NMDA receptor and retinal laser injury.
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Animals↗
Biomedical subjects
R Walz
Publications and source records attributed to R Walz.
[Comment on Deusch et al.: Patient knowledge about anesthesia practice and responsibilities of the anesthetist].
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Anesthesia↗
Drugs acting upon the cyclic adenosine monophosphate/protein kinase A signalling pathway modulate memory consolidation when given late after training into rat hippocampus but not amygdala.
Rats implanted bilaterally with cannulae in the CA1 region of the dorsal hippocampus or in the amygdala were trained in one-trial step-down inhibitory (passive) avoidance using a 0.4 mA footshock. At various times after training (0, 1.5, 3, 6 or 9 h for animals implanted in the hippocampus; 0 or 3 h for those implanted in the amygdala), they received infusions of 8-Br-cAMP (cyclic adenosine monophosphate) (1.25 micrograms/side), SKF38393 (7.5 micrograms/side), SCH23390 (0.5 microgram/side), norepinephrine ClH (0.3 microgram/side), timolol ClH (0.3 microgram/side), 8-HO-DPAT (2.5 micrograms/side), NAN-190 (2.5 micrograms/side), forskolin (0.5 microgram/side) or KT5720 (0.5 microgram/side). Rats were tested for retention 24 h after training. SKF38393 is an agonist and SCH23390 an antagonist at dopamine D1 receptors, timolol is a beta-adrenoceptor antagonist, 8-HO-DPAT is an agonist and NAN-190 an antagonist at 5HT1A receptors, forskolin enhances adenylyl cyclase, and KT5720 inhibits protein kinase A. When given into the hippocampus 0 h post-training, norepinephrine enhanced memory and KT5720 was amnestic. When given 1.5 h after training, all treatments were ineffective. When given 3 or 6 h post-training, 8-Br-cAMP, forskolin, SKF 38393, noradrenaline and NAN-190 caused memory facilitation, and KT5720, SCH23390, timolol and 8-HO-DPAT caused retrograde amnesia. At 9 h from training, all treatments were again ineffective. When given into the amygdala 0 or 3 h post-training all treatments were ineffective, except for noradrenaline at 0 h, which caused retrograde facilitation. The data agree with the suggestion that in the hippocampus, but not the amygdala, a cAMP/protein kinase A pathway is involved in memory consolidation at 3 and 6 h from training, and that this is regulated by D1, beta, and 5HT1A receptors. This correlates with a previous report of increased cAMP levels, protein kinase A activity and P-CREB levels at 3-6 h from training in rat hippocampus in this task. This may be taken to suggest that the hippocampus, but not the amygdala, is involved in the long-term storage of step-down inhibitory avoidance in the rat.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
A tube in the pharynx for emergency ventilation.
BACKGROUND: If the endotracheal placement of a nasal advanced tube fails, ventilation via this tube could bridge the time until a fibreoptic bronchoscope is available. This study investigates the efficiency of ventilation via a tube resting with its tip in the pharynx near the glottis. METHODS: In 20 patients respiratory data during ventilation via a pharyngeally placed tube were recorded by means of pulse oximetry, capnometry and side-stream spirometry. Results were compared with those measured previously in the same patients during conventional facemask ventilation. RESULTS: Oxygen saturation and end-tidal carbon dioxide concentration remained unchanged using ventilation via facemask (SO2 98.5 +/- 0.9%, FECO2 4.5 +/- 0.7 vol%) or pharyngeal tube (SO2 98.6 +/- 0.7%, FECO2 4.8 +/- 0.4 vol%). No significant differences were found between the two groups with regard to peak airway pressure, tidal volume leakage, compliance and resistance of the respiratory system. CONCLUSIONS: Our results suggest an effective ventilation and oxygenation via a tube placed with its tip in the pharynx. This technique may be helpful during difficult and prolonged nasal intubation.
Emergencies↗
Transient encephalopathy after Taxol infusion.
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Animals↗
Agents that affect cAMP levels or protein kinase A activity modulate memory consolidation when injected into rat hippocampus but not amygdala.
