Compounds > 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide

2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide and Pain

2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide has been researched along with Pain* in 1 studies

Other Studies

1 other study(ies) available for 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide and Pain

Article	Year
Activation of the NMDA receptor-neuronal nitric oxide synthase pathway within the ventral bed nucleus of the stria terminalis mediates the negative affective component of pain. Neuropharmacology, 2017, 05-15, Volume: 118 Pain consists of sensory and affective components. Although the neuronal mechanisms underlying the sensory component of pain have been studied extensively, those underlying its affective component are only beginning to be elucidated. Previously, we showed the pivotal role of the ventral part of the bed nucleus of the stria terminalis (vBNST) in the negative affective component of pain. Here, we examined the role of glutamate-nitric oxide (NO) signaling in the affective component of pain in rats using a conditioned place aversion (CPA) test. Intra-vBNST injection of either CNQX (an AMPA receptor antagonist) or MK-801 (an NMDA receptor antagonist) dose-dependently attenuated intraplantar formalin-induced CPA (F-CPA) without reducing nociceptive behaviors. In vivo microdialysis showed that extracellular oxidative NO metabolites (NOx) levels were significantly increased by intraplantar formalin injection. Intra-vBNST injection of NPLA (a selective neuronal NO synthase (nNOS) inhibitor), c-PTIO (a NO scavenger), or ZL006 (a postsynaptic density-95 (PSD-95)-nNOS interaction inhibitor) dose-dependently suppressed F-CPA without attenuating nociceptive behaviors. Intra-vBNST injection of NOR3 (a NO donor) produced CPA in a dose-dependent manner in the absence of noxious stimulation. Furthermore, whole-cell patch-clamp electrophysiology in the vBNST slices revealed that NOR3 induced depolarization of hyperpolarization-activated cation current (I Topics: Animals; Conditioning, Operant; Cyclic N-Oxides; Disease Models, Animal; Excitatory Postsynaptic Potentials; Formaldehyde; Free Radical Scavengers; Hydroxylamines; Imidazoles; Male; Membrane Potentials; Neurons; Nitric Oxide Synthase Type I; Nitro Compounds; Pain; Pain Management; Pain Measurement; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Septal Nuclei; Signal Transduction	2017

Article

Year

Activation of the NMDA receptor-neuronal nitric oxide synthase pathway within the ventral bed nucleus of the stria terminalis mediates the negative affective component of pain.

Neuropharmacology, 2017, 05-15, Volume: 118

Pain consists of sensory and affective components. Although the neuronal mechanisms underlying the sensory component of pain have been studied extensively, those underlying its affective component are only beginning to be elucidated. Previously, we showed the pivotal role of the ventral part of the bed nucleus of the stria terminalis (vBNST) in the negative affective component of pain. Here, we examined the role of glutamate-nitric oxide (NO) signaling in the affective component of pain in rats using a conditioned place aversion (CPA) test. Intra-vBNST injection of either CNQX (an AMPA receptor antagonist) or MK-801 (an NMDA receptor antagonist) dose-dependently attenuated intraplantar formalin-induced CPA (F-CPA) without reducing nociceptive behaviors. In vivo microdialysis showed that extracellular oxidative NO metabolites (NOx) levels were significantly increased by intraplantar formalin injection. Intra-vBNST injection of NPLA (a selective neuronal NO synthase (nNOS) inhibitor), c-PTIO (a NO scavenger), or ZL006 (a postsynaptic density-95 (PSD-95)-nNOS interaction inhibitor) dose-dependently suppressed F-CPA without attenuating nociceptive behaviors. Intra-vBNST injection of NOR3 (a NO donor) produced CPA in a dose-dependent manner in the absence of noxious stimulation. Furthermore, whole-cell patch-clamp electrophysiology in the vBNST slices revealed that NOR3 induced depolarization of hyperpolarization-activated cation current (I

Topics: Animals; Conditioning, Operant; Cyclic N-Oxides; Disease Models, Animal; Excitatory Postsynaptic Potentials; Formaldehyde; Free Radical Scavengers; Hydroxylamines; Imidazoles; Male; Membrane Potentials; Neurons; Nitric Oxide Synthase Type I; Nitro Compounds; Pain; Pain Management; Pain Measurement; Rats; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Septal Nuclei; Signal Transduction

2017