Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002622 (amnesia)
 5,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ACTH 4-9 analog, H-Met((O2)-Glu-His-Ph-D-Lys-Phe-OH (Or 2766), attenuates in rats CO2-induced amnesia for a one-trial passive avoidance step-through response when administered prior to the retrieval test but not when given prior to acquisition. Even a dose of 0.001 mug/rat Org 2766 yields an anti-amnesic effect. In this respect Org 2766 is more active than the ACTH fragment ACTH 4-10. An anti-amnesic effect was also obtained when Org 2766 was administered orally. ACTH 4-10 (100 mug/rat) has to be given SC within 8 hr of the retrieval test in order to be effective. A similar time span of effectiveness was observed when Org 2766 was SC injected in a dose of 0.1 mug/rat. The anti-amnesic effect of ACTH 4-10 remains when the time interval between acquisition and retrieval is extended beyond the usual 24 hr. The same appeared to be true for SC ADMINISTERED Org 2766. It is suggested that ACTH-like peptides, and particularly the orally active Org 2766, may be helpful in the treatment of deficient mental performance.
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PMID:Reversal of amnesia by an orally active ACTH 4-9 analog (Org 2766). 18 32

Application of footshock during the acquisition trial of a one-trial passive avoidance test is associated with a rise in the concentration of serotonin in the hippocampi of rats 24 hr after termination of the acquisition trial. Rats subjected to amnesic treatment with carbon dioxide (CO2) immediately after footshock do not show this rise in the hippocampal concentration of serotonin. The ACTH-analogues, ACTH 4-10 and ACTH 4-10 (7D-Phe), alleviate CO2-induced amnesia for the passive avoidance response when administered 1 hr before retrieval test 24 hr after acquisition. These peptides do not have anti-amnesic activity when given before acquistion. Another ACTH-analogue, ACTH 11-24 does not affect amnesia, given before either the acquisition or the retrieval test. The anti-amnesic effect of ACTH 4-10 AND ACTH 4-10 (7D-Phe), was correlated with a rise in the hippocampal serotonin concentration similar to that observed in non-amnesic animals. Pre-acquisition treatment with ACTH 4-10 or administration of ACTH 11-24 did not affect hippocampal serotonin concentrations. Changes in the hippocampal concentrations of noradrenaline, dopamine, tryptophan and tyrosine were not related to the behavioural activity of any of the peptides. It is suggested that alterations in hippocampal serotonin metabolism 24 hr after acquisition of a passive avoidance response are associated with the retrieveability of the passive avoidance response.
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PMID:Parallel changes in behaviour and hippocampal monoamine metabolism in rats after administration of ACTH-analogues. 20 81

Pituitary hormones profoundly influence behavior through direct actions on the brain. One of these behavioral effects is the attenuation of experimental amnesia. Traditionally, amnesia is considered as a "loss of memory." Memory comprises at least 2 stages: input (memory consolidation) and output (memory retrieval). Theoretically, disturbance of either aspect of memory may be the cause of amnesia. Also, it is possible that amnesia is based on a factor or factors not related to memory. Data and theories on amnesia in man were reviewed. Some salient features were mentioned: (1) amnesia can be induced by a variety of agents; (2) amnesia covers periods ranging from seconds to years; (3) amnesia gradients can be established; (4) amnesia is to a large extent reversible. From this survey, it seems possible that amnesia is not a homogeneous phenomenon and that even in one person a disturbance of both memory consolidation and memory retrieval may be produced by one and the same event. Animal studies in general have confirmed these conclusions. We have developed an animal model in order to study the effects of pituitary peptides on amnesia. This model is based on CO2-induced amnesia for a one-trial passive avoidance response in rats. This amnesia could be attenuated by treatment with ACTH-analogs 1 hour before the retrieval test. This anti-amnesic effect of ACTH-analogs was not dependent on the nature of the behavioral response or the amnesic treatment. The vasopressin-analog DGLVP similarly exerted an anti-amnesic effect when injected before the retrieval trial. In contrast to ACTH-analogs, however, it also reduced the amnesia when injected before acquisition. These results suggest that amnesia may comprise a "faulty-consolidation" and a "faulty-retrieval" component, which may be amended by different pituitary hormones. The study of the anti-amnesic activity of peptides therefore not only serves to characterize the nature of the behavioral effect of these peptides but may also prove to be helpful of the unraveling of processes involved in amnesia.
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PMID:Pituitary hormones and amnesia. 21 89

Application of a foot shock during the acquisition trial of a one-trial passive avoidance task is associated with a rise in the concentration of serotonin in the hippocampus 24 h after conclusion of the acquisition trial. Carbon dioxide (CO2) induces amnesia for the passive avoidance response when administered immediately upon termination of the acquisition trial. In rats subjected to CO2 treatment following foot shock the rise in hippocampal serotonin is not observed 24 h later. The vasopressin analogue desglycinamide lysine vasopressin attenuates CO2-induced amnesia for the passive avoidance response when given prior to either the acquisition or the retrieval test (24 h after acquisition). This attenuation of the passive avoidance response is associated with a rise in the hippocampal serotonin concentration similar to the one observed in non-amnesic animals. It is suggested that a correlation exists between changes in hippocampal serotonin metabolism and the retrievability of the passive avoidance response.
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PMID:Parallel changes in behaviour and hippocampal serotonin metabolism in rats following treatment with desglycinamide lysine vasopressin. 55 78

