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[Abstract Title]. - Society for Neuroscience

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242. Glial Neuronal Interactions: Glutamate and Calcium<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 242.9/I4<br />

Topic: B.11.b. Cell biology and signalling<br />

Support: The Council of Scientific and Industrial Research (CSIR) Grant<br />

<strong>Title</strong>: Acute effect of 17β-estradiol on signaling between astrocytes and neurons in mixed<br />

hippocampal cultures<br />

Authors: *S. P. RAO 1 , S. K. SIKDAR 2 ;<br />

1 Psychiatry/MRRC, Semel Inst, UCLA, Los Angeles, CA; 2 Mol. biophysics unit, Indian Inst. of<br />

Sci., Bangalore, India<br />

<strong>Abstract</strong>: The ovarian steroid hormone 17β-estradiol, in addition to its classical genomic effects<br />

in the brain through intracellular estrogen receptors, can bring about actions that are rapid in<br />

onset via a plasma membrane-associated <strong>for</strong>m of its receptor. In the hippocampus, estrogen<br />

receptors have been observed at extranuclear sites on both neurons and astrocytes suggesting a<br />

complex interplay between the two cell types in mediating the effects of the hormone. Neuronal<br />

activity can trigger intracellular calcium elevations in astrocytes, in turn leading to release of<br />

gliotransmitters that can modulate neuronal activity and synaptic transmission.<br />

We investigated the functional consequences of acute (5 min) estradiol treatment on astrocyteastrocyte<br />

and astrocyte-neuron signaling in rat hippocampal cultures using calcium imaging and<br />

electrophysiological techniques. Mechanical stimulation of an astrocyte in fluo-3 AM loaded<br />

cultures evoked a calcium rise in the stimulated astrocyte followed by calcium elevations in the<br />

surrounding astrocytes and neurons. Following acute treatment with estradiol, the amplitude of<br />

the calcium responses in the surrounding astrocytes and neurons was attenuated. Astrocyteevoked<br />

electrophysiological responses in neurons were affected by estradiol too. The incidence<br />

and amplitude of the astrocyte-evoked slow inward current in neurons was reduced in presence<br />

of estradiol. Also, acute estradiol treatment decreased the incidence of astrocyte-evoked increase<br />

in spontaneous postsynaptic current frequency in neurons. Astrocyte calcium responses to the<br />

metabotropic glutamate receptor agonist t-ACPD were reduced in presence of estradiol<br />

suggesting functional changes in astrocyte metabotropic glutamate receptors following acute<br />

treatment with estradiol. Our results indicate that glutamate-mediated astrocyte-astrocyte and<br />

astrocyte-neuron communication is sensitive to rapid estradiol-mediated hormonal control.<br />

Disclosures: S.P. Rao, None; S.K. Sikdar, None.<br />

Poster

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