bluuebunny/crossref_metadata_2025_split huggingface dataset:
Direction Tuning of Individual Retinal Inputs to the Turtle Accessory Optic System
Authors: Kogo Naoki , Rubio Doris McGartland , Ariel Michael 
Published: April 2018

Neurons in turtle accessory optic system [basal optic nucleus (BON)] were recorded to study convergence of retinal afferents, using whole-cell patch electrodes in a reducedin vitrobrainstem preparation with the eyes attached. BON cells primarily exhibit EPSPs from a contralateral retinal ganglion cell input and generate an output of action potentials. Visual responses were evoked by different directions of either full-field or local moving patterns. Direction tuning of action potentials was compared with that of EPSPs detected by passing the membrane voltage through an AC amplifier and window discriminator. This rough measure of retinal input indicated that the direction tuning of the full-field excitatory input from the retina matched that of the spike output for the same BON cell.Using local patterns within the receptive fields of the BON cells, it was estimated that one to four adjacent retinal inputs were being stimulated. The direction tuning of these inputs had preferred directions that were similar to that of the full-field spike output of the cell, irrespective of where the small window was placed within the receptive field. Because more than one retinal input may have been stimulated by the small stimulus window, subsets of those EPSPs that may represent responses of a single retinal afferent were identified based on their amplitude and rise time. Again, the preferred direction of those putative single retinal afferents matched the direction tuning of the spike output of the BON cell. These findings are discussed in terms of the formation of the retinal slip signal by the BON.
Zinc-Induced Cortical Neuronal Death: Contribution of Energy Failure Attributable to Loss of NAD+and Inhibition of Glycolysis
Authors: Sheline Christian T. , Behrens M. Margarita , Choi Dennis W. 
Published: April 2018

Excessive zinc influx may contribute to neuronal death after certain insults, including transient global ischemia. In light of evidence that levels of intracellular free Zn2+associated with neurotoxicity may be sufficient to inhibit glyceraldehyde-3-phosphate dehydrogenase (GAPDH), experiments were performed looking for reduced glycolysis and energy failure in cultured mouse cortical neurons subjected to lethal Zn2+exposure. As predicted, cultures exposed for 3–22 hr to 40 μmZn2+developed an early increase in levels of dihydroxy-acetone phosphate (DHAP) and fructose 1,6-bisphosphate (FBP) and a progressive loss of ATP levels, followed by neuronal cell death; furthermore, addition of the downstream glycolytic substrate pyruvate to the bathing medium attenuated the fall in ATP and neuronal death.However, an alternative to direct Zn2+inhibition of GAPDH was raised by the observation that Zn2+exposure also induced an early decrease in nicotinamide-adenine dinucleotide (NAD+) levels, an event itself capable of inhibiting GAPDH. Favoring this indirect mechanism of GAPDH inhibition, the neuroprotective effects of pyruvate addition were associated with normalization of cellular levels of NAD+, DHAP, and FBP. Zn2+-induced neuronal death was also attenuated by addition of the energy substrate oxaloacetate, the activator of pyruvate dehydrogenase, dichloroacetate, or the inhibitors of NAD+catabolism, niacinamide or benzamide. Acetyl carnitine, α-keto butyrate, lactate, and β-hydroxy-butyrate did not attenuate Zn2+-induced neurotoxicity, perhaps because they could not regenerate NAD+or be used for energy production in the presence of glucose.
Novel Hippocampal Interneuronal Subtypes Identified Using Transgenic Mice That Express Green Fluorescent Protein in GABAergic Interneurons
Authors: Oliva Anthony A. , Jiang Minghui , Lam Trang , Smith Karen L. , Swann John W. 
Published: April 2018

