bluuebunny/crossref_metadata_2025_split huggingface dataset:
Horizontal Cells in the Monkey Retina: Cone connections and dendritic network
Authors: Wässle H. , Boycott B. B. , Röhrenbeck J. 
Published: April 2006

AbstractHorizontal cells of the macaque monkey retina were quantified and the number of cones converging onto an individual horizontal cell as well as the number of horizontal cells contacting a single cone were determined. This was done by combining data from individual horizontal cells stained by the Golgi method with the results of immunocytochemical staining described in the preceding paper (Röhrenbeck et al., 1989).The observation (Boycott et al., 1987) that all horizontal cells contact all cones in their dendritic field irrespective of cone type was confirmed. The particular cones contacted by the terminal aggregates of each horizontal cell were found. The dendritic fields of H1 and H2 cells increase with increasing eccentricity; close to the fovea H1 cells are smaller than H2 cells, at 6 mm eccentricity they are about the same size and in peripheral retina H1 cells are much larger than H2 cells. The density gradients of the two cell types balance their denritic field changes so that throughout the retina each and every cone synapses with 3–5 horizontal cells of each type. Horizontal cells of both cat (Wässle et al., 1978) and monkey retina follow the general rule that all cones in the dendritic fields are contacted, their perikarya form a regular mosaic and the boundaries of their dendritic fields are marked by the perikarya of their homologous neighbours.
Membrane Characteristics and Synaptic Responsiveness of Superficial Dorsal Horn Neurons in a Slice Preparation of Adult Rat Spinal Cord
Authors: Thomson Alex M. , West David C. , Headley P. Max 
Published: April 2006

AbstractIntracellular recordings have been made from neurons of the superficial dorsal horn in slices of the lumbar and thoracic spinal cord of young adult rats. Three broad categories of neurons could be distinguished on the basis of their firing patterns to intracellular current pulses and their afterhyperpolarizations (AHP); there was no detectable difference in the regional distribution of the three types. Category 1 cells were characterized by maintained firing to intracellular depolarizing current pulses, brief action potential durations and polyphasic AHPs. Category 2 cells showed spike adaptation, without spike attenuation, during intracellular current pulses, and had monophasic AHPs. Category 3 cells fired only 1 or 2 spikes to maintained depolarizing pulses and had smaller monophasic AHPs than category 2 neurons. Spontaneous excitatory and inhibitory postsynaptic potential (epsp and ipsp) activity was seen with psp durations varying widely. Low intensity electrical stimulation of afferent fibres, or of superficial white matter, resulted in polyphasic epsps and/or ipsps. The spike discharge in response to such afferent inputs correlated with the membrane properties of the cells, such that the synaptic responses of category 1 neurons were usually bursts of spikes, whereas category 2 and 3 neurons either failed to fire or fired only a single spike. These results in adult rat spinal cord suggest that the discharge pattern within synaptic sensory responses of superficial dorsal horn neurons is determined by postsynaptic membrane properties as well as by the pattern of the afferent input.
The Functional Organization of the Olivo‐Cerebellar System as Examined by Multiple Purkinje Cell Recordings
Authors: Llinás R. , Sasaki K. 
Published: April 2006

AbstractMultiple recordings from Purkinje cells in the rat cerebellum allowed the mechanism responsible for the activation of rows of synchronous complex spikes to be investigated. By determining the spatial distribution of the climbing fibre reflex that follows electrical microstimulation of the cerebellar cortex, it was shown that the mechanism for the simultaneity of firing was the electrotonic interactions between neurons in the inferior olive (IO). The spatial organization of the complex spike activity was shown to be regulated by GABAergic inhibitory input into the IO, probably arising from the cerebellar nuclear neurons. The rostro‐caudal organizion of the complex spike activity following physiological stimulation (tactile stimulation of the upper and lower lip) demonstrated the same spatial distribution of synchronous activity in the cerebellar cortex as did the spontaneous activity and this was also disrupted by GABA blockers. Finally, complex spike responses to physiological stimulation indicate that the IO is capable of gating sensory inputs in accordance with its intrinsic autorhythmicity and that strong peripheral stimuli reset the oscillatory properties of the IO. The functional implications of the synchronicity and of the temporo‐spatial organizion of complex spikes in the cerebellar cortex are discussed in the context of motor coordination and timing.
17‐β Oestradiol Pretreatment of Mouse Striatal Neurons in Culture Enhances the Responses of Adenylate Cyclase Sensitive to Biogenic Amines
Authors: Maus M. , Cordier J. , Glowinski J. , Premont J. 
Published: April 2006

