66 research outputs found
Coordination Compounds of Lanthanides as Materials for Luminescent Turn Off Sensors
This review aims at describing the possible use of lanthanide coordination compounds as materials for luminescent sensors now more necessary due to the continuous requirements from the society of electroluminescent and lighting devices, for example analytical sensors and imaging instruments. This is the first part of a work describing the photophysical foundations of the luminescence of complex compounds of lanthanides in the context of design materials with a sensory response, and also considers in detail materials with the most common type of response - turn off sensors
Death of Neurons following Injury Requires Conductive Neuronal Gap Junction Channels but Not a Specific Connexin
A grant from the One-University Open Access Fund at the University of Kansas was used to defray the author's publication fees in this Open Access journal. The Open Access Fund, administered by librarians from the KU, KU Law, and KUMC libraries, is made possible by contributions from the offices of KU Provost, KU Vice Chancellor for Research & Graduate Studies, and KUMC Vice Chancellor for Research. For more information about the Open Access Fund, please see http://library.kumc.edu/authors-fund.xml.Pharmacological blockade or genetic knockout of neuronal connexin 36 (Cx36)-containing gap junctions reduces neuronal death caused by ischemia, traumatic brain injury and NMDA receptor (NMDAR)-mediated excitotoxicity. However, whether Cx36 gap junctions contribute to neuronal death via channel-dependent or channel-independent mechanism remains an open question. To address this, we manipulated connexin protein expression via lentiviral transduction of mouse neuronal cortical cultures and analyzed neuronal death twenty-four hours following administration of NMDA (a model of NMDAR excitotoxicity) or oxygen-glucose deprivation (a model of ischemic injury). In cultures prepared from wild-type mice, over-expression and knockdown of Cx36-containing gap junctions augmented and prevented, respectively, neuronal death from NMDAR-mediated excitotoxicity and ischemia. In cultures obtained form from Cx36 knockout mice, re-expression of functional gap junction channels, containing either neuronal Cx36 or non-neuronal Cx43 or Cx31, resulted in increased neuronal death following insult. In contrast, the expression of communication-deficient gap junctions (containing mutated connexins) did not have this effect. Finally, the absence of ethidium bromide uptake in non-transduced wild-type neurons two hours following NMDAR excitotoxicity or ischemia suggested the absence of active endogenous hemichannels in those neurons. Taken together, these results suggest a role for neuronal gap junctions in cell death via a connexin type-independent mechanism that likely relies on channel activities of gap junctional complexes among neurons. A possible contribution of gap junction channel-permeable death signals in neuronal death is discussed.National Institutes of Health (NIH) (R21 NS076925)University of Kansas Medical Center funds to A. B. B.NIH P20 GM104936, P30 AG035982UL1 TR000001NIH HD00252
Neuronal Glud1 (Glutamate Dehydrogenase 1) Over-Expressing Mice: Increased Glutamate Formation and Synaptic Release, Loss of Synaptic Activity, and Adaptive Changes in Genomic Expression
