A role for protein kinase C in the electrically evoked release of [3H]?-aminobutyric acid in rabbit caudate nucleus

1989 ◽  
Vol 339 (3) ◽  
Author(s):  
Peter Bartmann ◽  
Rolf Jackisch ◽  
Georg Hertting ◽  
Clemens Allgaier
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Caudate Nucleus ◽  
Aminobutyric Acid ◽  
Kinase C ◽  
Rabbit Caudate Nucleus

scholarly journals Activation of Protein Kinase C Induces γ-Aminobutyric Acid Type A Receptor Internalization inXenopusOocytes

1998 ◽  
Vol 273 (49) ◽  
pp. 32595-32601 ◽  
Author(s):  
Richard Chapell ◽  
Orlando F. Bueno ◽  
Xavier Alvarez-Hernandez ◽  
Lucy C. Robinson ◽  
Nancy J. Leidenheimer
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Type A ◽  
Receptor Internalization ◽  
Aminobutyric Acid ◽  
Kinase C ◽  
Acid Type

Involvement of Protein Kinase C in γ-Aminobutyric Acid Release from Xenopus Oocytes Injected with Rat Brain mRNA

2002 ◽  
Vol 67 (2) ◽  
pp. 868-871
Author(s):  
S. Kan ◽  
S. Mameya ◽  
Y. Kataoka ◽  
M. Kaibara ◽  
K. Yamashita ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Rat Brain ◽  
Xenopus Oocytes ◽  
Aminobutyric Acid ◽  
Kinase C ◽  
Acid Release ◽  
Brain Mrna

scholarly journals Feature Article: Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C

2018 ◽  
Vol 243 (13) ◽  
pp. 1046-1055 ◽  
Author(s):  
Nathanael O’Neill ◽  
Sergiy Sylantyev
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dentate Gyrus ◽  
Granule Cells ◽  
Tonic Inhibition ◽  
Aminobutyric Acid ◽  
Ionotropic Receptors ◽  
Kinase C ◽  
Inhibitory Signaling ◽  
Intracellular Mechanisms

Ionotropic receptors of γ-aminobutyric acid (GABAARs) produce two forms of inhibitory signaling: phasic inhibition triggered by activation of synaptic GABAARs at GABAergic synapses, and tonic inhibition generated in large part through persistent activation of extrasynaptic GABAARs. It has recently been demonstrated that tonic inhibition may also involve spontaneously opening GABAARs (s-GABAARs) whose activation does not require binding of γ-aminobutyric acid (GABA). Here, we examine intracellular mechanisms modulating GABAARs’ tonic effects in rat dentate gyrus granule cells (DGCs). Cellular control of s-GABAARs-delivered tonic current appears to involve signaling inputs from G-protein-dependent and -independent molecular cascades, whereas tonic GABA-dependent current in DGCs is regulated by protein kinase C. The intracellular agents that modulate s-GABAAR-generated inhibition could thus represent a generic mechanism controlling signal integration in central neural circuits. Impact statement Here we study intracellular mechanisms which regulate inhibitory signaling delivered through continuously (tonically) open ionotropic receptors of γ-aminobutyric acid (GABA) of dentate gyrus granule cells (DGCs). We found that, apart of classical GABA-A receptors (GABAARs) which can be activated by GABA binding, a significant part of tonic inhibitory current is delivered by newly discovered spontaneously opening GABAARs (s-GABAARs), which enter active state without binding of GABA. We have also found that conventional GABAARs and s-GABAARs are regulated by different intracellular mechanisms, which may overlap and thus induce various signaling repercussions. Our results demonstrate that s-GABAARs play a key role in the mechanism that implements DGCs functional role in the brain. On top of that, since regulatory mechanisms under study are affected in a number of pathological states, our results may have broad implications for treatment of neurological disorders.

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