1
40
2
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s11064-011-0591-2" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s11064-011-0591-2</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
134-142
Issue
1
Volume
37
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Differential Effect Of Nimodipine In Attenuating Iron-induced Toxicity In Brain- And Blood-brain Barrier-associated Cell Types
Publisher
An entity responsible for making the resource available
Neurochemical Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
Astrocytes; Biochemistry & Molecular Biology; central-nervous-system; cerebrospinal-fluid; cultured astrocytes; intracerebral hemorrhage; Iron in brain; Metal toxicity; Neurodegenerative diseases; neurodegenerative disorders; neurons; Neurosciences & Neurology; Nimodipine; oxidative; parkinsons-disease; redox-active iron; stress; substantia-nigra; transferrin receptor; Vascular endothelial cells
Creator
An entity primarily responsible for making the resource
Lockman J A; Geldenhuys W J; Bohn K A; DeSilva S F; Allen D D; Van der Schyf C J
Description
An account of the resource
Metal homeostasis is increasingly being evaluated as a therapeutic target in stroke and neurodegenerative diseases. Metal dysregulation has been shown to lead to protein aggregation, plaque formation and neuronal death. In 2007, we first reported that voltage-gated calcium channels act as a facile conduit for the entry of free ferrous (Fe2+) ions into neurons. Herein, we evaluate differential iron toxicity to central nervous system cells and assess the ability of the typical L-type voltage-gated calcium channel blocker nimodipine to attenuate iron-induced toxicity. The data demonstrate that iron sulfate induces a dose-dependent decrease in cell viability in rat brain endothelial cells (RBE4; LC50 = 150 mu M), neuronal cells (Neuro-2 alpha neuroblastoma; LC50 = 400 mu M), and in astrocytes (DI TNC1; LC50 = 1.1 mM). Pre-treatment with nimodipine prior to iron sulfate exposure provided a significant (P < 0.05) increase in viable cell numbers for RBE4 (2.5-fold), Neuro2-alpha (similar to 2-fold), and nearly abolished toxicity in primary neurons. Astrocytes were highly resistant to iron toxicity compared to the other cell types tested and nimodipine had no (P > 0.05) protective effect in these cells. The data demonstrate variable susceptibility to iron overload conditions in different cell types of the brain and suggest that typical L-type voltage-gated calcium channel blockers (here represented by nimodipine), may serve as protective agents in conditions involving iron overload, particularly in cell types highly susceptible to iron toxicity.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s11064-011-0591-2" target="_blank" rel="noreferrer noopener">10.1007/s11064-011-0591-2</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2012
Allen D D
Astrocytes
Biochemistry & Molecular Biology
Bohn K A
central-nervous-system
cerebrospinal-fluid
cultured astrocytes
DeSilva S F
Geldenhuys W J
intracerebral hemorrhage
Iron in brain
Journal Article or Conference Abstract Publication
Lockman J A
Metal toxicity
Neurochemical Research
Neurodegenerative Diseases
neurodegenerative disorders
Neurons
Neurosciences & Neurology
nimodipine
oxidative
parkinsons-disease
redox-active iron
Stress
substantia-nigra
transferrin receptor
Van der Schyf C J
Vascular endothelial cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/jn.1993.69.5.1541" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jn.1993.69.5.1541</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1541-1555
Issue
5
Volume
69
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role Of Hco3- Ions In Depolarizing Gaba-a Receptor-mediated Responses In Pyramidal Cells Of Rat Hippocampus
Publisher
An entity responsible for making the resource available
Journal of Neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
1993-05
Subject
The topic of the resource
central-nervous-system; cl-channels; cortical-neurons; cultured astrocytes; dendritic inhibition; gamma-aminobutyric acid; glial-cells; guinea-pig hippocampus; long-term potentiation; mammalian; Neurosciences & Neurology; Physiology; synaptic responses
Creator
An entity primarily responsible for making the resource
Grover L M; Lambert N A; Schwartzkroin P A; Teyler T J
Description
An account of the resource
1. Activation of GABA(A) receptors can produce both hyperpolarizing and depolarizing responses in CA1 pyramidal cells. The hyperpolarizing response is mediated by a Cl- conductance, but the ionic basis of the depolarizing response is not clear. We compared the GABA(A) receptor-mediated depolarizations induced by synaptically released gamma-aminobutyric acid [GABA; depolarizing inhibitory postsynaptic potentials (dIPSPs)] with those produced by exogenous GABA (depolarizing GABA responses). Short trains of high-frequency (200 Hz) stimuli were used to generate dIPSPs. We found that dIPSPs generated by trains of stimuli and depolarizing responses to exogenous GABA were accompanied by a conductance increase and had a similar reversal potential, indicating a similar ionic basis for both responses. 2. We wished to determine whether an HCO3- current contributed to the GABA(A)-mediated depolarizations. We found that dIPSPs and depolarizing GABA responses were sensitive to perfusion with HCO3--free medium. Interpretation of these data was complicated by the mixed nature of the responses: dIPSPs were invariably accompanied by conventional, Cl--mediated fast hyperpolarizing IPSPs (fIPSPs), and response to exogenous GABA usually consisted of biphasic hyperpolarizing and depolarizing responses. However, it was sometimes possible to elicit responses to GABA that appeared purely depolarizing (monophasic depolarizing GABA responses). 3. We analyzed monophasic depolarizing GABA responses and found no change in reversal potential when slices were perfused with HCO3--free medium. We also made whole-cell recordings from CA1 pyramidal cells, attempting to reduce [HCO3-]i, and compared the reversal potential for monophasic depolarizing GABA responses with similar responses recorded with fine intracellular microelectrodes. We found no difference in reversal potential. We also examined effects of the carbonic anhydrase inhibitor acetazolamide (ACTZ) on depolarizing GABA responses. ACTZ reduced these responses but did not change their reversal potential. 4. Effects of HCO3--free medium were not specific to GABA(A) receptor-mediated responses. GABA(B) receptor-mediated slow IPSPs (sIPSPs) were also reduced, as were excitatory postsynaptic potentials (EPSPs). Analyses of field potentials and spontaneous fIPSPs suggested a decrease in presynaptic excitability during perfusion with HCO3--free medium. In addition, pyramidal cells showed decreased input resistance when perfused with HCO 3--free medium. 5. The sensitivity of GABA(A) receptor-mediated depolarizations to HCO3--free medium can be explained by a decrease in presynaptic excitability and an increased resting conductance in postsynaptic neurons. Reduced presynaptic excitability and resting input resistance are also likely causes of the reduction in fast IPSPs, slow IPSPs, and EPSPs in HCO3--free medium. We suggest that these nonspecific effects of HCO3--free medium may be a consequence of an extracellular acidification. These data do not provide convincing evidence for involvement of an HCO3- conductance in the generation of dIPSPs and depolarizing GABA responses.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.1993.69.5.1541" target="_blank" rel="noreferrer noopener">10.1152/jn.1993.69.5.1541</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1993
central-nervous-system
cl-channels
cortical-neurons
cultured astrocytes
dendritic inhibition
gamma-aminobutyric acid
glial-cells
Grover L M
guinea-pig hippocampus
Journal Article or Conference Abstract Publication
Journal of neurophysiology
Lambert N A
Long-Term Potentiation
Mammalian
Neurosciences & Neurology
Physiology
Schwartzkroin P A
synaptic responses
Teyler T J