scholarly journals Cell swelling induced by water and glycerol gradients in hepatocytes from warm‐and cold‐acclimated Hyla chrysoscelis , a freeze‐tolerant amphibian

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
PonTi Tsou ◽  
Geetha Koneru ◽  
Luiz Finatti ◽  
Kara Bobka ◽  
James Frisbie ◽  
...  
Keyword(s):  
Cell Swelling ◽  
Hyla Chrysoscelis ◽  
Freeze Tolerant

scholarly journals Membrane trafficking of aquaglyceroporin HC‐3 in erythrocytes from the freeze tolerant anuran, Cope's gray treefrog, Hyla chrysoscelis

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Elizabeth Claire Wetzel ◽  
Philip Nickell ◽  
Venkateshwar Mutyam ◽  
James Frisbie ◽  
David L Goldstein ◽  
...  
Keyword(s):  
Membrane Trafficking ◽  
Hyla Chrysoscelis ◽  
Freeze Tolerant ◽  
Gray Treefrog

scholarly journals Glycosylation of aquaporins in the freeze tolerant tree frog, Hyla chrysoscelis

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Khadijeh Alnajjar ◽  
Ram Naresh Pandey ◽  
James Frisbie ◽  
David L. Goldstein
Keyword(s):  
Tree Frog ◽  
Hyla Chrysoscelis ◽  
Freeze Tolerant

scholarly journals Aquaglyceroporin expression and erythrocyte omoregulation in cultures from the freeze tolerant anuran, Cope's gray tree frog, Hyla chrysoscelis

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Venkateshwar Mutyam ◽  
James Frisbie ◽  
David L Goldstein ◽  
Carissa M Krane
Keyword(s):  
Tree Frog ◽  
Hyla Chrysoscelis ◽  
Freeze Tolerant ◽  
Gray Tree Frog

Imaging NMDA- and kainate-induced intrinsic optical signals from the hippocampal slice

1996 ◽  
Vol 76 (4) ◽  
pp. 2707-2717 ◽  
Author(s):  
R. D. Andrew ◽  
J. R. Adams ◽  
T. M. Polischuk
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Ampa Receptors ◽  
Hippocampal Slice ◽  
Field Potential ◽  
Nmda Receptor Antagonist ◽  
Light Transmittance ◽  
Stratum Radiatum ◽  
Cell Swelling ◽  
Tissue Resistance

1. Brain ischemia causes excess release and accumulation of glutamate that binds to postsynaptic receptors. This opens ionotropic channels that mediate neuronal depolarization and ionic fluxes that can lead to neuronal death. 2. The CA1 pyramidal cell region of the hippocampus is particularly susceptible to this neurotoxic process. Brain cell swelling is considered an early excitotoxic event, but remains poorly under stood and documented. As cells swell, light transmittance (LT) increases through brain tissue, so we hypothesized that brief exposure to glutamate agonists would elicit cell swelling that could be imaged in real time in the hippocampal slice. 3. A 1-min bath application of 100 microM N-methyl-D-aspartate (NMDA) or 100 microM kainate at 22 degrees C greatly increased LT, particularly in the dendritic regions of CA1. The response peaked by 2-3 min and slowly reversed over the subsequent 20 min following exposure. Peak LT increases were > 50% in CA1 stratum radiatum and > 20% in both CA1 stratum oriens and the dendritic region of the dentate gyrus, all areas with a high concentration of NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors. The CA3 stratum radiatum, which contains fewer of these receptors, showed a comparatively small LT increase. 4. The NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP-5) [but not 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)] blocked the CA1 response to NMDA, whereas the non-NMDA receptor antagonist CNQX (but not AP-5) blocked the response to kainate. The relative tissue resistance measured across CA1 stratum radiatum increased after NMDA or kainate exposure with a time course similar to the LT change described above. The increase in relative tissue resistance was blocked by kynurenate, a nonspecific glutamate antagonist. Increases in both LT and tissue resistance provide two independent lines of evidence that cell swelling rapidly developed in CA1 dendritic areas after activation of NMDA or AMPA receptors. 5. This swelling at 22 degrees C was accompanied by a temporary loss of the evoked CA1 field potential. However, at 37 degrees C the dendritic swelling rapidly progressed to an irreversible LT increase (swelling) of the CA1 cell bodies accompanied by a permanent loss of the evoked field. 6. We propose that dendritic swelling mediated by NMDA and AMPA receptors is an early excitotoxic event that can herald permanent damage to CA1 neurons, those cells most vulnerable to ischemic insult.

ATP potently modulates anion channel-mediated excitatory amino acid release from cultured astrocytes

2002 ◽  
Vol 283 (2) ◽  
pp. C569-C578 ◽  
Author(s):  
Alexander A. Mongin ◽  
Harold K. Kimelberg
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Atp Release ◽  
Anion Channel ◽  
P2y Receptors ◽  
Cell Swelling ◽  
Channel Blockers ◽  
Medium Osmolarity ◽  
Subsequent Activation

Volume-dependent ATP release and subsequent activation of purinergic P2Y receptors have been implicated as an autocrine mechanism triggering activation of volume-regulated anion channels (VRACs) in hepatoma cells. In the brain ATP is released by both neurons and astrocytes and participates in intercellular communication. We explored whether ATP triggers or modulates the release of excitatory amino acid (EAAs) via VRACs in astrocytes in primary culture. Under basal conditions exogenous ATP (10 μM) activated a small EAA release in 70–80% of the cultures tested. In both moderately (5% reduction of medium osmolarity) and substantially (35% reduction of medium osmolarity) swollen astrocytes, exogenous ATP greatly potentiated EAA release. The effects of ATP were mimicked by P2Y agonists and eliminated by P2Y antagonists or the ATP scavenger apyrase. In contrast, the same pharmacological maneuvers did not inhibit volume-dependent EAA release in the absence of exogenous ATP, ruling out a requirement of autocrine ATP release for VRAC activation. The ATP effect in nonswollen and moderately swollen cells was eliminated by a 5–10% increase in medium osmolarity or by anion channel blockers but was insensitive to tetanus toxin pretreatment, further supporting VRAC involvement. Our data suggest that in astrocytes ATP does not trigger EAA release itself but acts synergistically with cell swelling. Moderate cell swelling and ATP may serve as two cooperative signals in bidirectional neuron-astrocyte communication in vivo.

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