Male Wistar rats were trained in one-trial step-down inhibitory avoidance using a 0.4-mA footshock. At various times after training (0, 1.5, 3, 6 and 9 h for the animals implanted into the CA1 region of the hippocampus; 0 and 3 h for those implanted into the amygdala), these animals received microinfusions of SKF38393 (7.5 micrograms/side), SCH23390 (0.5 microgram/side), norepinephrine (0.3 microgram/side), timolol (0.3 microgram/side), 8-OH-DPAT (2.5 micrograms/side), NAN-190 (2.5 micrograms/side), forskolin (0.5 microgram/side), KT5720 (0.5 microgram/side) or 8-Br-cAMP (1.25 micrograms/side). Rats were tested for retention 24 h after training. When given into the hippocampus 0 h post-training, norepinephrine enhanced memory whereas KT5720 was amnestic. When given 1.5 h after training, all treatments were ineffective. When given 3 or 6 h post-training, 8-Br-cAMP, forskolin, SKF38393, norepinephrine and NAN-190 caused memory facilitation, while KT5720, SCH23390, timolol and 8-OH-DPAT caused retrograde amnesia. Again, at 9 h after training, all treatments were ineffective. When given into the amygdala, norepinephrine caused retrograde facilitation at 0 h after training. The other drugs infused into the amygdala did not cause any significant effect. These data suggest that in the hippocampus, but not in the amygdala, a cAMP/protein kinase A pathway is involved in memory consolidation at 3 and 6 h after training, which is regulated by D1, beta, and 5HT1A receptors. This correlates with data on increased post-training cAMP levels and a dual peak of protein kinase A activity and CREB-P levels (at 0 and 3-6 h) in rat hippocampus after training in this task. These results suggest that the hippocampus, but not the amygdala, is involved in long-term storage of step-down inhibitory avoidance in the rat.
8-Bromo Cyclic Adenosine Monophosphate↗
[Prolongation of fentanyl-induced decreased arousal by clonidine].
Both fentanyl and clonidine lead to a reduction of vigilance. We tested the influence of clonidine on a fentanyl induced change of vigilance using a cross-out concentration test (b-cross-out test). With local ethics committee approval, we conducted a randomised double-blinded cross-over study with 10 healthy male subjects (25-35 years old). Each volunteer received intravenously at two separate sessions 1.5 micrograms/kg fentanyl and 1.5 micrograms/kg fentanyl plus 3 micrograms/kg clonidine. For testing the level of vigilance a concentration test (b-cross-out) was used. The number of correctly revised marks was evaluated prior to drug administration (TI), directly after application, one hour later and two hours later. Our data underwent a multiple analysis of variance. With fentanyl two hours after application the mean increase of correctly revised marks was 12% when compared to those prior to application (p < 0.024). This means that with fentanyl a learning effect was achieved as described in the literature. With fentanyl and clonidine two hours after application, a decrease in vigilance of 7 1/4 in comparison with TI was seen (n.s.). This reduction of vigilance should be considered during the postoperative course and especially with regard to ambulant anaesthesia when using clonidine.
Adult↗
[Ventilation via a transnasally placed pharyngeal tube. Comparison with mask ventilation].
