Neuroscience 2004 Abstract
Presentation Number: | 383.14 |
---|---|
Abstract Title: | GABAergic signaling between neuronal precursors and astrocyte-like cells in the postnatal subventricular zone. |
Authors: |
Liu, X.*1
; Wang, Q.1
; Haydar, T.2
; Bordey, A.1
1Neurosurgery, Cell. and Mol. Physiology, Yale Univ. Sch. of Med., New Haven, CT 2DC, 333 Cedar Street, 06520-8082, |
Primary Theme and Topics |
Development - Neurogenesis and Gliogenesis -- Neural stem cells |
Secondary Theme and Topics | Development<br />- Neurogenesis and Gliogenesis<br />-- Proliferation |
Session: |
383. Neural Stem Cells II Poster |
Presentation Time: | Monday, October 25, 2004 9:00 AM-10:00 AM |
Location: | San Diego Convention Center - Hall A-H, Board # C7 |
Keywords: | STEM CELL, ASTROCYTE, PROLIFERATION, SYNAPTIC |
In the postnatal subventricular zone (SVZ) glial fibrillary acidic protein (GFAP)-immunopositive cells (called here astrocyte-like cells) are thought to be stem cells and closely encapsulate neuronal precursors. SVZ astrocyte-like cells are thus in a prime location to receive signals from neuronal precursors. As GABA and GABA synthetic enzyme are present in SVZ precursors, we examined whether GABA acts as a signaling molecule between SVZ cells using immunostaining and patch-clamp recordings in acute brain slices from transgenic mice expressing GFP on the promoter of GFAP. We found that astrocyte-like cells express functional GABAA receptors that are nonsynaptically activated following depolarization of SVZ precursors by either electrical stimulation or 5 mM-increase in extracellular K+. GABAA receptors were also tonically activated in 60% of recorded astrocyte-like cells. Furthermore, neuronal precursors contained GABA and displayed spontaneous depolarizations of similar amplitudes than those induced by K+ increases (10-20 mV), suggesting that they spontaneously release GABA that activates GABAA receptors in astrocyte-like cells. Bath application of dextran, which slows the diffusion of GABA, or inhibition of GABA transporters prolonged the decay of GABAA responses in astrocyte-like cells. Finally treatment of slices with bicuculline significantly increased the number of proliferative astrocyte-like cells. These data indicate the existence of nonsynaptic GABAergic signaling between neuronal precursors and astrocyte-like cells. As astrocyte-like cells generate neuronal precursors, GABA released from neuronal precursors represents a feedback mechanism to control astrocyte-like cell proliferation by activating GABAA receptors.
Supported by R21NS044161-01
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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