The chief inhibitory neurons of the mammalian brain, GABAergic neurons, are comprised of a myriad of diverse neuronal subtypes. To facilitate the study of these neurons, transgenic mice were generated that express enhanced green fluorescent protein (EGFP) in subpopulations of GABAergic neurons. In one of the resulting transgenic lines, called GIN (GFP-expressingInhibitoryNeurons), EGFP was found to be expressed in a subpopulation of somatostatin-containing GABAergic interneurons in the hippocampus and neocortex. In both live and fixed brain preparations from these mice, detailed microanatomical features of EGFP-expressing interneurons were readily observed. In stratum oriens of the hippocampus, EGFP-expressing interneurons were comprised almost exclusively of oriens/alveus interneurons with lacunosum-moleculare axon arborization (O-LM cells). In the neocortex, the somata of EGFP-expressing interneurons were largely restricted to layers II-IV and upper layer V.In hippocampal area CA1, two previously uncharacterized subtypes of interneurons were identified using the GIN mice: stratum pyramidale interneurons with lacunosum-moleculare axon arborization (P-LM cells) and stratum radiatum interneurons with lacunosum-moleculare axon arborization (R-LM cells). These newly identified interneuronal subtypes appeared to be closely related to O-LM cell, as they selectively innervate stratum lacunosum-moleculare. Whole-cell patch-clamp recordings revealed that these cells were fast-spiking and showed virtually no spike frequency accommodation. The microanatomical features of these cells suggest that they function primarily as “input-biasing” neurons, in that synaptic volleys in stratum radiatum would lead to their activation, which in turn would result in selective suppression of excitatory input from the entorhinal cortex onto CA1 pyramidal cells.
Extraretinal Control of Saccadic Suppression
Authors: Diamond Mark R. , Ross John , Morrone M. C. 
Published: April 2018

We measured the time course of saccadic suppression and tested whether suppression results entirely from retinal image motion or has an extraretinal source. We measured contrast thresholds for low-frequency gratings modulated either in luminance, at 17 cd/m2and 0.17 cd/m2, or color at 17 cd/m2. Gratings were flashed on a uniform background before, during, or after voluntary 12° saccades and, additionally in the case of luminance modulated gratings, saccades simulated by mirror motion.A 10-fold decrease in contrast sensitivity was found for luminance-modulated gratings with saccades, but little suppression was found with simulated saccades. Adding high-contrast noise to the display increased the magnitude and the duration of the suppression during simulated saccades but had little effect on suppression produced by real saccades.Suppression anticipates saccades by 50 msec, is maximal at the moment of saccadic onset, and outlasts saccades by ∼50 msec. At lower luminance, suppression is reduced, and its course is shallower than at higher luminance.Simulated saccades produce shallower suppression over a longer time course at both luminances. No suppression was found for chromatically modulated gratings.Differences between real and simulated saccades in the magnitude and time course of sensitivity loss suggest that saccadic suppression has an extraretinal component.We model the effects of saccades by adding a signal to the visual input, so as to saturate the nonlinear stage of visual processing and make detection of a test stimulus more difficult.
The “Waiting Period” of Sensory and Motor Axons in Early Chick Hindlimb: Its Role in Axon Pathfinding and Neuronal Maturation
Authors: Wang Guoying , Scott Sheryl A. 
Published: April 2018

During embryonic development motor axons in the chick hindlimb grow out slightly before sensory axons and wait in the plexus region at the base of the limb for ∼24 hr before invading the limb itself (Tosney and Landmesser, 1985a). We have investigated the role of this waiting period by asking, Is the arrest of growth cones in the plexus region a general property of both sensory and motor axons? Why do axons wait? Does eliminating the waiting period affect the further development of motor and sensory neurons?Here we show that sensory axons, like motor axons, pause in the plexus region and that neither sensory nor motor axons require cues from the other population to wait in or exit from the plexus region. By transplanting older or younger donor limbs to host embryos, we show that host axons innervate donor limbs on a schedule consistent with the age of the grafted limbs. Thus, axons wait in the plexus region for maturational changes to occur in the limb rather than in the neurons themselves. Both sensory and motor axons innervate their appropriate peripheral targets when the waiting period is eliminated by grafting older donor limbs. Therefore, axons do not require a prolonged period in the plexus region to sort out and project appropriately. Eliminating the waiting period does, however, accelerate the onset of naturally occurring cell death, but it does not enhance the development of central projections or the biochemical maturation of sensory neurons.
Interaction between Metabotropic and Ionotropic Glutamate Receptors Regulates Neuronal Network Activity
Authors: Krieger Patrik , Hellgren-Kotaleski Jeanette , Kettunen Petronella , El Manira Abdel Jabbar 
Published: April 2018

