Suppression of presynaptic calcium influx by metabotropic glutamate receptor agonists in neonatal rat hippocampus

Yoshino, Masatoshi; Kamiya, Haruyuki

doi:10.1016/0006-8993(95)00743-a

Cited by 28 publications

(18 citation statements)

References 23 publications

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“…Moreover, the inhibitory action of 1S,3R-ACPD on synaptic currents is occluded by voltage-dependent Ca 2ϩ channel blockers (Stefani et al, 1994;Glaum and Miller, 1995). Furthermore, reduction of evoked presynaptic Ca 2ϩ influx in the presence of an mGluR agonist is correlated with suppression of EPSPs (Yoshino and Kamiya, 1995). These findings suggest that reduction of Ca 2ϩ influx may underlie the presynaptic action of mGluRs.…”

Section: Presynaptic Action Of 1s3r-acpd Underlies Depression Of Synmentioning

confidence: 80%

Multiple Actions of 1S,3R-ACPD in Modulating Endogenous Synaptic Transmission to Spinal Respiratory Motoneurons

Dong¹,

Morin²,

Feldman

1996

J. Neurosci.

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To determine physiological roles of metabotropic glutamate receptors (mGluRs) affecting breathing, we examined the effects of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) on synaptic transmission and excitability of phrenic motoneurons (PMNs) in an in vitro neonatal rat brainstem/spinal cord preparation. The effects of 1S,3R-ACPD were multiple, including reduction of inspiratory-modulated synaptic currents and increase of neuronal excitability via an inward current (I acpd ) associated with a decrease of membrane conductance. The mechanism underlying synaptic depression was examined. We found that 1S,3R-ACPD reduced the frequency but not the amplitude of miniature excitatory postsynaptic currents. The current induced by exogenous AMPA was not significantly affected by 1S,3R-ACPD. These results suggest that 1S,3R-ACPD-induced reduction of inspiratory synaptic currents is mediated by presynaptic mGluRs. We also examined the ionic basis for I acpd . We found that I acpd had a reversal potential of approximately Ϫ100 mV, close to the estimated E K ϩ (Ϫ95 mV). Elevating extracellular [K ϩ ] to 9 mM reduced the I acpd reversal potential to Ϫ75 mV. The K ϩ channel blocker Ba 2ϩ induced an inward current with a reversal potential at Ϫ93 mV associated with a decrease of membrane conductance, closely resembling the effect of 1S,3R-ACPD. Moreover, Ba 2ϩ occluded 1S,3R-ACPD effects. In the presence of Ba 2ϩ , I acpd and the 1S,3R-ACPD-induced decrease of membrane conductance were diminished. Our data indicate that the dominant component of I acpd results from the blockade of a Ba 2ϩ -sensitive resting K ϩ conductance. We conclude that the activation of mGluRs affects the inspiratory-modulated activity of PMNs via distinct mechanisms at pre-and postsynaptic sites.

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Section: Presynaptic Action Of 1s3r-acpd Underlies Depression Of Synmentioning

confidence: 80%

Multiple Actions of 1S,3R-ACPD in Modulating Endogenous Synaptic Transmission to Spinal Respiratory Motoneurons

Dong¹,

Morin²,

Feldman

1996

J. Neurosci.

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“…Initial work focused on the potential of the mGluR system to modulate the release of intracellular calcium in a variety of animal models (Lachica, EA et al, 1995, Stefani, A et al, 1994, Yoshino, M and Kamiya, H, 1995. Subsequent investigations examined the ability of the mGluR system to directly inhibit excitatory transmission (Bonci, A et al, 1997) and offer protection through the inhibition of NMDA activity (Lafon-Cazal, M et al, 1999) and free radical generation (Maiese, K et al, 1995, Maiese, K et al, 1996, Vincent, AM et al, 2000.…”

Section: Targeting Injury Mechanisms To Main-tain Neuronal and Vasculmentioning

confidence: 99%

Driving Cellular Plasticity and Survival Through the Signal Transduction Pathways of Metabotropic Glutamate Receptors