AbstractEmbryonic striatal neurons from the mouse grown in primary culture (6 day old culture) were used in order to investigate the effects of 17‐β oestradiol (17‐β E2) on biogenic amine‐sensitive adenylate cyclases. Pretreatment (28 h) of intact cells with 17‐β E2 (10−9 M) enhanced cyclic AMP production induced by either dopamine, isoproterenol, serotonin, or 2‐chloro‐adenosine (maximal effective concentrations). These effects of 17‐β E2 on biogenic amine‐sensitive adenylate cyclases occurred after several hours (8 h at least) and were seen in most cases with a concentration as low as 10−11 M (EC50: 10−10 M). They were additive with those induced by phenol red (5.6 μg/l) and chemically specific since 17α‐oestradiol, 2(OH) 17‐β E2, progesterone, and dexamethasone were without effect. In addition, they were not seen in cells which had been pretreated (30 h) with cycloheximide or α‐amanitin, suggesting an involvement of de novo protein synthesis. Since 17‐β E2 did not influence cyclic AMP production induced by either forskolin or manganese ions, the stimulatory effects of 17‐β E2 pretreatment on biogenic amine‐sensitive adenylate cyclases were not linked to an increase in the amount of enzyme catalytic units. 17‐β E2 pretreatment enhanced twofold the number of β‐adrenergic receptors (as estimated by the specific binding of (125l)iodocyanopindolol) but did not, in contrast, affect either the number or the affinity of dopaminergic receptors (as estimated by (125l)SCH 23982 binding). Therefore, the enhancing effects of 17‐β E2 pretreatment on biogenic amine‐sensitive adenylate cyclases could be related either to an increased number of coupled receptors or to modifications of the adenylate cyclase transducing system (occurring probably at the G‐protein level) or to a combination of the two.
Host Corticostriatal Fibres Establish Synaptic Connections with Grafted Striatal Neurons in the Ibotenic Acid Lesioned Striatum
Authors: Wictorin K. , Clarke D. J. , Bolam J. P. , Björklund A. 
Published: April 2006

AbstractThe connections between host corticostriatal afferents and neurons in intrastriatal grafts of foetal striatal tissue have been studied with electron microscopic immunocytochemistry using Phaseolus vulgaris leucoagglutinin (PHA‐L) as a label of the host corticostriatal fibres. Adult rats with unilateral ibotenic acid lesions of the head of the caudate putamen received foetal cell suspension grafts from E14–15 rat embryos into the lesioned striatal area. Ten months after transplantation, multiple iontophoretic injections of PHA‐L were made into the host frontal cortex. These injections labelled large numbers of corticostriatal fibres which extended across the graft ‐ host border to form a rich axonal network mainly in the peripheral portions of the grafts. At the ultrastructural level a total of 134 PHA‐L‐labelled terminals were identified to form asymmetric synaptic contacts with neurons within the grafts. Of these contacts, 83% were in contact with dendritic spines, 12% with dendritic shafts, and 5% with small shafts or spines. The synaptic contacts were similar to those identified in intact regions of the host striatum that were spared by the lesion. However, the synapses in the host striatum were almost exclusively in contact with spines (98%). These results demonstrate that the corticostriatal projection, which constitutes a major source of afferent control in the normal striatum, not only extends axons into the intrastriatal striatal grafts, but also establishes synaptic connections with the implanted neuronal elements.
Intracellular Calcium and Control of Burst Generation in Neurons of Guinea‐Pig Neocortex in Vitro
Authors: Friedman A. , Gutnick M. J. 
Published: April 2006