It was found that in rats a gradient of retrograde amnesia for a passive avoidance response could be established when carbon dioxide (CO2) was used as the amnesic agent. The extent of passive avoidance increased as the period between application of a mild foot shock and CO2 treatment was increased. The amnesia gradient was found to cover a period of at least 60 min. Changes in hippocampal serotonin metabolism parallelled the amnesia gradient. Thus, the concent increased. The changes in hippocampal noradrenaline and dopamine did not correlate with the amnesia gradient.
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PMID:Hippocampal monoamine metabolism and the CO2 induced retrograde amnesia gradient in rats. 123 73

The time course of amnesia for a one-trial passive avoidance response after treatment with carbon dioxide (CO2) was studied. Amnesia developed gradually over the first 4 hr following the amnesic treatment. Once established, amnesia remained during a 4 week test period. Previously, we reported that acquisition of the passive avoidance response was attended with a rise in the hippocampal concentration of serotonin 24 hr later and that this rise was not observed when acquisition was followed by amnesic treatment. In the present study, it was found that a rise in hippocampal serotonin parallelled the transient retention of the avoidance response 2 hr after amnesic treatment. However, 2 weeks after acquisition and amnesic treatment no changes in hippocampal monomine metabolism could be detected. Hippocampal noradrenaline did not correlate with avoidance and amnesia.
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PMID:Time-dependent aspects of CO2 induced amnesia and hippocampal monoamine metabolism in rats. 123 74

The possible anti-amnesic effects of a dibenzoxazepine derivative, BY-1949 (3-methoxy-11-methyldibenz[b,f] [1, 4] oxazepine-8-carboxylate), were examined using the three learning paradigms. In the one-trial passive avoidance task in mice, BY-1949 (1-30 mg/kg, po) and aniracetam (3-30 mg/kg, po) reversed the shortening of the response latency in the retention test produced by exposure to 100% CO2 immediately after the acquisition trial. In the two-way active avoidance task in rats, BY-1949 (10, 30 mg/kg, po) reversed the decreased avoidance rate produced by the hypoxia treatment (5% O2:95% N2). In the radial-arm maze task in rats, BY-1949 (10 mg/kg, po) and aniracetam (10, 30 mg/kg, po) improved the impaired correct choices induced by scopolamine (0.25 mg/kg, ip). These results suggest that BY-1949, as well as aniracetam, exerts some improvement effects on experimental amnesia.
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PMID:[Effects of BY-1949 on three kinds of experimental amnesia in rodents]. 225 78

The side-effects of two opioid agonist-antagonists, nalbuphine and pentazocine, were assessed when used for patient-controlled postoperative analgesia. Forty ASA I or II patients scheduled for upper abdominal surgery were randomly allocated to two equal groups. The anaesthetic technique was the same for all the patients: premedication with atropine and diazepam, induction with thiopentone and suxamethonium and maintenance with fentanyl, pancuronium, nitrous oxide and halothane. Patient-controlled computer assisted analgesia (On-Demand Analgesia Computer) was started in the recovery room at least 2 h after the last administration of fentanyl. The parameters used were: a routine hourly dose (the half of that received during the previous hour), with on demand delivery of nalbuphine (15 micrograms.kg-1) or pentazocine (45 micrograms.kg-1) aliquots respectively, with a refractory period between two demands of 4 min and a total hourly maximum dose of 16 mg and 48 mg respectively. The following parameters were measured before the start of self-administration, and every hour afterwards for 24 h: systolic (Pasys) and diastolic blood pressures, heart rate, pressure-rate product (PRP), respiratory rate, end-tidal CO2 and pain (by way of a three point scale). Analgesia was assessed on a four-point scale every 6 h. The total doses of nalbuphine and pentazocine administered were 94 +/- 43 mg and 251 +/- 150 mg respectively. The only parameters significantly different between the two groups were Pasys and PRP, being higher in the pentazocine group. There were no significant differences in the side-effects (drowsiness, nausea, vomiting, headache, amnesia, logorrhoea and urine retention). All patients in both groups were satisfied with this technique.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Comparison of nalbuphine and pentazocine in the treatment of postoperative pain by self-administration]. 266 Jun 40

The effects of sufoxazine on various experimental amnesia models were studied using passive avoidance behavior in mice. Sufoxazine had no influence on learning and memory in intact mice. Sufoxazine, administered either immediately after CO2 exposure or 30 min prior to the acquisition trial, improved CO2 induced amnesia. It also improved both electroconvulsive shock (ECS) induced amnesia (administered immediately after the amnestic treatment) and scopolamine induced amnesia (administered immediately after the acquisition trial). The anti-depressant drugs, imipramine and desipramine had no ameliorative activity in any of these experimental amnesia models. These results suggest that sufoxazine improves amnesia experimentally induced by various methods.
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PMID:[Pharmacological studies on sufoxazine (Y-8894). (I) Effects on experimental amnesia in mice]. 285 38

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.
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PMID:[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice]. 299 54


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