scholarly journals Presynaptic kainate receptor facilitation of glutamate release involves protein kinase A in the rat hippocampus

2004 ◽  
Vol 557 (3) ◽  
pp. 733-745 ◽  
Author(s):  
Antonio Rodríguez-Moreno ◽  
Talvinder S. Sihra
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Glutamate Release ◽  
Rat Hippocampus ◽  
Kainate Receptor ◽  
Kinase A

scholarly journals Kainate Receptor–Mediated Inhibition of Glutamate Release Involves Protein Kinase A in the Mouse Hippocampus

2006 ◽  
Vol 96 (4) ◽  
pp. 1829-1837 ◽  
Author(s):  
José V. Negrete-Díaz ◽  
Talvinder S. Sihra ◽  
José M. Delgado-García ◽  
Antonio Rodríguez-Moreno
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Mossy Fiber ◽  
Glutamate Release ◽  
Pyramidal Cells ◽  
Kainate Receptors ◽  
Mouse Hippocampus ◽  
Ca3 Pyramidal Cells ◽  
Kinase A ◽  
Stimulation Of

The mechanisms involved in the inhibition of glutamate release mediated by the activation of presynaptic kainate receptors (KARs) at the hippocampal mossy fiber–CA3 synapse are not well understood. We have observed a long-lasting inhibition of CA3 evoked excitatory postsynaptic currents (eEPSCs) after a brief application of kainate (KA) at concentrations ranging from 0.3 to 10 μM. The inhibition outlasted the change in holding current caused by the activation of ionotropic KARs in CA3 pyramidal cells, indicating that this action is not contingent on the opening of the receptor channels. The inhibition of the eEPSCs by KA was prevented by G protein and protein kinase A (PKA) inhibitors and was enhanced after stimulation of the adenylyl cyclase (AC) with forskolin. We conclude that KARs present at mossy fiber terminals mediate the inhibition of glutamate release through a metabotropic mechanism that involves the activation of an AC-second messenger cAMP-PKA signaling cascade.

11-Keto-β-Boswellic Acid Attenuates Glutamate Release and Kainic Acid-Induced Excitotoxicity in the Rat Hippocampus

Planta Medica ◽  
2020 ◽  
Vol 86 (06) ◽  
pp. 434-441 ◽  
Author(s):  
Cheng Wei Lu ◽  
Tzu Yu Lin ◽  
Su Jane Wang
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Kainic Acid ◽  
Neuronal Death ◽  
Glutamate Release ◽  
Boswellic Acid ◽  
Glutamate Concentration ◽  
Kainic Acid Injection ◽  
Kinase A

AbstractExcessive glutamate concentration induces neuronal death in acute brain injuries and chronic neurodegenerative diseases. Natural compounds from medicinal plants have attracted considerable attention for their use in the prevention and treatment of neurological disorders. 11-Keto-β-boswellic acid, a triterpenoid found in the medicinal plant Boswellia serrata, has neuroprotective potential. The present study investigated the effect of 11-keto-β-boswellic acid on glutamate release in vitro and kainic acid-induced glutamate excitotoxicity in vivo in the rat hippocampus. In rat hippocampal nerve terminals (synaptosomes), 11-keto-β-boswellic acid dose-dependently inhibited 4-aminopyridine-stimulated glutamate release. This effect was dependent on extracellular calcium, persisted in the presence of the glutamate transporter inhibitor DL-threo-β-benzyloxyaspartate, and was blocked by the vesicular transporter inhibitor bafilomycin A1. In addition, 11-keto-β-boswellic acid reduced the 4-aminopyridine-induced increase in intrasynaptosomal Ca2+ levels. The N- and P/Q-type channel blocker ω-conotoxin MVIIC and the protein kinase A inhibitor H89 significantly suppressed the 11-keto-β-boswellic acid-mediated inhibition of glutamate release, whereas the intracellular Ca2+-releasing inhibitors dantrolene, CGP37157, and xestospongin C, mitogen-activated protein kinase inhibitor PD98059, as well as protein kinase C inhibitor calphostin C had no effect. In a rat model of excitotoxicity induced by intraperitoneal kainic acid injection (15 mg/kg), intraperitoneal 11-keto-β-boswellic acid administration (10 or 50 mg/kg) 30 min before kainic acid injection considerably ameliorated kainic acid-induced glutamate concentration elevation and CA3 neuronal death. These data suggested that 11-keto-β-boswellic acid inhibits glutamate release from the rat hippocampal synaptosomes by suppressing N- and P/Q-type Ca2+ channels and protein kinase A activity, as well as exerts protective effects against kainic acid-induced excitotoxicity in vivo.

scholarly journals Kainate Receptor-Mediated Depression of Glutamate Release Involves Protein Kinase A in the Cerebellum

2019 ◽  
Vol 20 (17) ◽  
pp. 4124
Author(s):  
Falcón-Moya ◽  
Losada-Ruiz ◽  
Rodríguez-Moreno
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Ampa Receptors ◽  
Calcium Release ◽  
Glutamate Release ◽  
Patch Clamp Technique ◽  
Protein Kinase C Inhibitors ◽  
Action Mechanisms ◽  
Kinase C ◽  
Kinase A

Kainate (KA) receptors (KAR) have important modulatory roles of synaptic transmission. In the cerebellum, the action mechanisms of KAR-mediated glutamatergic depression are unknown. We studied these mechanisms by recording evoked excitatory postsynaptic currents (eEPSCs) from cerebellar slices using the whole-cell configuration of the patch-clamp technique. We observed that 3 μM KA decreased the amplitude of eEPSCs and increased the number of failures at the synapses established between parallel fibers (PF) and Purkinje neurons, and the effect was antagonized by NBQX under the condition where AMPA receptors were previously blocked. The inhibition of protein kinase A (PKA) suppressed the effect of KAR activation on eEPSC, and effect was not prevented by protein kinase C inhibitors. Furthermore, in the presence of Pertussis toxin, the depression of glutamate release mediated by KAR activation was prevented, invoking the participation of a Gi/o protein in this modulation. Finally, the KAR-mediated depression of glutamate release was not prevented by blocking calcium-permeable KARs or by treatments that affect calcium release from intracellular stores. We conclude that KARs present at these synapses mediate an inhibition of glutamate release through a mechanism that involves the activation of G-protein and protein kinase A.

Novelty promotes recognition memory persistence by D1 dopamine receptor and protein kinase A (PKA) signaling in rat hippocampus

2021 ◽  
Author(s):  
Karine Ramires Lima ◽  
Ana Carolina Souza da Rosa ◽  
Steffanie Severo Picua ◽  
Shara Souza Silva ◽  
Náthaly Marks Soares ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Recognition Memory ◽  
Protein Kinase A ◽  
Dopamine Receptor ◽  
Rat Hippocampus ◽  
D1 Dopamine Receptor ◽  
Memory Persistence ◽  
Kinase A
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