[Abstract Title]. - Society for Neuroscience

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 242.12/I7
Topic: B.11.b. Cell biology and signalling
Title: Eph receptors mediate gliotransmitter release from astrocytes
Authors: *Z.-Y. ZHUANG, J. HUANG, C. NELERSA, J. SAGEN, D. J. LIEBL;
The Miami Project to Cure Para, Univ. of Miami, Miami, FL
Abstract: Astrocytes regulate synaptic transmission by releasing gliotransmitters such as
glutamate, ATP and D-serine. Eph receptors, the largest family of receptor tyrosine kinases, and
their membrane bound ligand, the ephrins, are very known for their functions in regulating
axonal growth/guidance, synaptic formation/plasticity in the developing nervous system. Our
previous data have shown that ephrinB3 KO null mutant mice exhibit reductions in CA3-CA1
long-term potentiation that is associated with defective leaning and memory (Rodenas-Ruano et
al., 2006). Here, we explored mechanisms regulating EphB3/EphA4-mediated release of
gliotransmitters from astrocytes. First, we used reverse-transcription PCR and
immunohistochemistry to study the mRNA and protein expression of ephrins (B1, B2, and B3)
and Eph receptors B1, B2, B3, and A4) in purified cultured cortex astrocytes. We found
ephrinB1, ephrinB3, EphB1, EphB2, EphB3 and EphA4 were strongly expressed in cultured
astrocytes while ephrinB2 was weakly expressed in astrocytes. Second, we employed HPLC and
chemiluminescence to measure the release of glutamate, D-serine and ATP from astrocytes, and
found that ephrinB3 stimulation could increase glutamate, D-serine and ATP release. Our data
demonstrate that Eph receptors can regulate gliotransmitter release from cultured astrocytes,
which may have important implication on synaptic function and plasticity.
Disclosures: Z. Zhuang , None; J. Huang, None; C. Nelersa, None; J. Sagen, None; D.J.
Liebl, None.
Poster
242. Glial Neuronal Interactions: Glutamate and Calcium
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 242.13/I8
Topic: B.11.b. Cell biology and signalling
Support: Ministerio de Educación y Ciencia (BFU2007-64764)