OBJECTIVE: The present prospective study was designed to investigate the respiratory function during ventilation via a tube inserted through the nose into the pharynx. Results were compared with respiratory parameters measured during conventional mask ventilation in the same patients. METHODS: 20 ASA physical status I-II patients were studied after approval by the local Ethics Committee. Anaesthesia was induced with alfentanil 15 micrograms/kg and propofol 2.5-3.0 mg/kg and maintained with propofol, 12-15 mg/kg/h. Patients were ventilated via a facemask with oxygen and a tidal volume of approximately 8ml/kg (measurement A). After insertion of a tube (I.D. 7.0-7.5 mm) through the nostril into the pharynx ventilation was repeated in the same manner (measurement B). To secure airway seal a second person closed the patient's mouth and exerted cricoid pressure. Following neuromuscular blockade with suxamethonium (1.5 mg/kg) respiratory parameters were measured again (C). Measurements included pulse oximetry and side stream spirometry with continuous collection of the following data: airway pressure, inspired and expired tidal volume, dynamic compliance, expired volume in one second, inspiratory and expiratory oxygen and carbon dioxide concentration. Pressure-volume and flow-volume loops were displayed continuously. RESULTS: Ventilation via facial mask or via pharyngeal tube with and without relaxation showed normal endtidal FECO2. The mean values were 4.5 +/- 0.7%, 4.8 +/- 0.4% and 4.6 +/- 0.7%, respectively. Mean oxygen saturation exceeded 98% in each period. Leakage during mask ventilation was 59.3 +/- 65.5 mL and decreased to 40.5 +/- 62.1 mL with the pharyngeal tube, whereas relaxation resulted in a significant increase to 92.3 75.0 mL. Compliance (Cdyn) and expired volume in one second (V 1.0) did not change significantly during the entire period of measurement. CONCLUSION: The use of a pharyngeally placed tube proved adequate compared to conventional mask ventilation in 20 patients without underlying airway disease.
Adolescent↗
[Muscle relaxation with atracurium in myasthenia gravis].
This report concerns a narcosis in a 42-year-old female patient suffering from myasthenia gravis in a state of clinical remission after thymectomia. Six months after thymectomia relaxometric control (Datex AMG) was performed while the patient underwent major colorectal surgery. We found a persisting sensitivity to relaxants during isoflurane anaesthesia supplemented with fentanyl. During 270 minutes of anaesthesia we needed only 25 mg atracurium (0.4 mg/kg bodyweight) only 57% of a theoretical normal dose. This is the result of a continuing muscular weakness in asymptomatic patients suffering from clinically reliable myasthenia gravis. Therefore, a reduced demand for muscle relaxants can be expected in these patients.
Adult↗
CNQX infused into entorhinal cortex blocks memory expression, and AMPA reverses the effect.
Rats were trained in a step-down inhibitory avoidance task using a 0.8-mA foot shock and tested for retention 26 days later. Three to five days prior to the retention test they were bilaterally implanted with cannulae aimed at the entorhinal cortex. Ten minutes before testing they received an infusion, into the entorhinal cortex, of vehicle, ciano-nitro-quinoxaline-dione (CNQX; 0.5 micrograms), amino-hydroxy-methyl-isoxalone-propionate (AMPA; 1.0 or 2.5 micrograms), or AMPA (1.0 micrograms) plus CNQX (0.5 micrograms). CNQX blocked memory expression; the effect lasted less than 90 min. AMPA had no effect of its own, but at the lower dose level it counteracted the depressant influence of CNQX. It is not likely that the effect of CNQX could have been due to an influence on performance: In separate sets of experiments the bilateral intraentorhinal infusion of CNQX (0.5 micrograms) 10 min before training did not affect either acquisition or retention of the avoidance task or general activity during 3 min of free exploration in the training box. The results indicate that the integrity of AMPA receptors in the entorhinal cortex is necessary for memory expression.
6-Cyano-7-nitroquinoxaline-2,3-dione↗
Effect of antagonists of platelet-activating factor receptors on memory of inhibitory avoidance in rats.
Platelet-activating factor (PAF) is present in the brain. It enhances glutamate release and long-term potentiation (LTP) through an action on synaptic membrane receptors sensitive to the antagonist, BN 52021, and has been proposed as a retrograde messenger in the genesis of LTP. In addition, PAF has other, metabolic actions mediated by microsomal receptors sensitive to the antagonist, BN 50730. We investigated the effect on memory of the pre- or post-training infusion of BN 52021 or BN 50730 into the hippocampus and that of BN 52021 in the amygdala and the entorhinal cortex. Male Wistar rats were implanted bilaterally with cannulae aimed at these brain regions. After recovery from surgery, the animals were trained in step-down inhibitory avoidance using a 0.5-mA foot shock and tested for retention 24 h later. BN 52021 (0.5 microgram/side) was amnestic when given into the hippocampus or the amygdala either before or immediately after training but not 30 or 100 min later. BN 52021 was also amnestic when given into the entorhinal cortex 100 but not 0 or 300 min after training. Intrahippocampally administered BN 50730 had no effect on memory. The findings are compatible with the suggestion from previous findings that memory of this task depends on the generation of LTP at the time of training in hippocampus and amygdala and, 90-180 min later, in the entorhinal cortex.
