bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diversity of Potassium Channels Contributing to Differences in Brain Area‐specific Seizure Susceptibility: Sensitivity of Different Potassium Channels to the Epileptogenic Agent Pentylenetetrazol
Authors: Madeja Michael , Musshoff Ulrich , Speckmann Erwin‐Josef 
Published: April 2006

AbstractThe effect of the epileptogenic agent pentylenetetrazol on eight cloned voltage‐operated mammalian potassium channels (expressed in oocytes of Xenopus laevis) was investigated in order to contribute to an explanation for the brain area‐specific differences in seizure susceptibility. Pentylenetetrazol increased the potassium currents at more negative and decreased them at more positive potentials for the channels of the Kvl gene family, whereas for the other channels the currents were decreased over the whole potential range. The sensitivities of the different potassium channels to the epileptogenic agent were different. At a potential of 0 mV, for example, there were strong reductions for the Kvl.1, Kvl.4 and Kv2.1 currents, whereas the decrease was smaller for the Kvl.3 and Kvl.6 currents and was negligible for the Kvl.2, Kvl.5 and Kv3.4 currents. Correlating these data with the distribution patterns of the potassium channels in the hippocampus, the neocortex and the cerebellum (representing examples of brain areas of distinct seizure susceptibility) revealed that in brain areas with higher seizure susceptibility the overall sensitivity of the potassium channels to the epileptogenic agent is augmented. As a whole, the findings give the first evidence that the differences in distributions and properties of potassium channels contribute to differences in the seizure susceptibility of brain areas.
Arm Movement‐related Neurons in the Visual Area V6A of the Macaque Superior Parietal Lobule
Authors: Galletti C. , Fattori P. , Kutz D. F. , Battaglini P. P. 
Published: April 2006

AbstractArea V6A is a cortical visual area located in the posterior face of the superior parietal lobule in the macaque monkey. It contains visual neurons as well as neurons not activated by any kind of visual stimulation. The aim of this study was to look for possible features able to activate these latter neurons. We tested 70 non‐visual V6A neurons. Forty‐three of them showed an arm movement–related neural discharge due to somatosensory stimulation and/or skeletomotor activity of the upper limbs of the animal. The arm movement‐related neural discharge started before the onset of arm movement, often before the earliest lectromyographic activity. Thus, although the discharge is probably supported by proprioceptive and tactile inputs it is not fully dependent on them. Arm movement‐related neurons of area V6A seem to be well equipped for integrating motor signals related to arm movements with somatosensory signals evoked by those ovements. Taking into account also the visual characteristics of V6A neurons, it seems likely that area V6A as a whole is involved in the visual guiding of reaching
The Synapse Between LE Sensory Neurons and Gill Motoneurons Makes Only a Small Contribution to the Aplysia Gill‐withdrawal Reflex
Authors: Hickie Christopher , Cohen Lawrence B. , Balaban Pavel M. 
Published: April 2006

AbstractThe monosynaptic connection between the mechano‐sensory neurons in the LE cluster and gill motoneurons has been extensively studied and used as a model for the gill‐withdrawal reflex and its behavioural plasticity. In an attempt to evaluate the contribution of this synapse to the behaviour, we used voltage‐sensitive dye recording to determine the number of activated LE neurons and the number of spikes made by each neuron in response to a light touch. In five preparations, light touch activated a median of five sensory cells with a median of 1.6 spikes per cell. From a comparison of the sizes of the motoneuron synaptic potentials elicited by LE spikes and elicited by a light siphon touch, we estimate that the LE sensory neurons contribute ˜5% of the motoneuron synaptic potential in response to this touch. This result casts doubt on the validity of using this synaptic connection as a model for gill‐withdrawal behaviour. Siphon nerve recordings reveal the existence of short‐latency, low‐threshold neurons that may provide much of the sensory input in response to a light touch.
Experience‐dependent Facilitating Effect of Corticosterone on Spatial Memory Formation in the Water Maze
Authors: Sandi Carmen , Loscertales Maria , Guaza Carmen 
Published: April 2006