AbstractResponse properties of neurons in brain slices of guinea pig parietal neocortex were examined following intracellular injection of the Ca2+ chelators, EGTA and BAPTA. Although chelator injection did not cause any consistent change in passive membrane properties, it did induce 81% of neurons encountered at all sub‐pial depths to become ‘bursters’, in that just‐threshold depolarizing current pulses triggered all‐or‐none bursts of 2–5 fast action potentials. Transition to ‘burstiness’ was associated with disappearance of an AHP and appearance of a DAP. Although chelator caused a slight increase in steady‐state firing rate, marked accommodation persisted. Extracellular Co2+ or Mn2+ had an effect on steady‐state firing rate similar to that of the intracellular chelators; however, exposure to these Ca2+ channel blockers also caused steady state depolarization, increased resting input resistance and time constant, and profound spike broadening. This treatment never induced transition to ‘burstiness’. Chelator‐injected neurons ceased to generate bursts when Ca2+ was replaced by Mn2+ in the Ringer's solution. During exposure to 10−6 M TTX and 20 mM TEA, 50–200 msec Ca2+ spikes followed brief depolarizing pulses. As chelator was injected into the cell, there was progressive prolongation of the Ca2+ plateaus, which was associated with slowing of the rate at which membrane resistance gradually recovered following the initial increase in conductance.These findings indicate that under normal conditions, activity‐related increases in intracellular Ca2+ activate processes which prevent most neocortical neurons from being bursters. These processes probably include Ca2+ ‐dependent K+ currents, and Ca2+ ‐dependent Ca2+ channel inactivation.
The role of the medial caudate nucleus, but not the hippocampus, in a matching‐to sample task for a motor response
Authors: Kesner Raymond P. , Gilbert Paul E. 
Published: April 2006

AbstractA delayed‐match‐to‐sample task was used to assess memory for motor responses in rats with control, hippocampus, or medial caudate nucleus (MCN) lesions. All testing was conducted on a cheeseboard maze in complete darkness using an infrared camera. A start box was positioned in the centre of the maze facing a randomly determined direction on each trial. On the sample phase, a phosphorescent object was randomly positioned to cover a baited food well in one of five equally spaced positions around the circumference of the maze forming a 180‐degree arc 60 cm from the box. The rat had to displace the object to receive food and return to the start box. The box was then rotated to face a different direction. An identical baited phosphorescent object was placed in the same position relative to the start box. A second identical object was positioned to cover a different unbaited well. On the choice phase, the rat must remember the motor response made on the sample phase and make the same motor response on the choice phase to receive a reward. Hippocampus lesioned and control rats improved as a function of increased angle separation used to separate the correct object from the foil (45, 90, 135, and 180 degrees) and matched the performance of controls. However, rats with MCN lesions were impaired across all separations. Results suggest that the MCN, but not the hippocampus, supports working memory and/or a process aimed at reducing interference for motor response selection based on vector angle information.
The essential haematopoietic transcription factor Scl is also critical for neuronal development
Authors: Bradley Cara K. , Takano Elena A. , Hall Mark A. , Göthert Joachim R. , Harvey Alan R. , Begley C. Glenn , van Eekelen J. Anke M. 
Published: April 2006

AbstractThe basic helix‐loop‐helix (bHLH) transcription factor Scl displays tissue‐restricted expression and is critical for the establishment of the haematopoietic system; loss of Scl results in embryonic death due to absolute anaemia. Scl is also expressed in neurons of the mouse diencephalon, mesencephalon and metencephalon; however, its requirement in those sites remains to be determined. Here we report conditional deletion of Scl in neuronal precursor cells using the Cre/LoxP system. Neuronal‐Scl deleted mice died prematurely, were growth retarded and exhibited an altered motor phenotype characterized by hyperactivity and circling. Moreover, ablation of Scl in the nervous system affected brain morphology with abnormal neuronal development in brain regions known to express Scl under normal circumstances; there was an almost complete absence of Scl‐null neurons in the hindbrain and partial loss of Scl‐null neurons in the thalamus and midbrain from early neurogenesis onwards. Our results demonstrate a crucial role for Scl in the development of Scl‐expressing neurons, including γ‐aminobutyric acid (GABA)ergic interneurons. Our study represents one of the first demonstrations of functional overlap of a single bHLH protein that regulates neural and haematopoietic cell development. This finding underlines Scl's critical function in cell fate determination of mesodermal as well as neuroectodermal tissues.
Tight covariation of BOLD signal changes and slow ERPs in the parietal cortex in a parametric spatial imagery task with haptic acquisition
Authors: Schicke Tobias , Muckli Lars , Beer Anton L. , Wibral Michael , Singer Wolf , Goebel Rainer , Rösler Frank , Röder Brigitte 
Published: April 2006