Maiese¹,

Chong²,

Li³

2005

CNR

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Metabotropic glutamate receptors (mGluRs) share a common molecular morphology with other G protein-linked receptors, but there expression throughout the mammalian nervous system places these receptors as essential mediators not only for the initial development of an organism, but also for the vital determination of a cell's fate during many disorders in the nervous system that include amyotrophic lateral sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, Multiple Sclerosis, epilepsy, trauma, and stroke. Given the ubiquitous distribution of these receptors, the mGluR system impacts upon neuronal, vascular, and glial cell function and is activated by a wide variety of stimuli that includes neurotransmitters, peptides, hormones, growth factors, ions, lipids, and light. Employing signal transduction pathways that can modulate both excitatory and inhibitory responses, the mGluR system drives a spectrum of cellular pathways that involve protein kinases, endonucleases, cellular acidity, energy metabolism, mitochondrial membrane potential, caspases, and specific mitogen-activated protein kinases. Ultimately these pathways can converge to regulate genomic DNA degradation, membrane phosphatidylserine (PS) residue exposure, and inflammatory microglial activation. As we continue to push the envelope for our understanding of this complex and critical family of metabotropic receptors, we should be able to reap enormous benefits for both clinical disease as well as our understanding of basic biology in the nervous system.

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“…Inhibition of transmitter release from presynaptic terminals may result from the reduction of presynaptic Ca 2+ influx (915). Inhibition of voltage-dependent Ca 2+ currents after mGluR activation occurs in neuronal soma (219,428,730,1089,1185,1204,1272,1410); perhaps a similar mechanism underlies the presynaptic inhibitory action of mGluR agonists. Another possible mechanism is the direct modulation of the exocytotic machinery by influencing the availability of vesicles or their probability of release (468).…”

Section: Modulation Of Synaptic Transmission To Motoneurons-activatiomentioning

confidence: 99%

Synaptic Control of Motoneuronal Excitability

Rekling

Funk

Bayliss

et al. 2000

Physiological Reviews

535

482

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Movement, the fundamental component of behavior and the principal extrinsic action of the brain, is produced when skeletal muscles contract and relax in response to patterns of action potentials generated by motoneurons. The processes that determine the firing behavior of motoneurons are therefore important in understanding the transformation of neural activity to motor behavior. Here, we review recent studies on the control of motoneuronal excitability, focusing on synaptic and cellular properties. We first present a background description of motoneurons: their development, anatomical organization, and membrane properties, both passive and active. We then describe the general anatomical organization of synaptic input to motoneurons, followed by a description of the major transmitter systems that affect motoneuronal excitability, including ligands, receptor distribution, pre-and postsynaptic actions, signal transduction, and functional role. Glutamate is the main excitatory, and GABA and glycine are the main inhibitory transmitters acting through ionotropic receptors. These amino acids signal the principal motor commands from peripheral, spinal, and supraspinal structures. Amines, such as serotonin and norepinephrine, and neuropeptides, as well as the glutamate and GABA acting at metabotropic receptors, modulate motoneuronal excitability through pre-and postsynaptic actions. Acting principally via second messenger systems, their actions converge on common effectors, e.g., leak K + current, cationic inward current, hyperpolarization-activated inward current, Ca 2+ channels, or presynaptic release processes. Together, these numerous inputs mediate and modify incoming motor commands, ultimately generating the coordinated firing patterns that underlie muscle contractions during motor behavior.

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Suppression of presynaptic calcium influx by metabotropic glutamate receptor agonists in neonatal rat hippocampus

Cited by 28 publications

References 23 publications

Multiple Actions of 1S,3R-ACPD in Modulating Endogenous Synaptic Transmission to Spinal Respiratory Motoneurons

Multiple Actions of 1S,3R-ACPD in Modulating Endogenous Synaptic Transmission to Spinal Respiratory Motoneurons

Driving Cellular Plasticity and Survival Through the Signal Transduction Pathways of Metabotropic Glutamate Receptors

Synaptic Control of Motoneuronal Excitability

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