bluuebunny/crossref_metadata_2025_split huggingface dataset:
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

AbstractDevelopment 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

AbstractElectroencephalographic 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

AbstractWe 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.
A nonopioid analgesic acts upon the PAG‐RVM axis to reverse inflammatory hyperalgesia
Authors: Vazquez Enrique , Escobar William , Ramirez Karla , Vanegas Horacio 
Published: January 2007

AbstractMetamizol (dipyrone) and other nonsteroidal anti‐inflammatory drugs (NSAIDs) induce antinociception by acting upon peripheral tissues and upon central nervous system structures, notably the periaqueductal grey matter (PAG) and the spinal cord. Inflammation‐induced hyperalgesia is prevented by spinal application of NSAIDs before the inflammation, but once central sensitization is established the spinal effect of NSAIDs is uncertain. The present study examines whether the action upon the PAG contributes to the attenuation of inflammation‐induced spinal hyperalgesia by NSAIDs. In deeply anaesthetized rats, responses of spinal multireceptive neurons to mechanical stimulation of the ipsilateral paw and leg were recorded. An inflammation in the paw was induced with carrageenan. Fifty minutes later, neuronal responses to innocuous and noxious stimulation had, respectively, increased to 206 and 304% for paw, and 160 and 190% for leg. When metamizol (150 µg in 0.5 µL) was microinjected into PAG before the inflammation, neuronal hyperexcitability was delayed for ∼ 60 min and was much reduced by 215 min. More interestingly, microinjection of metamizol into PAG when hyperexcitability was fully developed depressed neuronal responses down to baseline for ∼ 1 h. The effect of PAG metamizol was reversed by microinjection of a GABAAagonist into the rostral ventromedial medulla (RVM), which indicates that RVM relays the metamizol effect from PAG onto the spinal cord. These results suggest that, upon clinical administration of NSAIDs, a joint action upon PAG and spinal cord contributes to preventing the development of hyperalgesia but it is mainly the action upon PAG which contributes to reducing fully established hyperalgesia.
Truncated TrkB‐T1 regulates the morphology of neocortical layer I astrocytes in adult rat brain slices
Authors: Ohira Koji , Funatsu Nobuo , Homma Koichi J. , Sahara Yoshinori , Hayashi Motoharu , Kaneko Takeshi , Nakamura Shun 
Published: January 2007

AbstractBy altering their morphology, astrocytes, including those involved in the maintenance and plasticity of neurons and in clearance of transmitter, play important roles in synaptic transmission; however, the mechanism that regulates the morphological plasticity of astrocytes remains unclear. Recently, we reported that T1, a subtype of TrkB (a family of BDNF‐specific receptors), altered astrocytic morphology through the control of Rho GTPases in primary astrocyte cultures. In this study, we extended this observation to investigate acute neocortical slices from adult rats. T1 siRNA‐expression vectors were electroporated into astrocytes in neocortical layer I of living rats. In both normal slices and control vector‐electroporated slices, BDNF induced the elongation of the astrocytic processes and increased the branching of processes in slices after 1 h incubation. In contrast, in T1 siRNA‐electroporated slices, no such significant morphological changes were observed in the astrocytes. In addition, the number of synaptophysin+ sites in contact with GFAP+ processes increased in a BDNF–T1‐dependent manner without the increase in the total synaptophysin+ sites. Therefore, the present study provides evidence of the regulation of layer I astrocytic morphology by the BDNF–T1 signal in adult rat neocortical slices.
Differentiating allocation of resources and conflict detection within attentional control processing
Authors: Blasi Giuseppe , Goldberg Terry E. , Elvevåg Brita , Rasetti Roberta , Bertolino Alessandro , Cohen Jessica , Alce Guilna , Zoltick Brad , Weinberger Daniel R. , Mattay Venkata S. 
Published: January 2007