AbstractThe present study investigated the relation of brain activity patterns measured with functional magnetic resonance imaging (fMRI) and slow event‐related potentials (ERPs) associated with a complex cognitive task. A second goal was to examine the neural correlates of spatial imagery of haptically – instead of visually – acquired representations. Using a mental image scanning task, spatial imagery requirements were systematically manipulated by parametrically varying the distance between haptically acquired landmarks. Results showed a close relation between slow ERPs and the blood oxygenation level dependent (BOLD) signal in human parietal lobe. Reaction times of mental scanning correlated with the distances between landmarks on the learned display. In parallel, duration and amplitude of slow ERPs and duration of the haemodynamic response systematically varied as a function of mental scanning distance. Source analysis confirmed that the ERP imagery effect likely originated from the same cortical substrate as the corresponding BOLD effect. This covariation of the BOLD signal with slow ERPs is in line with recent findings in animals demonstrating a tight link between local field potentials and the BOLD signal. The parietal location of the imagery effect is consistent with the idea that externally triggered (perceptual) and mentally driven (imagery) spatial processes are both mediated by the same supramodal brain areas.
Nitric oxide impairs mitochondrial movement in cortical neurons during hypoxia
Authors: Zanelli Santina A. , Trimmer Patricia A. , Solenski Nina J. 
Published: April 2006

AbstractCortical nitric oxide (NO) production increases during hypoxia/ischemia in the immature brain and is associated with both neurotoxicity and mitochondrial dysfunction. Mitochondrial redistribution within the cell is critical to normal neuronal function, however, the effects of hypoxia on mitochondrial dynamics are not known. This study tested the hypothesis that hypoxia impairs mitochondrial movement via NO‐mediated pathways. Fluorescently labeled mitochondria were studied using time‐lapse digital video microscopy in cultured cortical neurons exposed either to hypoxia/re‐oxygenation or to diethyleneamine/nitric oxide adduct, DETA‐NO (100–500 µm). Two NO synthase inhibitors, were used to determine NO specificity. Mitochondrial mean velocity, the percentage of movement (i.e. the time spent moving) and mitochondrial morphology were analyzed. Exposure to hypoxia reduced mitochondrial movement to 10.4 ± 1.3% at 0 h and 7.4 ± 1.7% at 1 h of re‐oxygenation, versus 25.6 ± 1.4% in controls (p < 0.05). Mean mitochondrial velocity (µm s−1) decreased from 0.374 ± 0.01 in controls to 0.146 ± 0.01 at 0 h and 0.177 ± 0.02 at 1 h of re‐oxygenation (p < 0.001). Exposure to DETA‐NO resulted in a significant decrease in mean mitochondrial velocity at all tested time points. Treatment with NG‐nitro‐l‐arginine methyl ester (l‐NAME) prevented the hypoxia‐induced decrease in mitochondrial movement at 0 h (30.1 ± 1.6%) and at 1 h (26.1 ± 9%) of re‐oxygenation. Exposure to either hypoxia/re‐oxygenation or NO also resulted in the rapid decrease in mitochondrial size. Both hypoxia and NO exposure result in impaired mitochondrial movement and morphology in cultured cortical neurons. As the effect of hypoxia on mitochondrial movement and morphology can be partially prevented by a nitric oxide synthase (NOS) inhibitor, these data suggest that an NO‐mediated pathway is at least partially involved.
Pseudophosphorylation of tau at serine 422 inhibits caspase cleavage: in vitro evidence and implications for tangle formation in vivo
Authors: Guillozet‐Bongaarts Angela L. , Cahill Michael E. , Cryns Vincent L. , Reynolds Matthew R. , Berry Robert W. , Binder Lester I. 
Published: April 2006

AbstractThe tangles of Alzheimer's disease (AD) are comprised of the tau protein displaying numerous alterations, including phosphorylation at serine 422 (S422) and truncation at aspartic acid 421 (D421). Truncation at the latter site appears to result from activation of caspases, a class of proteases that cleave specifically at aspartic acid residues. It has been proposed that phosphorylation at or near caspase cleavage sites could regulate the ability of the protease to cleave at those sites. Here, we use tau pseudophosphorylated at S422 (S422E) to examine the effects of tau phosphorylation on its cleavage by caspase 3. We find that S422E tau is more resistant to proteolysis by caspase 3 than non‐pseudophosphorylated tau. Additionally, we use antibodies directed against the phosphorylation site and against the truncation epitope to assess the presence of these epitopes in neurofibrillary tangles in the aged human brain. We show that phosphorylation precedes truncation during tangle maturation. Moreover, the distribution of the two epitopes suggests that a significant length of time (perhaps as much as two decades) elapses between S422 phosphorylation and cleavage at D421. We further conclude that tau phosphorylation at S422 may be a protective mechanism that inhibits cleavage in vivo.
Apolipoprotein A‐I increases association of cytosolic cholesterol and caveolin‐1 with microtubule cytoskeletons in rat astrocytes
Authors: Ito Jin‐ichi , Kheirollah Alireza , Nagayasu Yuko , Lu Rui , Kato Koichi , Yokoyama Shinji 
Published: April 2006