AbstractStress‐related adrenal steroid hormones modulate brain and cognitive function. Electrophysiological studies, including primed burst potentiation and long‐term potentiation, have indicated concentration‐dependent inverted U‐shape effects of corticosterone in hippocampal function and plasticity. Here, we explored the role of corticosterone in the consolidation and long‐term retrieval of spatial learning in the Morris water maze task in rats. We postulated that corticosterone actions might be experience‐dependent with regard to stimulus intensity, such as differential water temperatures. Indeed, rats trained at 19°C showed a quicker rate of acquisition and better long‐term retention than rats trained at 25°C water. In addition, post‐training corticosterone levels, on the first training day, were significantly higher in rats in the 19°C group than in the 25°C group. Performance of rats trained at 25°C, but not at 19°C, water was improved by injecting them i.p. with corticosterone immediately after each training session. Thus, the effect of exogenously administered corticosterone appears to be experience‐dependent, with the experience‐induced corticosterone concentrations as a critical factor determining the cognitive consequences of steroid treatment. Therefore, this work indicates a facilitating corticosterone action, during the post‐training period, on the neural mechanisms determining the strength of information storage under acute, physiological conditions.
Visual Activation in α‐Chloralose‐anaesthetized Cats Does Not Cause Lactate Accumulation in the Visual Cortex as Detected by [1HINMR Difference Spectroscopy
Authors: Kauppinen Risto A. , Eleff Scott M. , Ulatowski John A. , Kraut Michael , Soher Brian , van Zijl Peter C.M. 
Published: April 2006

AbstractThe hypothesis that neuronal activation results in lactate accumulation due to mismatch between glucose and oxygen consumption was tested in the cat model of visual activation by monitoring cerebral metabolism with localized 1H nuclear magnetic resonance spectroscopy (MRS). Adult cats were anaesthetized with α‐chloralose, paralysed and mechanically ventilated. Visual evoked potentials measured over the occipital cortex showed maximal amplitude at 2 Hz stimulation, but the latencies of the early cortical potentials, N1 and P1, were independent of stimulation frequency. High signal‐to‐noise ratio, short echo time volume‐selected [1H]MRS was used to monitor cerebral lactate with a temporal resolution of 70 s. Difference proton spectroscopy unambiguously showed no lactate peak in the visual cortex during visual activation at stimulation frequencies ranging from 1 to 16 Hz. Absence of change in lactate concentration during visual stimulation was confirmed by averaging all the spectra acquired during activation and subtracting them from reference spectra collected in darkness, a procedure that had a calculated lactate detection limit of 0.17 mM. We also reduced the O2 in the inspired air to 13%, which decreased pO2 from 94.5 ± 8.9 to 47.0 ± 6.8 mmHg, during visual stimulation at 2 or 4 Hz. At this low pO2 level, visual stimulation did not cause lactate accumulation in the visual cortex, however. The present data show that neuronal activation to this degree in the cat brain is not associated with aerobic lactate production to an extent that can be detected with 1H MRS.
Molecular and Functional Diversity at Synapses of Individual Neurons In Vitro
Authors: Staple Julie K. , Osen‐Sand Astrid , Benfenati Fabio , Pich Emilio Merlo , Catsicas Stefan 
Published: April 2006

AbstractWe have quantified activity‐dependent uptake of the fluorescent dye FM1–43 in combination with immunocytochemistry for synaptic vesicle‐associated proteins (SVPs) at individual synapses in primary cultures of rat cortical neurons. We show that expression of synaptic proteins is highly variable and that the levels of synaptophysin (p38), synapsin I and sv2, but not synapsin II, correlate with the extent of FM1–43 labelling at synapses. The data indicate that SVP levels affect the uptake of FMI‐43 with different efficacy (p38 > synapsin I > sv2 or synapsin 11). We also found that the relative levels of SVPs vary at individual boutons of single neurons grown in isolation, which indicates that differential regulation of specific SVPs may contribute to the selective modulation of activity at synapses of the same neuron.
Zinc Blocks Acetylcholine Release but not Vesicle Fusion at the Torpedo Nerve–Electroplate Junction
Authors: Parducz Arpad , Corrèges Philippe , Sors Patrick , Dunant Yves 
Published: April 2006

AbstractThe combined effects of Zn2+ treatment and nerve stimulation were studied on cholinergic synapses of the Torpedo rnarmorafa electric organ. Incubation of small pieces of electric tissue in 250 μM ZnCI2 for 2 h irreversibly blocked synaptic transmission by inhibiting the release of acetylcholine. This treatment, however, did not cause any significant fine structural alteration in the nerve‐electroplate junctions. Preparations treated with Zn2+ were submitted to electrical stimulation. In spite of the fact that no transmitter was released, stimulation resulted in the accumulation of calcium in the tissue, and in marked ultrastructural changes. The density of synaptic vesicles was significantly reduced and many of the remaining vesicles were found in close proximity to the presynaptic membrane. Images of vesicles fused with the plasmalemma were abundant, indicating that numerous vesicles were caught in different phases of exocytosis or endocytosis. Freeze‐fracture replicas made from quick‐frozen or chemically fixed material showed a high number of vesicle openings (pits) in the presynaptic plasmalemma. No recovery occurred even after a prolonged period of rest, indicating that retrieval was impaired by zinc treatment. In conclusion, the present experimental paradigm created an unusual situation where fusion of synaptic vesicles to the plasma membrane could be activated independently from the release of transmitter.
Importance of the Different |β Subunits in the Membrane Expression of the α1A and α2 Calcium Channel Subunits: Studies Using a Depolarization‐sensitive α1A Antibody
Authors: Brice N. L. , Berrow N. S. , Campbell V. , Page K. M. , Brickley K. , Tedder I. , Dolphin A. C. 
Published: April 2006