AbstractIncreasing demands for conflict detection and for allocation of attentional resources increase the need for attentional control. While prior evidence suggests that different cortical regions are preferentially engaged by these two attentional processes, the effect of increasing demand for conflict detection and/or allocation of attentional resources has been relatively unexplored. We designed a novel task (the ‘variable attentional control’– VAC – task) that varies the demand for attentional control by increasing conflict detection and allocation of attentional resources within the same stimuli. We studied 34 subjects who underwent event‐related functional magnetic resonance imaging while performing the VAC task. Increasing demand for attentional control, as reflected by longer reaction time and reduced accuracy, was associated with greater activation in the dorsolateral prefrontal cortex, parietal cortex and dorsal cingulate. Furthermore, an increase in conflict detection was associated with greater dorsal cingulate activity, whereas an increase in demand for allocation of attentional resources implied greater activation in the dorsolateral prefrontal and parietal cortices. In essence, in addition to allowing the exploration of the overall effects of increasing demand for attentional control, our novel task also allowed parsing of the neural components of attentional control into those related to allocation of attentional resources and those related to conflict detection.
In vivoadministration of epidermal growth factor and its homologue attenuates developmental maturation of functional excitatory synapses in cortical GABAergic neurons
Authors: Nagano Tadasato , Namba Hisaaki , Abe Yuichi , Aoki Hiroyuki , Takei Nobuyuki , Nawa Hiroyuki 
Published: January 2007

AbstractThe ErbB1 ligand family includes epidermal growth factor (EGF), transforming growth factor‐α (TGFα), heparin‐binding EGF‐like growth factor, amphiregulin and betacellulin. Previously, we demonstrated that TGFα decreases α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA)‐type glutamate receptors in cultured neocortical γ‐aminobutyric acid (GABA) neurons. In the present study, we examinedin vivoeffects of EGF and TGFα in the mouse neocortex using electrophysiological and biochemical techniques. In mouse neonates, subcutaneously administered EGF penetrated the blood–brain barrier and activated ErbB1 in the neocortex. Daily administration of EGF or TGFα attenuates developmental increases in expression of the AMPA receptor subunits (GluR1 and GluR2/3) in the neocortex of postnatal mice. Immunohistochemistry revealed that the reduction in AMPA receptor expression was significant in the GABAergic neurons, especially those positive for parvalbumin. Using cortical slices prepared from EGF‐treated mice, we recorded miniature excitatory postsynaptic currents (mEPSCs) in both GABAergic and pyramidal neurons. Subchronic treatment with EGF decreased the amplitude and frequency of mEPSCs in GABAergic neurons, but its effects were negligible on pyramidal neurons. We conclude that EGF or other ErbB1 ligand(s) attenuates a developmental increase in AMPA receptor expression and function in cortical GABAergic neurons.
Selectivity of human retinotopic visual cortex to S‐cone‐opponent, L/M‐cone‐opponent and achromatic stimulation
Authors: Mullen Kathy T. , Dumoulin Serge O. , McMahon Katie L. , De Zubicaray Greig I. , Hess Robert F. 
Published: January 2007

AbstractOur aim was to make a quantitative comparison of the response of the different visual cortical areas to selective stimulation of the two different cone‐opponent pathways [long‐ and medium‐wavelength (L/M)‐ and short‐wavelength (S)‐cone‐opponent] and the achromatic pathway under equivalent conditions. The appropriate stimulus‐contrast metric for the comparison of colour and achromatic sensitivity is unknown, however, and so a secondary aim was to investigate whether equivalent fMRI responses of each cortical area are predicted by stimulus contrast matched in multiples of detection threshold that approximately equates for visibility, or direct (cone) contrast matches in which psychophysical sensitivity is uncorrected. We found that the fMRI response across the two colour and achromatic pathways is not well predicted by threshold‐scaled stimuli (perceptual visibility) but is better predicted by cone contrast, particularly for area V1. Our results show that the early visual areas (V1, V2, V3, VP and hV4) all have robust responses to colour. No area showed an overall colour preference, however, until anterior to V4 where we found a ventral occipital region that has a significant preference for chromatic stimuli, indicating a functional distinction from earlier areas. We found that all of these areas have a surprisingly strong response to S‐cone stimuli, at least as great as the L/M response, suggesting a relative enhancement of the S‐cone cortical signal. We also identified two areas (V3A and hMT+) with a significant preference for achromatic over chromatic stimuli, indicating a functional grouping into a dorsal pathway with a strong magnocellular input.
Pigmentation predicts the shift in the line of decussation in humans with albinism
Authors: Von Dem Hagen Elisabeth A. H. , Houston Gavin C. , Hoffmann Michael B. , Morland Antony B. 
Published: January 2007

