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G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...

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GABA uptake-dependent Ca(2+) signaling in developing olfactory bulb astrocytes.

Michael Doengi1, Daniela Hirnet, Philippe Coulon

  • 1Abteilung für Allgemeine Zoologie, Universität Kaiserslautern, Postfach 3049, D-67653 Kaiserslautern, Germany.

Proceedings of the National Academy of Sciences of the United States of America
|October 7, 2009
PubMed
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GABA signaling in astrocytes involves GABA transporters, not just receptors. This process triggers calcium release, influencing blood flow and astrocyte function.

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Area of Science:

  • Neuroscience
  • Astrocyte Biology
  • Neurotransmission

Background:

  • GABAergic signaling is crucial in the central nervous system.
  • Astrocytes play active roles in neuronal communication and regulation.
  • The precise mechanisms of GABAergic influence on astrocytes are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms of GABAergic signaling in olfactory bulb astrocytes.
  • To determine the role of GABA transporters and intracellular calcium release in astrocyte responses to GABA.
  • To explore the functional consequences of astrocyte GABAergic signaling on blood flow.

Main Methods:

  • Confocal Ca(2+) imaging and two-photon Na(+) imaging in olfactory bulb slices.
  • Application of GABA receptor antagonists (GABA(A), GABA(B)) and GABA uptake inhibitors (SNAP 5114).
  • Manipulation of extracellular Ca(2+) and intracellular Ca(2+) stores (cyclopiazonic acid).
  • Inhibition of ryanodine receptors and InsP(3) receptors (2-APB).
  • Pharmacological inhibition of Na(+)/Ca(2+) exchange (KB-R7943).
  • Stimulation of endogenous GABA release via afferent axon stimulation or NMDA application.

Main Results:

  • GABA evoked Ca(2+) transients in astrocytes, dependent on extracellular Ca(2+) but primarily mediated by intracellular Ca(2+) release via InsP(3) receptors.
  • GABA uptake inhibition by SNAP 5114 suppressed these Ca(2+) transients.
  • GABA induced Na(+) increases, which were shown to reduce Na(+)/Ca(2+) exchange, mimicking GABA-induced Ca(2+) transients.
  • Endogenous GABA release also triggered astrocyte Ca(2+) transients.
  • SNAP 5114-sensitive blood vessel constriction was observed, linking astrocyte GABA signaling to blood flow regulation.

Conclusions:

  • GABAergic signaling in astrocytes is primarily mediated by GABA uptake, leading to intracellular Na(+) increases and subsequent Ca(2+) release via InsP(3) receptors.
  • GABA transporters play a dual role, clearing extracellular GABA and modulating intracellular Ca(2+) signaling.
  • Astrocyte GABAergic signaling contributes to the regulation of cerebral blood flow.