Experimental and computational techniques have been used to investigate the group I metabotropic glutamate receptor (mGluR)-mediated increase in the frequency of spinal cord network activity underlying locomotion in the lamprey. Group I mGluR activation potentiated the amplitude of NMDA-induced currents in identified motoneurons and crossed caudally projecting network interneurons. Group I mGluRs also potentiated NMDA-induced calcium responses. This effect was blocked by a group I mGluR-specific antagonist, but not by blockers of protein kinase A, C, or G. The effect of group I mGluRs activation was also tested on NMDA-induced oscillations known to occur during fictive locomotion. Activation of these receptors increased the duration of the plateau phase and decreased the duration of the hyperpolarizing phase. These effects were blocked by a group I mGluR antagonist. To determine its role in the modulation of NMDA-induced oscillations and the locomotor burst frequency, the potentiation of NMDA receptors by mGluRs was simulated using computational techniques. Simulating the interaction between these receptors reproduced the modulation of the plateau and hyperpolarized phases of NMDA-induced oscillations, and the increase in the frequency of the locomotor rhythm.Our results thus show a postsynaptic interaction between group I mGluRs and NMDA receptors in lamprey spinal cord neurons, which can account for the regulation of the locomotor network output by mGluRs.
Evidence for Spatial Modules Mediated by Temporal Synchronization of Carbachol-Induced Gamma Rhythm in Medial Entorhinal Cortex
Authors: Dickson Clayton T. , Biella Gerardo , de Curtis Marco 
Published: April 2018

Fast (γ) oscillations in the cortex underlie the rapid temporal coordination of large-scale neuronal assemblies in the processing of sensory stimuli. Cortical γ rhythm is modulatedin vivoby cholinergic innervation from the basal forebrain and can be generatedin vitroafter exogenous cholinergic stimulation. Using the isolated guinea pig brain, anin vitropreparation that allows for the study of an intact cerebrum, we studied the spatial features of γ activity evoked by the cholinomimetic carbachol (CCh) in the medial entorhinal cortex (mEC). γ activity induced by either arterial perfusion or intraparenchymal application of CCh showed a phase reversal across mEC layer II and was reduced or abolished in a spatially localized region by focal infusions of atropine, bicuculline, and CNQX. In addition, a spatially restricted zone of γ activity could be induced by passive diffusion of CCh from a recording pipette. Finally, γ oscillations recorded at multiple sites across the surface of the mEC using array electrodes during arterial perfusion of CCh demonstrated a decline in synchronization (coherence) as the interelectrode distance increased. This effect was independent of the signal amplitude and was specific for γ as opposed to theta-like activity induced by CCh in the same experiments.These results suggest that CCh-induced γ oscillations in the mEC are mediated through direct muscarinic excitation of a highly localized reciprocal inhibitory–excitatory network located in superficial layers. We propose that functional cortical modules of highly synchronous γ oscillations may organize incoming (cortical) and outgoing (hippocampal) information in the mEC.
Neuronal Activity and Brain-Derived Neurotrophic Factor Regulate the Density of Inhibitory Synapses in Organotypic Slice Cultures of Postnatal Hippocampus
Authors: Marty Serge , Wehrlé Rosine , Sotelo Constantino 
Published: April 2018

Hippocampal interneurons inhibit pyramidal neurons through the release of the neurotransmitter GABA. Given the importance of this inhibition for the proper functioning of the hippocampus, the development of inhibitory synapses must be tightly regulated. In this study, the possibility that neuronal activity and neurotrophins regulate the density of GABAergic inhibitory synapses was investigated in organotypic slice cultures taken from postnatal day 7 rats.In hippocampal slices cultured for 13 d in the presence of the GABAAreceptor antagonist bicuculline, the density of glutamic acid decarboxylase (GAD) 65-immunoreactive terminals was increased in the CA1 area when compared with control slices. Treatment with the glutamate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione decreased the density of GAD65-immunoreactive terminals in the stratum oriens of CA1. These treatments had parallel effects on the density of GABA-immunoreactive processes. Electron microscopic analysis after postembedding immunogold labeling with antibodies against GABA indicated that bicuculline treatment increased the density of inhibitory but not excitatory synapses. Application of exogenous BDNF partly mimicked the stimulatory effect of bicuculline on GAD65-immunoreactive terminals. Finally, antibodies against BDNF, but not antibodies against nerve growth factor, decrease the density of GAD65-immunoreactive terminals in bicuculline-treated slices.Thus, neuronal activity regulates the density of inhibitory synapses made by postnatal hippocampal interneurons, and BDNF could mediate part of this regulation. This regulation of the density of inhibitory synapses could represent a feedback mechanism aimed at maintaining an appropriate level of activity in the developing hippocampal networks.
Interleukin-1β-Induced Changes in Blood–Brain Barrier Permeability, Apparent Diffusion Coefficient, and Cerebral Blood Volume in the Rat Brain: A Magnetic Resonance Study
Authors: Blamire A. M. , Anthony D. C. , Rajagopalan B. , Sibson N. R. , Perry V. H. , Styles P. 
Published: April 2018