Glutamate dehydrogenase 1 (GLUD1) is a mitochondrial enzyme expressed in all tissues, including brain. Although this enzyme is expressed in glutamatergic pathways, its function as a regulator of glutamate neurotransmitter levels is still not well defined. In order to gain an understanding of the role of GLUD1 in the control of glutamate levels and synaptic release in mammalian brain, we generated transgenic (Tg) mice that over-express this enzyme in neurons of the central nervous system. The Tg mice have increased activity of GLUD, as well as elevated levels and increased synaptic and depolarization-induced release of glutamate. These mice suffer age-associated losses of dendritic spines, nerve terminals, and neurons. The neuronal losses and dendrite structural changes occur in select regions of the brain. At the transcriptional level in the hippocampus, cells respond by increasing the expression of genes related to neurite growth and synapse formation, indications of adaptive or compensatory responses to the effects of increases in the release and action of glutamate at synapses. Because these Tg mice live to a relatively old age they are a good model of the effects of a βhyperglutamatergicβ state on the aging process in the nervous system. The mice are also useful in defining the molecular pathways affected by the over-activation of GLUD in glutamatergic neurons of the brain and spinal cord
Transgenic Expression of Glud1 (Glutamate Dehydrogenase 1) in Neurons: In Vivo Model of Enhanced Glutamate Release, Altered Synaptic Plasticity, and Selective Neuronal Vulnerability
This is the published version. Copyright 2009 Society for Neuroscience.The effects of lifelong, moderate excess release of glutamate (Glu) in the CNS have not been previously characterized. We created a transgenic (Tg) mouse model of lifelong excess synaptic Glu release in the CNS by introducing the gene for glutamate dehydrogenase 1 (Glud1) under the control of the neuron-specific enolase promoter. Glud1 is, potentially, an important enzyme in the pathway of Glu synthesis in nerve terminals. Increased levels of GLUD protein and activity in CNS neurons of hemizygous Tg mice were associated with increases in the in vivo release of Glu after neuronal depolarization in striatum and in the frequency and amplitude of miniature EPSCs in the CA1 region of the hippocampus. Despite overexpression of Glud1 in all neurons of the CNS, the Tg mice suffered neuronal losses in select brain regions (e.g., the CA1 but not the CA3 region). In vulnerable regions, Tg mice had decreases in MAP2A labeling of dendrites and in synaptophysin labeling of presynaptic terminals; the decreases in neuronal numbers and dendrite and presynaptic terminal labeling increased with advancing age. In addition, the Tg mice exhibited decreases in long-term potentiation of synaptic activity and in spine density in dendrites of CA1 neurons. Behaviorally, the Tg mice were significantly more resistant than wild-type mice to induction and duration of anesthesia produced by anesthetics that suppress Glu neurotransmission. The Glud1 mouse might be a useful model for the effects of lifelong excess synaptic Glu release on CNS neurons and for age-associated neurodegenerative processes
Thermogenetic neurostimulation with single-cell resolution