AbstractThe plasma membrane expression of the rat brain calcium channel subunits α1A, α2‐Δ and the β subunits β1b, β2a, β3b and β4 was examined by transient expression in COS‐7 cells. Neither α1A nor α2‐Δ localized to the plasma membrane, either alone or when coexpressed. However, coexpression of α1A or α2‐Δ/α1A with any of the p subunits caused α1A and α2 to be targetted to the plasma membrane. The α1A antibody is directed against an exofacial epitope at the mouth of the pore, which is not exposed unless cells are depolarized, both for native α1A channels in dorsal root ganglion neurons and for α1A expressed with a β subunit. This subsidiary result provides evidence that either channel opening or inactivation causes a conformational change at the mouth of the pore of α1A. Immunostaining for α1A was obtained in depolarized non‐permeabilized cells, indicating correct orientation in the membrane only when it was coexpressed with a subunit. In contrast, β1b and β2a were associated with the plasma membrane when expressed alone. However, this is not a prerequisite to target α1A to the membrane since β3 and β4 alone showed no differential localization, but did direct the translocation of α1A to the plasma membrane, suggesting a chaperone role for the β subunits
Gradation of Kainic Acid‐induced Rat Limbic Seizures and Expression of Hippocampal Heat Shock Protein‐70
Authors: Zhang Xia , Gelowitz Douglas L. , Lai Chien‐Tsai , Boulton Alan A. , Yu Peter H. 
Published: April 2006

AbstractSystemic injection of kainic acid (KA) induces limbic seizures in rats, which resemble human temporal lobe epilepsy, the most common form of adult human epilepsy. In this study, we have investigated KA‐elicited limbic seizures in the rats by correlating the severity of the seizure attacks with the expression of hippocampal heat shock protein‐70 (HSP70) which has been suggested to be a marker for neuronal injury/death in this model of seizures. After a systemic injection of KA, six stages of limbic seizures have been classified, namely, staring (stage 1), wet dog shake (stage 2), hyperactivity (stage 3), rearing (stage 4), rearing and falling (stage 5), and jumping (stage 6). Stages 4, 5 and 6 were further divided into mild and severe sub‐stages. HSP70 expression was not detected in animals with stages 1 and 2 seizures. At stage 3 a small amount of HSP70 immunoreactive neurons was detected in the CA3 field and the dentate hilus. From stage 4 to stage 5 the degree of HSP70 immunoreactivity increased in the CA1 field from a few positive cells in stage 4 mild to large numbers of immunoreactive neurons in stage 5 severe. HSP70 became detectable in pyramidal cells in the CA2 field from stage 5 severe and higher. In animals with stage 6 seizures, the majority of HSP70 expression became located in glial cells throughout the whole hippocampus. We concluded that HSP70 expression in the hippocampus positively correlates with the severity of KA‐elicited limbic seizures.
Sequential Role of Hippocampus and Amygdala, Entorhinal Cortex and Parietal Cortex in Formation and Retrieval of Memory for Inhibitory Avoidance in Rats
Authors: Izquierdo I. , Quillfeldt J. A. , Zanatta M. S. , Quevedo J. , Schaeffer E. , Schmitz P. K. , Medina J. H. 
Published: April 2006