The cytokine interleukin-1β (IL-1β) is implicated in a broad spectrum of CNS pathologies, in which it is thought to exacerbate neuronal loss. Here, the effects of injecting recombinant rat IL-1β into the striatum of 3-week-old rats were followed noninvasively from 2 to 123 hr using magnetic resonance imaging and spectroscopy. Four hours after injection of IL-1β (1 ng in 1 μl), cerebral blood volume was significantly increased, the blood–brain barrier (BBB) became permeable to intravenously administered contrast agent between 4.5 and 5 hr, and the apparent diffusion coefficient (ADC) of brain water fell by 6 hr (5.42 ± 0.35 × 10−4mm2/sec treated, 7.35 ± 0.77 × 10−4mm2/sec control;p< 0.001). At 24 hr the BBB was again intact, but the ADC, although partially recovered, remained depressed at both 24 and 123 hr (p< 0.03). Depleting the animals of neutrophils before IL-1β injection prevented the BBB permeability at all time points, but the ADC was still depressed at 6 hr (6.64 ± 0.34 × 10−4mm2/sec treated, 7.49 ± 0.38 × 10−4mm2/sec control;p< 0.005). No changes were seen in brain metabolites using proton spectroscopy at 6 hr after IL-1β.Intraparenchymal injection of IL-1β caused a neutrophil-dependent transient increase in BBB permeability. The presence of neutrophils within the brain parenchyma significantly contributed to the IL-1β-induced changes in cerebral blood volume and the ADC of brain water. However, IL-1β apparently had a direct effect on the resident cell populations, which persisted well after all recruited leukocytes had disappeared. Thus the action of IL-1β alone can give rise to magnetic resonance imaging-visible changes that are normally attributed to alterations to cellular homeostasis.
Independence of and Interactions between GABA-, Glutamate-, and Acetylcholine-Activated Cl Conductances inAplysiaNeurons
Authors: Kehoe JacSue , Vulfius Catherine 
Published: April 2018

In certainAplysianeurons, glutamate, GABA, and acetylcholine (ACh) all elicit desensitizing Cl-dependent responses. This fact and the finding that the glutamate and GABA responses “cross-desensitize” led to the suggestion (Swann and Carpenter, 1975; King and Carpenter, 1987) that the responses to these transmitters were mediated by the same receptor–channel complex.This hypothesis is incompatible with the demonstration given here that the GABA- and glutamate-gated channels are clearly distinct; the GABA channel, but not the glutamate channel, shows outward rectification (Matsumoto, 1982; King and Carpenter, 1987, 1989) and is selectively blocked by intracellular sulfate. Exploiting these distinctive characteristics and the independent expression of the receptors in some cells, we have been able to reevaluate the so-called cross-desensitization by analyzing the ability of GABA, glutamate, and other agonists to interact with each of the receptor molecules.The cross-desensitization was found to be exclusively attributable to the ability of GABA to interact with the glutamate receptor (Oyama et al., 1990). The GABA receptor is unaffected by glutamate. Nevertheless, in cells expressing both receptors, glutamate can reduce the GABA response by auto-desensitizing the part of the response that is mediated by the glutamate receptor. No interactions were observed between ACh-induced responses and either of the responses elicited by the amino acids.The invertebrate glutamate-gated Cl channels that have been cloned resemble the vertebrate glycine receptor (Vassilatis et al., 1997). Our pharmacological evaluation of the molluscan glutamate receptor points in the same direction.
Age and Gender Predict Volume Decline in the Anterior and Posterior Hippocampus in Early Adulthood
Authors: Pruessner J. C. , Collins D. L. , Pruessner M. , Evans A. C. 
Published: April 2018