AbstractIn albinism a large proportion of nerve fibres originating in temporal retina cross the midline at the chiasm and project to the contralateral hemisphere. Studies in rodents with albinism have suggested that the extent of this misrouting at the chiasm is inversely related to pigmentation levels. Here, we examine whether there is evidence for a similar relationship in humans with albinism. Functional MRI was performed on 18 subjects with albinism, 17 control subjects and six controls with nystagmus as they underwent hemifield visual stimulation of nasal or temporal retina. Functional activation in 16 coronal slices beginning at the posterior occipital lobes were analysed and the extent of hemispheric response lateralization at each slice position was determined. During temporal retina stimulation, the control response was lateralized to the hemisphere ipsilateral to the stimulated eye for all slices. In albinos, the response in posterior slices was predominantly in the contralateral hemisphere, consistent with misrouting of temporal retina fibres. However, as slice location became progressively anterior, response lateralization reverted to the ipsilateral hemisphere. The slice location at which the transition from contra‐ to ipsilateralization occurred provided an estimate of the extent of fibre misrouting in the individual. The slice transition location correlated negatively with pigmentation level, providing the first evidence for a relationship between pigmentation and the extent of misrouting in humans with albinism.
Local synthesis of axonal and presynaptic RNA in squid model systems
Authors: Eyman Maria , Cefaliello Carolina , Ferrara Eugenia , De Stefano Rosanna , Lavina Zeno Scotto , Crispino Marianna , Squillace Angela , Van Minnen Jan , Kaplan Barry B. , Giuditta Antonio 
Published: January 2007

AbstractThe presence of active systems of protein synthesis in axons and nerve endings raises the question of the cellular origin of the corresponding RNAs. Our present experiments demonstrate that, besides a possible derivation from neuronal cell bodies, axoplasmic RNAs originate in periaxonal glial cells and presynaptic RNAs derive from nearby cells, presumably glial cells. Indeed, in perfused squid giant axons, delivery of newly synthesized RNA to the axon perfusate is strongly stimulated by axonal depolarization or agonists of glial glutamate and acetylcholine receptors. Likewise, incubation of squid optic lobe slices with [3H]uridine leads to a marked accumulation of [3H]RNA in the large synaptosomes derived from the nerve terminals of retinal photoreceptor neurons. As the cell bodies of these neurons lie outside the optic lobe, the data demonstrate that presynaptic RNA is locally synthesized, presumably by perisynaptic glial cells. Overall, our results support the view that axons and presynaptic regions are endowed with local systems of gene expression which may prove essential for the maintenance and plasticity of these extrasomatic neuronal domains.
Early electrophysiological abnormalities in lumbar motoneurons in a transgenic mouse model of amyotrophic lateral sclerosis
Authors: Bories Cyril , Amendola Julien , Lamotte d'Incamps Boris , Durand Jacques 
Published: January 2007

AbstractAmyotrophic lateral sclerosis is a lethal, adult‐onset disease characterized by progressive degeneration of motoneurons. Recent data have suggested that the disease could be linked to abnormal development of the motor nervous system. Therefore, we investigated the electrical properties of lumbar motoneurons in an in‐vitro neonatal spinal cord preparation isolated from SOD1G85R mice, which is a transgenic model of amyotrophic lateral sclerosis. The study was performed on young animals at the beginning of their second week, between postnatal days 6 and 10. Measurements of resting membrane potential and action potential characteristics of motoneurons were similar in wild‐type and SOD1G85R mice. However, the input resistance of motoneurons from transgenic mice was significantly lower than that of wild‐type animals, whereas their membrane capacitance was increased, strongly suggesting larger SOD1G85R motoneurons. Furthermore, the slope of the frequency–intensity curve was steeper in motoneurons from wild‐type pups. Interestingly, the input resistance as well as the slope of the frequency–intensity curves of other spinal neurons did not show such differences. Finally, the amplitude of dorsal root‐evoked potentials following high‐intensity stimulation was significantly smaller in SOD1G85R motoneurons. The superoxide dismutase 1 mutation thus induces specific alterations of the functional properties of motoneurons early in development.
The operant serial implicit learning task reveals early onset motor learning deficits in the HdhQ92 knock‐in mouse model of Huntington's disease
Authors: Trueman Rebecca C. , Brooks Simon P. , Jones Lesley , Dunnett Stephen B. 
Published: January 2007

