elicited during the earlier infusion period were still present at P45. In PARV neurons, NT‐4 caused a long‐lasting stabilization of CB and NPY expression. Furthermore, NT‐4 accelerated the expression of GAD‐65 mRNA in a subset of non‐PARV neurons of layer V, which normally up‐regulate GAD‐65 towards the end of the critical period. Most of these effects were shared by NT‐4 and BDNF. Some were unexpectedly also shared by NGF, which promoted growth of layer V PARV neurons, stabilized the CB expression and accelerated the GAD‐65 expression. The results suggest that neurotrophins act on critical period plasticity by strengthening inhibition.
Mechanisms of selective inhibition in visual spatial attention are indexed by α‐band EEG synchronization
Authors: Rihs Tonia A. , Michel Christoph M. , Thut Gregor
Published: January 2007

Electroencephalographic studies in humans have demonstrated that orienting of visual attention induces a decrease in oscillatory α‐band activity (α‐desynchronization) over cortical areas tuned to the attended visual space. This is interpreted as reflecting intentionally enhanced excitability of these areas to facilitate upcoming visual processing. However, the inverse mechanism might also apply. Brain areas that process task‐irrelevant space might be actively suppressed by increased α‐activity (α‐synchronization) to protect against input of distracter information. In the present study, we demonstrate that such suppression mechanisms are highly selective and are taking place even without distracters that need to be ignored. During voluntary orienting of attention, we found α‐synchronization to dominate over desynchronization, to be topographically specific for each of eight attention positions, and to occur over areas processing unattended space in a retinotopically organized pattern. This indicates that α‐synchronization is an important component of selective attention, serving active suppression of unattended positions during visual spatial orienting.
Binaral interaction and centrifugal input enhances spatial contrast in olfactory bulb activation
Authors: Singer Benjamin H. , Kim Soyoun , Zochowski Michal
Published: January 2007

We used paired‐pulse odorant stimulation, with a conditioning stimulus delivered either ipsilateral or contralateral to a test stimulus, to unmask the effects of centrifugal feedback on olfactory bulb responses. In reptiles and mammals there are no direct connections between the paired olfactory bulbs, and thus all information transfer between the olfactory bulbs depends on feedback from retrobulbar structures. We measured odor‐induced activity in the turtle olfactory bulb using a voltage‐sensitive dye and a 464‐element photodiode array, which allowed us to monitor the spatial variation in activation of the olfactory bulb. We found that both contralateral and ipsilateral conditioning stimuli evoked long‐lasting inhibition of olfactory bulb activation. In contrast to previous studies using local field potential recording to monitor activity at a single site, we found that this inhibition increased contrast in the spatial patterning of activation over the dorsal surface of the olfactory bulb. Inhibition was also increased when different odorants were used as conditioning and test stimuli, suggesting a role for centrifugal feedback in olfactory discrimination. These results highlight the functional importance of centrifugal feedback and information processing in a broadly distributed olfactory network.