Potent antagonists at the L-AP4- and (1S,3S)-ACPD-sensitive presynaptic metabotropic glutamate receptors in the neonatal rat spinal cord

Jane, David E.; Thomas, Nicola; Tse, H. W.; Watkins, Johnathan

doi:10.1016/s0028-3908(96)00048-2

Cited by 129 publications

(67 citation statements)

References 34 publications

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“…To preclude endogenous G-protein-mediated modulation during trains of stimuli, the GABA B receptor antagonist CGP55845a (2 M) (Davies et al, 1993), the adenosine A 1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPC PX) (5 M) (Haleen et al, 1987), and the mGlu-RIII antagonist ( RS)-␣-cyclopropyl-4-phosphonophenylglycine (C PPG) (30 M) (Jane et al, 1996) were included in the external saline. These antagonists had no effect on EPSC amplitudes during low-frequency stimulation (Ͻ0.1 Hz) (n ϭ 3; data not shown).…”

Section: Methodsmentioning

confidence: 99%

Modulation of Transmission during Trains at a Cerebellar Synapse

Kreitzer

Regehr

2000

J. Neurosci.

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Activity-dependent processes dynamically regulate synapses on the time scale of milliseconds to seconds. Here, we examine the factors governing synaptic strength during repetitive stimulation, both in control conditions and during presynaptic inhibition. Field recordings of presynaptic volleys, optical measurements of presynaptic calcium, and voltage-clamp recordings of postsynaptic currents were used to examine parallel fiber to Purkinje cell synapses in cerebellar brain slices at 34°C. In control conditions, regular stimulus trains (1-50 Hz) evoked up to a 250% peak synaptic enhancement, whereas during irregular stimulation, a threefold variability in EPSC amplitude was observed. When initial EPSC amplitudes were reduced by 50%, either by lowering external calcium or by activating adenosine A 1 or GABA B receptors, the peak enhancement during regular trains was 500%, and synaptic variability during irregular trains was nearly sixfold. By contrast, changes in fiber excitability and calcium influx per pulse were small during trains. Presynaptic calcium measurements indicated that by pulse 10, stimulusevoked calcium influx had increased by ϳ15%, which on the basis of the measured relationship between calcium influx and release corresponds to an EPSC enhancement of 50%. This enhancement was the same in all experimental conditions, even in the presence of N 6 -cyclopentyladenosine or baclofen, suggesting that repetitive stimulation does not relieve the G-protein inhibition of calcium channels by these modulators. Therefore, for our experimental conditions, changes in synaptic strength during trains are primarily attributable to residual calcium (Ca res )-dependent short-term plasticities, and the actions of neuromodulators during repetitive stimulation result from their inhibition of initial calcium influx and the resulting effects on Ca res and calcium-driven processes.

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Section: Methodsmentioning

confidence: 99%

Modulation of Transmission during Trains at a Cerebellar Synapse

Kreitzer

Regehr

2000

J. Neurosci.

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“…However, the effects of LY341495 cannot be ascribed solely to group III mGluRs in photoreceptor terminals, because LY341495 is an antagonist of both group II and group III mGluRs (Kingston et al, 1998;Wright et al, 2000;Kogo et al, 2004). Surprisingly, CPPG (300 M), known as a group III mGluR antagonist (Jane et al, 1996;von Gersdorff et al, 1997;Awatramani and Slaughter, 2001;Nawy, 2004), could not suppress the inhibitory effect of L-AP-4 (20 -200 M) on the cone I Ca (n ϭ 4). MPPG (300 M), another group III mGluR antagonist (Jane et al, 1995;Koulen et al, 1999), was also ineffective in antagonizing L-AP-4-induced outward current in ON bipolar cells of the newt retina (data not shown).…”

Section: L-ap-4 Inhibited L-type I Ca In Conesmentioning

confidence: 98%

Group III Metabotropic Glutamate Receptors and Exocytosed Protons Inhibit L-Type Calcium Currents in Cones But Not in Rods

Hosoi¹,

Arai²,

Tachibana³

2005

J. Neurosci.

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“…Activation of group II and III mGluRs also inhibits glutamatergic transmission in many brain regions and in the normal spinal cord (Jane et al, 1996;Conn and Pin, 1997;Gerber et al, 2000). Activation of group II and III mGluRs attenuates the firing activity of spinal dorsal horn neurons in acute and chronic pain models (Neugebauer et al, 2000;Chen and Pan, 2005).…”

Section: Effect Of Group II and Iii Metabotropic Glutamate Receptor Amentioning

confidence: 99%

Modulation of pain transmission by G-protein-coupled receptors

Pan

Zhou

et al. 2008

Pharmacology & Therapeutics

167

116

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The heterotrimeric G protein-coupled receptors (GPCRs) represent the largest and most diverse family of cell surface receptors and proteins. GPCRs are widely distributed in the peripheral and central nervous systems and are one of the most important therapeutic targets in pain medicine. GPCRs are present on the plasma membrane of neurons and their terminals along the nociceptive pathways and are closely associated with the modulation of pain transmission. GPCRs that can produce analgesia upon activation include opioid, cannabinoid, α 2 -adrenergic, muscarinic acetylcholine, γ-aminobutyric acid B (GABA B ), group II and III metabotropic glutamate, and somatostatin receptors. Recent studies have led to a better understanding of the role of these GPCRs in the regulation of pain transmission. Here, we review the current knowledge about the cellular and molecular mechanisms that underlie the analgesic actions of GPCR agonists, with a focus on their effects on ion channels expressed on nociceptive sensory neurons and on synaptic transmission at the spinal cord level.

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Potent antagonists at the L-AP4- and (1S,3S)-ACPD-sensitive presynaptic metabotropic glutamate receptors in the neonatal rat spinal cord

Cited by 129 publications

References 34 publications

Modulation of Transmission during Trains at a Cerebellar Synapse

Modulation of Transmission during Trains at a Cerebellar Synapse

Group III Metabotropic Glutamate Receptors and Exocytosed Protons Inhibit L-Type Calcium Currents in Cones But Not in Rods

Modulation of pain transmission by G-protein-coupled receptors

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