AbstractThe hippocampus and amygdala, the entorhinal cortex and the parietal cortex participate, in that sequence, both in the formation and in the expression of memory for a step‐down inhibitory avoidance task in rats. Bilateral infusion of AP5 or muscimol caused retrograde amnesia when given O min after training into both hippocampus and amygdala, when given or 180 min after training into the entorhinal cortex, or when given 180 min after training into the parietal cortex. Therefore, memory formation requires the sequential and integrated activity of all these areas mediated by glutamate NMDA receptors in each case. Pre‐test administration of CNQX 1 day after training into hippocampus and amygdala, 1 or 31 days after training in entorhinal cortex, or 1, 31 or 60 days after training in the parietal cortex temporarily blocked retention test performance. Therefore, 1 day after training, all these brain structures are necessary for retrieval; 1 month later, the hippocampus and amygdala are no longer necessary for retrieval but the entorhinal and parietal cortex still are; and 60 days after training only the parietal cortex is needed. In all cases the mechanisms of retrieval require intact glutamate AMPA receptors.
Spontaneous and Repetitive Calcium Transients in C2C12 Mouse Myotubes during In Vitro Myogenesis
Authors: Lorenzon Paola , Giovannelli Aldo , Ragozzino Davide , Eusebi Fabrizio , Ruzzier Fabio 
Published: April 2006

AbstractFluorescence videomicroscopy was used to monitor changes in the cytosolic free Ca2+ concentration ([Ca2+]i in the mouse muscle cell line C2C12 during in vitro myogenesis. Three different patterns of changes in [Ca2+]i were observed: (i) [Ca2+]i oscillations; (ii) faster Ca2+ events confined to subcellular regions (localized [Ca2+]i spikes) and (iii) [Ca2+]i spikes detectable in the entire myotube (global [Ca2+]i spikes). [Ca2+]i oscillations and localized [Ca2+]i spikes were detectable following the appearance of caffeine‐sensitivity in differentiating C2C12 cells. Global [Ca2+]i spikes appeared later in the process of myogenesis in cells exhibiting coupling between voltage‐operated Ca2+ channels and ryanodine receptors. In contrast to [Ca2+]i oscillations and localized [Ca2+]i spikes, the global events immediately stopped when cells were perfused either with a Ca2+‐free solution, or a solution with TTX, TEA and verapamil. To explore further the mechanism of the global [Ca2+]i spikes, membrane currents and fluorescence signals were measured simultaneously. These experiments revealed that global [Ca2+]i spikes were correlated with an inward current. Moreover, while the depletion of the Ca2+ stores blocked [Ca2+]i oscillations and localized [Ca2]i spikes, it only reduced the amplitude of global [Ca2+]i spikes. It is suggested that, during the earlier stages of the myogenesis, spontaneous and repetitive [Ca2+]i changes may be based on cytosolic oscillatory mechanisms. The coupling between voltage‐operated Ca2+ channels and ryanodine receptors seems to be the prerequisite for the appearance of global [Ca2+]i spikes triggered by a membrane oscillatory mechanism, which characterizes the later phases of the myogenic process.
Multiple Types of Ca2+ Channels in Mouse Motor Nerve Terminals
Authors: Lin Min‐Jon , Lin‐Shiau Shoei‐Yn 
Published: April 2006

AbstractWe measured neurotransmitter release and motor nerve terminal currents in mouse phrenic nerve‐diaphragm and triangularis sterni preparations, to evaluate the role of Ca2+‐channel subtypes in regulating transmitter release. Saturated concentrations of either ωagatoxin IVA [ω‐Aga‐IVA (0.3 μM), a blocker of P‐type Ca2+channels] or ω‐conotoxin MVIIC [ω‐CTx‐MVIIC (2 μM), a P‐and Q‐type Ca2+‐channel blocker], inhibited nerve‐evoked muscle contractions and the amplitude of endplate potentials respectively. In contrast, combined treatment with nifedipine (50 μM, a blocker of L‐type Ca2+ channels) plus ω‐conotoxin GVIA [ω‐CTx‐GVIA (2 μM), a blocker of N‐type Ca2+ channels] did not elicit inhibitory effects on nerve‐evoked muscle contractions, endplate potentials or nerve terminal waveforms. Because of the non‐linear relationship between endplate potentials and Ca2+ signals, a small decrease in presynaptic Ca2+ entry can significantly reduce the amplitude of the endplate potential. Thus, we applied 3, 4‐diaminopyridine (3, 4‐DAP, a k+‐channel blocker) or high Ca2+(10 mM) to accelerate and amplify the endplate potentials and Ca2+ currents. The endplate potentials amplified by 3, 4‐DAP or by high Ca2+ correspondingly proved to be quite resistant to both ω‐Aga‐IVA and ω‐CTx‐MVIIC; ωAga‐IVA exerted only a partial inhibitory effect on endplate potentials, and the ω‐Aga‐IVA‐resistant component was further inhibited by ω‐CTx‐MVIIC. The component that was resistant to the two toxins could be completely blocked by the non‐selective Ca2+ channel blocker Cd2+ (300 μM). A combination of the two toxins had no significant effects on either spontaneous transmitter release or postsynaptic resting membrane potentials of the diaphragm preparation and the Na+ and K+ waveforms of the triangularis sterni preparations. This finding suggests a preferential inhibitory effect at a presynaptic site. Measuring the Ca2+ currents in the triangularis sterni also revealed partial inhibition by ω‐CTx‐MVIIC with further incomplete inhibition by ω‐Aga‐IVA. Cd2+ (300 μM) abolished the toxin‐resistant component of the Ca2+ current. In contrast, a combination of nifedipine (50 μM) with ω‐CTx‐GVIA (2 μM) was without inhibitory effect. We conclude that multiple types of Ca2+channels, i.e. ω‐Aga‐IVA‐sensitive, ω‐CTx‐MVIIC‐sensitive and toxin‐resistant Ca2+ channels, coexist in mouse motor nerve terminals.
Susceptibility of Cerebellar Granule Neurons Derived from Bcl‐2‐Deficient and Transgenic Mice to Cell Death
Authors: Tanabe Hiroki , Eguchi Yutaka , Kamada Shinji , Martinou Jean‐Claude , Tsujimoto Yoshihide 
Published: April 2006

