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Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
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Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
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Direct Imaging of ER Calcium with Targeted-Esterase Induced Dye Loading TED
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Calcium Release from Stores Inhibits GIRK.

Paul F Kramer1, John T Williams1

  • 1Vollum Institute, Oregon Health and Science University, Portland, OR 97239, USA.

Cell Reports
|December 24, 2016
PubMed
Summary
This summary is machine-generated.

Group 1 metabotropic glutamate receptors (mGluRs) transiently inhibit GIRK currents in rat dopamine neurons. This calcium-dependent, postsynaptic mechanism reduces GABAB receptor-mediated inhibition, impacting central neuron activity.

Keywords:
D2GABA(B)GIRK inhibitionIP(3)calciumdopamine neuronsgroup I mGluR

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Area of Science:

  • Neuroscience
  • Cellular signaling
  • Synaptic plasticity

Background:

  • Synaptic transmission relies on ionotropic and metabotropic receptors.
  • Metabotropic receptors modulate ion channels and other receptors.
  • Group 1 mGluRs and GABAB/D2 receptors influence neuronal firing patterns.

Purpose of the Study:

  • To investigate the interaction between group 1 mGluR-mediated calcium release and GABAB/D2-mediated GIRK currents.
  • To elucidate the postsynaptic mechanisms regulating neuronal inhibition in rat dopamine neurons.

Main Methods:

  • Electrophysiological recordings in rat substantia nigra dopamine neurons.
  • Pharmacological manipulation of mGluRs and downstream signaling pathways.
  • Measurement of GIRK currents and calcium release from intracellular stores.

Main Results:

  • Transient mGluR activation transiently decreased GABAB and D2 receptor-evoked GIRK currents.
  • The inhibition was calcium-dependent, peaking at 1 second and recovering within 5 seconds.
  • Inhibition was greater for transient than tonic currents and independent of PLC, PKC, PLA2, or calmodulin.

Conclusions:

  • Group 1 mGluR activation inhibits GIRK currents via intracellular calcium release.
  • This postsynaptic mechanism broadly reduces GIRK-dependent inhibition in central neurons.
  • Provides insight into the regulation of neuronal excitability and synaptic transmission.