Ketamine Inhibits Glutamate-, N-Methyl-D-Aspartate-, and Quisqualate-Stimulated cGMP Production in Cultured Cerebral Neurons

Gonzales, Jerry M.; Loeb, Alex L.; Reichard, Peter S.; Irvine, Steven

doi:10.1097/00132586-199512000-00008

Cited by 14 publications

(20 citation statements)

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“…This study provides in vitro data that directly show the suppressive effects of ketamine on NO production in HUVECs. In cultured cerebral neurons, Gonzales et al reported that N-methyl-Daspartate-and non-N-methyl-D-aspartate-specific analogs increased NO synthesis, but ketamine reduced this effect (29). Ketamine has been reported to reduce NO production in lipopolysaccharide-activated macrophages (30).…”

Section: Discussionmentioning

confidence: 99%

Ketamine reduces nitric oxide biosynthesis in human umbilical vein endothelial cells by down-regulating endothelial nitric oxide synthase expression and intracellular calcium levels*

Chen

Lin

et al. 2005

Critical Care Medicine

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Section: Discussionmentioning

confidence: 99%

Ketamine reduces nitric oxide biosynthesis in human umbilical vein endothelial cells by down-regulating endothelial nitric oxide synthase expression and intracellular calcium levels*

Chen

Lin

et al. 2005

Critical Care Medicine

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“…Regarding the different effect of ether and ketamine on the acrophases of T, H and A, the effect of ketamine could be interpreted according to its mechanisms of action. The glutamatergic neurotransmission is involved in the hypnotic activity of ketamine as shown in vivo (Yamamura et al 1990) or in vitro (Gonzales et al 1995) by inhibition of the excitatory amino acid (NMDA) receptors' activity. Elsewhere, monoaminergic neurotransmission is also concerned by ketamine since this drug has been shown to inhibit synaptic norepinephrine re-uptake (Cook et al 1991).…”

Section: Discussionmentioning

confidence: 99%

Daily rhythms of heart rate, temperature and locomotor activity are modified by anaesthetics in rats: a telemetric study

Prudian¹,

Gantenbein²,

Pélissier³

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The aim of this study was to evaluate the effect of anaesthesia (ether or ketamine) on daily rhythms of temperature (T), heart rate (H) and locomotor activity (A) in unrestrained rats by using implanted radio-telemetry transmitters. T, H and A were measured every 10 min, in Wistar male rats, and analysed using Cosinor. The mean +/- SEM days needed, after surgical implantation, to detect a daily rhythm in H, T and A were also assessed. Six rats were anaesthetized for about 50 min either by ketamine or ether in a 3 by 3 cross-over design. Mesors, amplitudes and acrophases of T, H and A were calculated three days before (D-3; D-2; D-1), the day of anaesthesia (D0) as well as the three following days (D1; D2; D3). ANOVA was performed in order to detect, firstly a possible effect due to the order of application of anaesthesia, secondly a significant difference between ether or ketamine-induced anaesthesia and finally a modification of the mesors, amplitudes and acrophases of T, H and A, induced by each anaesthesia, for D0, D1, D2 and D3 when compared to D-1. Our results indicate: (1) Alterations of the acrophases, mesors and amplitudes, except for the amplitude of A, of the daily rhythms of T, H and A on D0 of ketamine anaesthesia while regarding ether anaesthesia only amplitude of T and H and acrophase of A were modified on D0. Some of these modifications were still observed on the days following anaesthesia. A significant difference between ether and ketamine-induced anaesthesia was also observed. (2) A non-detection of T, H and A daily rhythms after surgical implantation, which was not observed after injection of either ether or ketamine alone. Almost 10 days were needed to detect a significant daily rhythm for T, H and A. The authors suggest that, the general anaesthetic agent was responsible for a perturbation of the mesors, amplitudes and acrophases of the daily rhythms of H, T and A while the non-detection of these rhythms after implantation was more due to the surgical aggression.

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“…Although stimulation of NOS with the subsequent production of NO triggered by activation of NMDA receptors plays an important role in the spinal nociceptive processing of information (see Introduction), there are other receptor systems that can also activate the NO pathway. For instance, activation of glutamate receptors other than NMDA receptors can also increase cGMP concentrations in spinal cord slices from neonate rats (Morris et al, 1994) and in cultured cerebellar cortical neurones from fetal rats (Gonzales et al, 1999). In both cases, NOS inhibitors, including L-NAME, blocked the increase in cGMP concentrations (Morris et al, 1994;Gonzales et al, 1999).…”

Section: Ketamine and Ketoprofen Combinationmentioning

confidence: 99%

Synergistic depression of NMDA receptor‐mediated transmission by ketamine, ketoprofen and L‐NAME combinations in neonatal rat spinal cords in vitro

Lizarraga

Chambers

Johnson

2008

British J Pharmacology

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Background and purpose: Spinal N-methyl-D-aspartate (NMDA) receptor/cyclooxygenase (COX) and nitric oxide synthase (NOS) pathways play a major role in nociceptive processing, and influencing them simultaneously may induce synergistic analgesia. This study determined the spinal antinociceptive interactions between ketamine (NMDA receptor channel blocker), ketoprofen (COX inhibitor) and L-NAME (NOS inhibitor) combinations. Experimental approach: Using an in vitro neonatal rat spinal cord preparation, two A-fibre-mediated reflexes, the monosynaptic reflex (MSR) and the low-intensity excitatory postsynaptic potential (epsp), and one C-fibre-mediated reflex, the high-intensity epsp, were evoked electrically. The effect of drugs and drug combinations on these reflexes was assessed and the type of interaction determined by isobolographic analysis. Key results: Infusion of ketamine alone decreased all three reflexes. That of ketoprofen decreased both the low and the highintensity epsp only. Infusion of L-NAME alone produced no significant effects. Co-infusion of fixed ratios of IC 40 fractions of both (ketamine þ ketoprofen) and (ketamine þ L-NAME) were synergistic for depressing the low and the high-intensity epsps. The interaction was sub-additive for both combinations on the MSR. The only significant effect for the (ketoprofen þ L-NAME) combination was synergism on the high-intensity epsp. Conclusions and implications: All three combinations synergistically depressed nociceptive spinal transmission, and both ketamine and ketoprofen and ketamine and L-NAME combinations did so with potentially decreased motor side effects. If such combination profiles also occur in vivo, the present findings raise the possibility of ultimate therapeutic exploitation of increased analgesia with fewer side effects.

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Ketamine Inhibits Glutamate-, N-Methyl-D-Aspartate-, and Quisqualate-Stimulated cGMP Production in Cultured Cerebral Neurons

Cited by 14 publications

References 0 publications

Ketamine reduces nitric oxide biosynthesis in human umbilical vein endothelial cells by down-regulating endothelial nitric oxide synthase expression and intracellular calcium levels*

Ketamine reduces nitric oxide biosynthesis in human umbilical vein endothelial cells by down-regulating endothelial nitric oxide synthase expression and intracellular calcium levels*

Daily rhythms of heart rate, temperature and locomotor activity are modified by anaesthetics in rats: a telemetric study

Synergistic depression of NMDA receptor‐mediated transmission by ketamine, ketoprofen and L‐NAME combinations in neonatal rat spinal cords in vitro

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