AbstractOverproduced Bcl‐2 oncoprotein has been shown to suppress cell death induced by a variety of stimuli in many cell types, including neuronal cells. Because bcl‐2 is expressed in the nervous system where massive cell death is observed during development, endogenous Bcl‐2 is likely to be involved in regulating neuronal cell death. Here we examined the possible role of endogenous Bcl‐2 in the regulation of neuronal cell survival in the central nervous system using primary cultured cerebellar granule neurons from bcl‐2‐deficient, wild‐type and NSE‐bcl‐2‐ transgenic mice. Cerebellar granule neurons from bcl‐2‐deficient mice were more susceptible than those from normal littermates to death induced by reducing the K+ concentration of the medium from high (25 mM) to low (5 mM), and neurons from bcl‐2‐transgenic mice were least susceptible. Similar results were obtained when cell death was induced by serum withdrawal under high K+ conditions or by the presence of etoposide, A23187 or nimodipine. Consistently, bcl‐2 deficiency reduced the number of cerebellar granule neurons per mouse. These results indicate that Bcl‐2 impedes neuronal cell death induced by various stimuli in a dose‐dependent manner, and that endogenous levels of Bcl‐2 are able to regulate neuronal cell survival in the central nervous system.
Expression of GABAA Receptor Subunit mRNAs by Layer V Pyramidal Cells of the Rat Primary Visual Cortex
Authors: Ruano Diego , Perrais David , Rosier Jean , Ropert Nicole 
Published: April 2006

AbstractThe expression of the GABAA receptor subunit mRNAs by layer V pyramidal neurons of the primary visual cortex and cerebellar Purkinje cells was analysed by single‐cell reverse transcription of the mRNAs and amplification of the resulting cDNAs by the polymerase chain reaction. Neurons were identified by infrared Videomicroscopy, and GABAA‐mediated miniature inhibitory postsynaptic currents were recorded. In Purkinje cells, α1, β2, β3, γ2s and γ2L subunit mRNAs were detected within a single cell. In layer V pyramidal cells, a total of ten GABAA receptor subunit mRNAs could be detected, with a mean of seven subunit mRNAs per cell, suggesting GABAA receptor heterogeneity within a single pyramidal cell.
Fluorescent Dye Prelabelled Microglial Cells Migrate into Organotypic Hippocampal Slice Cultures and Ramify
Authors: Hailer Nils P. , Heppner Frank L. , Haas Dorit , Nitsch Robert 
Published: April 2006

AbstractMicroglial cells with their characteristic ramified morphology are exclusively found in healthy CNS tissue, whereas various pathologies are associated with the occurrence of amoeboid, macrophage‐like cells. It is still a matter of discussion whether amoeboid cells are blood‐derived macrophages, or whether a characteristic change in morphology, reflecting activation of previously ramified microglia, takes place. Cells in dissociated microglia culture obtained from healthy rat brains, inevitably developing this amoeboid morphology, were labelled with a fluorescent dye and transferred onto organotypic hippocampal slice cultures. Prelabelled cells with amoeboid morphology invaded these slice cultures and had, after 9 days in vitro, gradually transformed into highly ramified cells. Our findings strengthen the hypothesis that the observed amoeboid and ramified cells belong to a single population of microglia, appearing with different morphologies depending on the presence of stimuli provided by the CNS microenvironment. Microglial cells obviously appear in different shapes and can switch from immunologically resting to activated modes and vice versa.