AbstractA range of genetic mouse models of Huntington's disease have been created. However, as knock‐in models typically have milder phenotypes, they have frequently been overlooked as therapeutic tools in favour of the transgenic models that display severe behavioural symptoms. More sensitive tests are therefore required to reveal abnormalities and release the potential of knock‐in lines. An implicit learning task for mice has been developed in the nine‐hole operant box test apparatus, in which mice must respond to a sequence of lights in order to earn a reward. A light stimulus was presented randomly in one of five holes, to which a nose poke response resulted in the light being extinguished and a second light illuminated in a different hole. Response to the second light resulted in a liquid reward. To probe implicit learning, a predictable stimulus sequence was embedded among many unpredictable sequences. In the current study, the HdhQ92 mouse model of Huntington's disease was examined. At 4 months of age, HdhQ92/Q92 mice demonstrated clear and significant deficits in both accuracy and reaction time on all trials of the implicit learning task, with improved performance on predictable trials. We believe this to be the earliest reported behavioural deficit in the HdhQ92 knock‐in mouse line. The results of this study validate the serial implicit learning task as a sensitive tool for the examination of implicit and motor learning deficits in mutant mice, and may provide a powerful test for probing potential treatments for Huntington's disease.
Effect of neurotrophin‐3 on reinnervation of the larynx using the phrenic nerve transfer technique
Authors: Kingham Paul J. , Hughes Alexandra , Mitchard Louisa , Burt Rachel , Murison Pamela , Jones Alan , Terenghi Giorgio , Birchall Martin A. 
Published: January 2007

AbstractCurrent techniques for reinnervation of the larynx following recurrent laryngeal nerve (RLN) injury are limited by synkinesis, which prevents functional recovery. Treatment with neurotrophins (NT) may enhance nerve regeneration and encourage more accurate reinnervation. This study presents the results of using the phrenic nerve transfer method, combined with NT‐3 treatment, to selectively reinnervate the posterior cricoarytenoid (PCA) abductor muscle in a pig nerve injury model. RLN transection altered the phenotype and morphology of laryngeal muscles. In both the PCA and thyroarytenoid (TA) adductor muscle, fast type myosin heavy chain (MyHC) protein was decreased while slow type MyHC was increased. These changes were accompanied with a significant reduction in muscle fibre diameter. Following nerve repair there was a progressive normalization of MyHC phenotype and increased muscle fibre diameter in the PCA but not the TA muscle. This correlated with enhanced abductor function indicating the phrenic nerve accurately reinnervated the PCA muscle. Treatment with NT‐3 significantly enhanced phrenic nerve regeneration but led to only a small increase in the number of reinnervated PCA muscle fibres and minimal effect on abductor muscle phenotype and morphology. Therefore, work exploring other growth factors, either alone or in combination with NT‐3, is required.
A different regional response by mouse oligodendrocyte progenitor cells (OPCs) to high‐dose X‐irradiation has consequences for repopulating OPC‐depleted normal tissue
Authors: Irvine Karen‐Amanda , Blakemore William F. 
Published: January 2007

AbstractThis study was designed to investigate whether the residual, dysfunctional oligodendrocyte progenitor cells (OPCs) observed following X‐irradiation of the mouse spinal cord [D. M. Chari et al. (2003) Exp. Neurol., 198, 145–153], the presence of which prevented the endogenous repopulation of these areas from normal tissue, reflects a general response of OPCs in the mouse central nervous system (CNS) to X‐irradiation. The brains of adult mice were exposed to 40 Gy of X‐irradiation and the effect of X‐irradiation on the OPCs was assessed up to 4 weeks post‐irradiation using anti‐NG2 antibodies. X‐irradiation resulted in almost complete depletion of OPCs within the telencephalon (cortex, corpus callosum and hippocampus) by 7 days post‐irradiation, which was followed by progressive repopulation of OPCs from non‐irradiated areas of the cortex. By contrast, within the lower brain centres (the diencephalon and mesencephalon) OPC loss occurred much more slowly so that 26% of the OPCs still remained 4 weeks after X‐irradiation. The consequence of this heterogeneous response to X‐irradiation was that whereas transplanted and endogenous OPCs rapidly established themselves in the OPC‐depleted telencephalon this did not occur in the areas where there was incomplete depletion of endogenous OPCs. Our findings confirm not only the requirement for almost complete OPC depletion in order to establish transplanted OPCs in normal tissue but also highlight a heterogeneity of progenitor populations in different areas of the mouse CNS.