Time-lapse animation of fura-2 calcium images of a single cortical astrocyte exposed to 250 nM V1 agonist. Calcium was initially increased in both the cytoplasm and nucleus.
The cytoplasmic calcium rise was followed by a rapid and transient calcium localization into the nucleus. Following the nuclear rise in calcium, translocation of nuclear calcium
back to the cytoplasm occurred before the decrease of total intracellular calcium concentration took place.
Time-lapse animation of confocal fluo-3 calcium images of V1 agonist-induced nuclear calcium rise in cortical astrocytes. Following addition of V1 agonist, the fluo-3 fluorescence
intensity was increased in both cytoplasmic and nuclear compartments followed by a much higher calcium signal in the nucleus for several seconds. The signal covered the whole nucleus
and then spread back to the cytoplasm followed by the decrease in total intracellular calcium, consistent with the fura-2 calcium imaging data.
Fura-2 calcium fluorescence in hippocampal neurons exposed to synaptically relevant glutamate in presence or absence of estrogen replacement therapy. At rest, [Ca++]i is low
in neurons under control conditions (top panel) and in neurons treated with the estrogen replacement therapy, conjugated equine estrogens (CEE 100ng/ml; bottom panel). Following
exposure to glutamate (25 micromolar) CEE-pretreated neurons (bottom panel) exhibit a greater rise in [Ca++]i than control neurons (upper panel)
(Brain Research Interactive, 930:216-234, 2002).
Images of calcium fluorescence in neurons exposed to 200 microM glutamate in hippocampal neurons grown in presence and absence of the estrogen replacement therapy. At rest,
[Ca++]i is low in neurons treated with CEE (100 ng/ml) bottom panel) or control (top panel). Following exposure to glutamate (200 micromolar) CEE-pretreated neurons (bottom panel)
exhibit a lower rise in [Ca++]i than control neurons (upper panel).
Time-lapse animation of color topographical maps of 17 -estradiol enhancement of synaptic transmission in CA3. The hippocampal slice was stimulated at CA3 for every 30 sec, and
EPSPs were recorded from the entire hippocampal slice. During baseline recording, the slice was perfused with ACSF for 30mins and, then, was perfused with 100pM 17 -estradiol
ACSF. The amplitudes of the EPSPs were analyzed to generate a topographical map based on the difference from the baseline recordings. The initial increase of amplitude occurs
at the dentate gyrus and traverses up through CA3 to CA1.