Amygdala↗
Post-training intrahippocampal infusion of protein kinase C inhibitors causes amnesia in rats.
This experiment investigated the effect on memory, in rats, of the bilateral intrahippocampal post-training infusion of two different inhibitors of protein kinase C activity, staurosporin and CGP41231. Male Wistar rats were implanted bilaterally with cannulae aimed at the CA1 region of the dorsal hippocampus. After recovery from surgery, they were trained in step-down inhibitory avoidance using a 0.5-mA footshock and tested for retention 24 h later. Immediately or 30, 120, or 180 min after training they received, through the cannulae, infusions of vehicle, staurosporin (1.0 microgram), or CGP41231 (2.5 micrograms). The two drugs caused full retrograde amnesia when given immediately or 30 min post-training, partial amnesia when given 120 min after training, and had no effect when given 180 min after training. The results support the suggestion that memory involves long-term potentiation initiated at the time of training in the hippocampus. Inhibitors of protein kinase C block the development of long-term potentiation when administered in the first 2 h after induction.
Alkaloids↗
Effect of the infusion of the GABA-A receptor agonist, muscimol, on the role of the entorhinal cortex, amygdala, and hippocampus in memory processes.
Rats were bilaterally implanted with cannulae in the entorhinal cortex, amygdala, and hippocampus; after recovery, they were trained in a step-down inhibitory avoidance task and tested for retention 24 h later. Muscimol (0.03 microgram) or D-amino-5-phosphonovalerate (5.0 micrograms) infused in the entorhinal cortex 20 min prior to training inhibited the amnestic effect of the same dose of muscimol infused into this area 100 min after training. Thus, memory-relevant information must be processed by the entorhinal cortex at the time of training in order that this cortex may play a late post-training role in memory processing. Pretraining intraentorhinal muscimol administration did not affect the amnestic effect of the post-training infusion of muscimol into the amygdala and hippocampus, or the inhibition of memory expression induced by a pretest infusion of CNQX into the amygdala and hippocampus or into the entorhinal cortex. Pretest intraentorhinal muscimol also did not influence the effect of pretest intra-amygdala and intrahippocampal CNQX administration. These data indicate that the cells of the entorhinal cortex that are sensitive to pretraining muscimol are not part of the inputs that lead to post-training processing by the amygdala and hippocampus, or to the intervention of the amygdala, hippocampus, and entorhinal cortex in memory expression. The present findings are compatible with the possibility that, instead, the entorhinal cortex may be an output of the amygdala and hippocampus at the time of memory expression.
2-Amino-5-phosphonovalerate↗
Memory processing by the limbic system: role of specific neurotransmitter systems.
Experiments using localized infusions into selected brain structures of agonists and antagonists of various synaptic receptors, given before or after behavioral training, have led to the following conclusions: (1) Memory is processed shortly after training in the amygdala, medial septum and hippocampus by glutamatergic NMDA and AMPA receptors activated in that sequence. Cholinergic muscarinic receptors are activated concurrently with the former. GABAA receptors modulated by brain benzodiazepines and by beta-noradrenergic receptors inhibit the process. (2) The sequential involvement of NMDA and AMPA receptors suggests that long-term potentiation (LTP) of the synapses activated by the learning experiences in the hippocampus and/or amygdala and medial septum is the crucial event. Expression of this LTP at the time of testing is necessary for retrieval: AMPA receptor blockade in the hippocampus and amygdala at the time of testing hinders retrieval. This suggests that the LTP underlies the memory process itself. (3) The amygdala, medial septum and hippocampus mediate different types of memory and/or different components of memories. The entorhinal cortex, through mechanisms that require intact NMDA receptors and are inhibited by GABAA receptors, intervenes in post-training memory processing 90-180 min after the other limbic regions. The entorhinal cortex integrates consecutively acquired memories; this role could be maintained by the LTP that is generated after training in the amygdala, hippocampus and medial septum. Post-training intervention of the entorhinal cortex does not occur if this region is inhibited at the time of training.