Magnetic Resonance Imaging (MRI) provides a noninvasive method for investigating brain morphology. Within the medial temporal lobe, special attention has been paid to the hippocampus (HC) and amygdala (AG) because of their role in memory, depression, emotion, and learning. Volume changes in these areas have been observed in conjunction with certain disease states, e.g. Alzheimer's disease, post-traumatic stress disorder, and depression. Aging has also been shown to result in gray matter volume loss of the overall brain, including the HC. With regard to gender specificity, results suggest a larger shrinkage for men of brain gray matter, with controversial observations being made for the HC.With recently refined MRI acquisition and segmentation protocols, the HC and AG of 80 subjects in early adulthood (39 men and 41 women, age 18–42 years) were investigated. Whereas the volume of the AG appeared to be independent of age and gender, a significant negative correlation with age for both left and right HC was found in men (r= −0.47 and −0.44, respectively) but not in women (r= 0.01 and 0.02, respectively). The volume decline in men appeared to be linear, starting at the beginning of the third life decade and approximating 1.5% per annum. Using voxel-based regressional analysis, it was shown that changes with age occurred mostly in the head and tail of the HC. This finding underscores the need to include sociodemographic variables in functional and anatomical MRI designs.
Expression of Neuronal Connexin36 in AII Amacrine Cells of the Mammalian Retina
Authors: Feigenspan Andreas , Teubner Barbara , Willecke Klaus , Weiler Reto 
Published: April 2018

We have studied the expression pattern of neuronal connexin36 (Cx36) in the mouse and rat retina. In vertical sections of both retinas, a polyclonal antibody directed against Cx36 produced punctate labeling in the inner plexiform layer (IPL). Intense immunoreactivity was localized to the entire OFF sublamina of the IPL, and much weaker staining could be observed in the ON sublamina. Double-labeling experiments in the rat retina with antibodies directed against parvalbumin indicate that Cx36 is expressed on dendrites of AII amacrine cells. Cx36-like immunoreactivity in sublamina a of the IPL did not overlap with lobular appendages or cell bodies of AII amacrine cells. In a mouse retinal slice preparation, AII amacrine and ON cone bipolar cells were intracellularly injected with Neurobiotin and counterstained with antibody against Cx36. Punctate labeling appeared to be in register with dendritic arborization of AII amacrines and cone bipolar cells in the ON sublamina of the IPL. Whereas AII amacrine cells isolated from the rat retina clearly displayed Cx36-like immunoreactivity, isolated ON cone bipolar cells were negative for Cx36. Axon terminals of rod bipolar cells were decorated with Cx36-positive contacts but did not express Cx36 themselves.These results indicate that Cx36 is expressed by AII amacrine cells in homologous and heterologous gap junctions made with AII amacrines and cone bipolar cells, respectively. The heterologous gap junctions appear to be heterotypic, because ON cone bipolar cells do not express Cx36.
Identification of Domains and Amino Acids Involved in GluR7 Ion Channel Function
Authors: Strutz Nathalie , Villmann Carmen , Thalhammer Agnes , Kizelsztein Pablo , Eisenstein Miriam , Teichberg Vivian I. , Hollmann Michael 
Published: April 2018

The kainate receptors GluR6 and GluR7 differ considerably in their ion channel properties, despite sharing 86% amino acid sequence identity. When expressed inXenopusoocytes GluR6 conducts large agonist-evoked currents, whereas GluR7 lacks measurable currents. In the present study, we localized the determinants that are responsible for the functional differences between GluR6 and GluR7 to the extracellular loop domain L3. In addition, we generated several GluR7 point mutants that are able to conduct currents that can be readily measured inXenopusoocytes.In GluR6, glutamate- and kainate-evoked maximal currents are of the same magnitude when desensitization is inhibited with the lectin concanavalin A. By contrast, all functional GluR7 mutants were found to have glutamate current amplitudes significantly larger than those evoked by kainate. We localized the domain that determines the relative agonist efficacies to the C-terminal half of the L3 domain of GluR7.Our data show that EC50values for glutamate (but not for kainate) in GluR7 mutants or chimeras tend to be increased in comparison to the EC50values in GluR6. The high EC50for wild-type GluR7 reported in the literature appears to be linked to the S1 portion of the agonist-binding domain.Finally, we determined the C-terminal half of the L3 domain plus the far C-terminal domain of GluR7 to be responsible for the recently reported reduction of current amplitude seen when GluR7 is coexpressed with GluR6. We conclude that coexpression of GluR6 and GluR7 leads to nonstochastical assembly of heteromeric receptor complexes.