AbstractThermogenetics is a promising innovative neurostimulation technique, which enables robust activation of neurons using thermosensitive transient receptor potential (TRP) cation channels. Broader application of this approach in neuroscience is, however, hindered by a limited variety of suitable ion channels, and by low spatial and temporal resolution of neuronal activation when TRP channels are activated by ambient temperature variations or chemical agonists. Here, we demonstrate rapid, robust and reproducible repeated activation of snake TRPA1 channels heterologously expressed in non-neuronal cells, mouse neurons and zebrafish neurons in vivo by infrared (IR) laser radiation. A fibre-optic probe that integrates a nitrogenβvacancy (NV) diamond quantum sensor with optical and microwave waveguide delivery enables thermometry with single-cell resolution, allowing neurons to be activated by exceptionally mild heating, thus preventing the damaging effects of excessive heat. The neuronal responses to the activation by IR laser radiation are fully characterized using Ca2+ imaging and electrophysiology, providing, for the first time, a complete framework for a thermogenetic manipulation of individual neurons using IR light.</jats:p
Electrochromic Oxide Materials
Π ΡΡΠ°ΡΡΠ΅ ΡΠ°ΡΡΠΌΠΎΡΡΠ΅Π½Ρ ΡΠ΅ΠΎΡΠ΅ΡΠΈΡΠ΅ΡΠΊΠΈΠ΅ ΠΎΡΠ½ΠΎΠ²Ρ ΡΠ»Π΅ΠΊΡΡΠΎΡ
ΡΠΎΠΌΠΈΠ·ΠΌΠ°, ΠΏΡΠΈΠ½ΡΠΈΠΏΠΈΠ°Π»ΡΠ½Π°Ρ ΡΡ
Π΅ΠΌΠ°
ΡΠ»Π΅ΠΊΡΡΠΎΡ
ΡΠΎΠΌΠ½ΡΡ
ΡΡΡΡΠΎΠΉΡΡΠ² ΠΈ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Ρ, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΌΠΎΠ³ΡΡ Π±ΡΡΡ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½Ρ Π΄Π»Ρ ΠΈΡ
ΡΠΎΠ·Π΄Π°Π½ΠΈΡ. ΠΠ°ΠΈΠ±ΠΎΠ»ΡΡΠ΅Π΅ Π²Π½ΠΈΠΌΠ°Π½ΠΈΠ΅ ΡΠ΄Π΅Π»Π΅Π½ΠΎ ΠΎΠΊΡΠΈΠ΄Π½ΡΠΌ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»Π°ΠΌ, ΡΠ°ΠΊΠΈΠΌ ΠΊΠ°ΠΊ WO3, V2O5, TiO2,
Cr3O8, NiO, MoO3. ΠΠΎΠΊΠ°Π·Π°Π½Ρ Ρ
Π°ΡΠ°ΠΊΡΠ΅ΡΠΈΡΡΠΈΠΊΠΈ ΡΡΠΈΡ
ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π»ΠΎΠ² ΠΈ Π²ΠΎΠ·ΠΌΠΎΠΆΠ½ΡΠ΅ ΠΌΠ΅ΡΠΎΠ΄Ρ ΠΈΡ
ΠΏΠΎΠ»ΡΡΠ΅Π½ΠΈΡ. ΠΡΠΈΠ²Π΅Π΄Π΅Π½Ρ ΡΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΡΠ΅ Π΄Π°Π½Π½ΡΠ΅ ΠΏΠΎ ΠΏΠΎΠ»ΡΡΠ΅Π½ΠΈΡ ΡΠΎΠ½ΠΊΠΈΡ
ΠΏΠ»Π΅Π½ΠΎΠΊ ΠΎΠΊΡΠΈΠ΄Π° Π½ΠΈΠΊΠ΅Π»Ρ
Ρ ΠΏΡΠΈΠΌΠ΅Π½Π΅Π½ΠΈΠ΅ΠΌ ΡΠ°ΡΡΠ²ΠΎΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠΎΠ΄Π°, ΠΏΠΎΠ·Π²ΠΎΠ»ΡΡΡΠ΅Π³ΠΎ Π½Π°Π½ΠΎΡΠΈΡΡ ΠΏΠΎΠΊΡΡΡΠΈΡ Π±Π΅Π· ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΡ
Π²Π°ΠΊΡΡΠΌΠ°. ΠΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ ΠΏΠΎΠ»ΡΡΠ΅Π½Π½ΡΠΉ ΠΈ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Π½ΡΠΉ ΡΠ»Π΅ΠΊΡΡΠΎΡ
ΡΠΎΠΌΠ½ΡΠΉ ΠΌΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΌΠ΅Π½ΡΠ΅Ρ
ΡΠ²Π΅ΡΠΎΠΏΡΠΎΠΏΡΡΠΊΠ°Π½ΠΈΠ΅ ΠΏΡΠΈ ΠΏΡΠΈΠ»ΠΎΠΆΠ΅Π½ΠΈΠΈ Π½Π°ΠΏΡΡΠΆΠ΅Π½ΠΈΡ ΠΈ ΠΌΠΎΠΆΠ΅Ρ ΡΠΈΠΊΠ»ΠΈΡΠΎΠ²Π°ΡΡ ΠΏΡΠΎΡΠ΅ΡΡΡ Π·Π°ΡΠ΅ΠΌΠ½Π΅Π½ΠΈΡ
ΠΈ ΠΎΠ±Π΅ΡΡΠ²Π΅ΡΠΈΠ²Π°Π½ΠΈΡ Π΄Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅ Π²ΡΠ΅ΠΌΡThe paper discusses the theoretical basis of electrochromism, the concept of electrochromic devices
and materials that can be used to create them. Most attention is paid to oxide materials such as WO3,
V2O5, TiO2, Cr3O8, NiO, MoO3. Characteristics of these materials and their preparation methods are
shown. The paper presents experimental data on the nickel oxide thin films production using a solution
method to be applied without vacuum equipment. It is shown that the obtained and investigated
electrochromic material changes the light transmittance upon application of a voltage and can cycling
the processes of darkening and discoloration for a long tim
Homeostatic Plasticity: Comparing and Contrasting Cortical and Hippocampal Studies. A Review
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