Animals↗
A peptide muscarinic toxin from the Green Mamba venom shows agonist-like action in an inhibitory avoidance learning task.
A peptide, muscarinic toxin 2 (MTX2), isolated from Dendroaspis angusticeps venom was previously shown to displace the specific binding of [3H]pirenzepine, a muscarinic M1 receptor ligand, from rat brain synaptosomal membranes. We have tested MTX2 for muscarinic agonist or antagonist actions in an inhibitory avoidance task in rats. Infusion of the muscarinic receptor antagonist scopolamine into the hippocampus of rats immediately after the training period produced amnesia, whereas the muscarinic agonist oxotremorine increased retention. When MTX2 was injected into the hippocampus of rats after the inhibitory avoidance task, it caused memory facilitation, which could be suppressed by the concomitant infusion of scopolamine. Hence, in this test, MTX2 showed muscarinic receptor agonist-like actions, which are probably mediated by the M1 subtype of muscarinic acetylcholine receptors.
Animals↗
Memory expression is blocked by the infusion of CNQX into the hippocampus and/or the amygdala up to 20 days after training.
Bilateral infusion of CNQX (0.5 microgram) into the amygdala and the dorsal hippocampus prior to a retention test blocked the expression of step-down inhibitory avoidance in rats 6, 13, or 20 days after training. Retention test performance recovered 90 min after the infusions. Pretest intrahippocampal CNQX (0.5 microgram) blocked the expression of habituation to a novel environment measured 20 days after training. The data suggest that memory expression depends on non-NMDA receptor-mediated mechanisms, perhaps the expression of LTP, up to at least 20 days after acquisition. These mechanisms operate in the hippocampus in both tasks and in the amygdala in the avoidance task.
Amygdala↗
CNQX infused into rat hippocampus or amygdala disrupts the expression of memory of two different tasks.
The bilateral infusion of CNQX (0.5 or 1.25 micrograms) into the amygdala or dorsal hippocampus 10 min prior to a retention test partially blocked the expression of stepdown inhibitory avoidance in rats 24 h after training. When infused into both the amygdala and the hippocampus at a dose of 0.5 microgram. CNQX caused a complete blockade of the expression of that task. Retention test performance recovered 2 h after the infusions. In rats trained for habituation to a novel environment and tested 24 h later, pretest intrahippocampal CNQX (0.5 microgram) blocked the expression of retention at a dose of 0.5 microgram, and intra-amygdala CNQX (0.5 or 1.25 micrograms) had no effect. The data suggest that, up to at least 1 day after training, memory of the avoidance task depends on glutamate acting on non-NMDA receptors in both the hippocampus and the amygdala, whereas memory of the habituation task depends on non-NMDA receptor activity in the hippocampus but not the amygdala.
6-Cyano-7-nitroquinoxaline-2,3-dione↗
Amnesia by post-training infusion of glutamate receptor antagonists into the amygdala, hippocampus, and entorhinal cortex.
The blockers of glutamate receptors, aminophosphonovaleric acid (AP5) (5.0 micrograms) and cyano-nitroquinoxaline-dione (CNQX) (0.5 microgram), were infused bilaterally into the amygdala, dorsal hippocampus, or entorhinal cortex of rats through indwelling cannulae 0, 90, 180, or 360 min after step-down inhibitory avoidance training. Animals were tested for retention 24 h after training. In the amygdala or hippocampus, AP5 was amnestic when given 0 min after training and CNQX was amnestic when given 0, 90, or 180 min after training. In the entorhinal cortex, AP5 was amnestic when given 90 or 180 min after training and CNQX had no effect. The results suggest that a phenomenon sensitive first to AP5 and then to CNQX in the amygdala and hippocampus, probably long-term potentiation (LTP), is crucial to post-training memory processing. LTP in these two structures could underlie their role in memory consolidation and could explain the late involvement of the entorhinal cortex in post-training memory processing.
Amnesia, Retrograde↗