AbstractApolipoprotein (apo) A‐I induces rapid translocation of protein kinase Cα and phospholipase Cγ, and slow translocation of caveolin‐1 and newly synthesized cholesterol to the cytosolic lipid‐protein particle (CLPP) fraction in rat astrocytes. In order to understand the function of CLPP, we investigated the interaction with cytoskeletons of CLPP‐related proteins such as caveolin‐1 and protein kinase Cα and of CLPP‐related lipids in rat astrocytes. Under the conditions that microtubules were depolymerized, association of cytosolic caveolin‐1 with protein kinase Cα and α‐tubulin was enhanced when the cells were treated with apoA‐I for 5 min. This association was suppressed by a scaffolding domain‐peptide of caveolin‐1. Association with the microtubule‐like filaments of cytosolic lipids, caveolin‐1 and protein kinase Cα was also increased by the apoA‐I treatment and inhibited by the scaffolding domain peptide. Paclitaxel (taxol), a compound to stabilize microtubules, suppressed the apoA‐I‐mediated intracellular translocation and release from the cells of the de novo synthesized cholesterol and phospholipid. The findings suggested that the association of CLPP with microtubules is mediated by a scaffolding domain of caveolin‐1, induced by apoA‐I and involved in regulation of intracellular cholesterol trafficking for assembly of cellular lipids to apoA‐I–high‐density lipoprotein (HDL).
Direct interaction of post‐synaptic density‐95/Dlg/ZO‐1 domain‐containing synaptic molecule Shank3 with GluR1 α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid receptor
Authors: Uchino Shigeo , Wada Hidenori , Honda Shizuyo , Nakamura Yasuko , Ondo Yumiko , Uchiyama Takayoshi , Tsutsumi Moe , Suzuki Eri , Hirasawa Takae , Kohsaka Shinichi 
Published: April 2006

AbstractA class of scaffolding protein containing the post‐synaptic density‐95/Dlg/ZO‐1 (PDZ) domain is thought to be involved in synaptic trafficking of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA) receptors during development. To clarify the molecular mechanism of AMPA receptor trafficking, we performed a yeast two‐hybrid screening system using the cytoplasmic tail of the GluR1 subunit of AMPA receptor as a bait and identified a synaptic molecule, Shank3/ProSAP2, as a GluR1 subunit‐interacting molecule. Shank3 is a PDZ domain‐containing multidomain protein and is predominantly expressed in developing neurons. Using the glutathione S‐transferase pull‐down assay and immunoprecipitation technique we demonstrated that the GluR1 subunit directly binds to the PDZ domain of Shank3 via its carboxyl terminal PDZ‐binding motif. We raised anti‐Shank3 antibody to investigate the expression of Shank3 in cortical neurons. The pattern of Shank3 immunoreactivity was strikingly punctate, mainly observed in the spines, and closely matched the pattern of post‐synaptic density‐95 immunoreactivity, indicating that Shank3 is colocalized with post‐synaptic density‐95 in the same spines. When Shank3 and the GluR1 subunit were overexpressed in primary cortical neurons, they were also colocalized in the spines. Taken together with the biochemical interaction of Shank3 with the GluR1 subunit, these results suggest that Shank3 is an important molecule that interacts with GluR1 AMPA receptor at synaptic sites of developing neurons.
Laser treatment for pigmented lesions: a review
Authors: Jones Christina E. , Nouri Keyvan 
Published: April 2006

SummaryBackground  Just a few decades ago, before lasers were introduced into dermatologic practice, many cutaneous lesions were untreatable. Since the introduction of lasers in dermatology in the 1960s and its revolution by Anderson and Parrish in the 1980s based on the selective photothermolysis theory, lasers have become a main component of many dermatology practices. With the advent of these selective lasers and their constant technological advancements, many lesions can now be easily removed with a low incidence of complications, creating a high demand for laser surgery.Aims  This paper will review current laser systems used for pigmented lesions.Methods  An English‐language literature search and review through Medline from January 1994 to October 2004. Review of the latest techniques and lasers used in treating pigmentary disorders and possible future applications and treatment options.Conclusions  Laser technique and technology has greatly advanced producing more effacious treatment with minimal complications.