Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An experimental model of amnesia induced by cerebral ischemia after one-trial passive avoidance learning was established to test the effects of a novel compound, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619), and some commonly used drugs in rats. One day after the vertebral artery was electrocauterized bilaterally, the common carotid artery was transiently occluded bilaterally to produce cerebral ischemia. The amnesia was estimated by the response latency for a rat to step from a light safety compartment to a dark compartment in which a foot-shock was given. The results of the retention test given 24 hr after the ischemia indicated that amnesia was successfully produced when the 200-600 sec ischemia was provided within 20 min after the avoidance learning. The effects of drugs on the amnesia induced by a 200-sec ischemia immediately after the avoidance learning were as follows: CV-2619 (10, 30 mg/kg, i.p. or p.o.) given before the retention test significantly increased the response latency, indicating a reversal effect on the amnesia. Physostigmine (0.1, 0.2 mg/kg, i.p.) and arginine-vasopressin (10 micrograms/kg, s.c.) were also effective, and calcium hopantenate (500 mg/kg, p.o.) showed a slight reversal action. Furthermore, CV-2619 (10 mg/kg, i.p.), given before or after the ischemia, significantly inhibited the appearance of amnesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effect of idebenone (CV-2619) on cerebral ischemia-induced amnesia in rats. 654 47

Amnesia in mice for a passive avoidance response induced by anisomycin injection immediately after training was reversed by 40 micrograms of lysine-vasopressin given one hour before testing. Control groups receiving non-contingent shock instead of training were used to demonstrate that the effects of vasopressin were due to memory of shock received in a particular place, rather than non-specific suppression of locomotion. The effects of vasopressin on retention were not mimicked by either pentylenetetrazol or epinephrine suggesting that the enhanced latencies were probably not the result of increases in fear or arousal. These data support the hypothesis that the retrieval of memory can be facilitated by vasopressin. The possibility of a relationship between the effects of vasopressin and those of catecholamine manipulations on memory is discussed.
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PMID:Alleviation of anisomycin-induced amnesia by pre-test treatment with lysine- vasopressin. 707 82

[Ile3, Arg8]vasopressin (arginine-vasotocin), as well as the C-terminal tripeptides of the neurohypophyseal hormones arginine and lysine vasopressin, Pro-Arg-Gly-NH2 and Pro-Lys-Gly-NH2, were protective against puromycin-induced amnesia in mice when administered 24h before training. The N-protected tripeptide derivative, Z-Pro-Lys-Gly-NH2, was effective when given 5 days before training. The effectiveness of all peptides to attenuate puromycin-induced amnesia decreased as the interval between training and peptide treatment increased, indicating that the peptides influence memory processes, rather than general arousal. Z-Pro-Lys-Gly-NH2 was active at 24h after training, when the other peptides were no longer effective. Although it seems clear that neurohypophyseal hormones per se can attenuate puromycin-induced amnesia, these results are in line with the possibility that some portion of hormone action may be mediated via formation of longer-lived hormone fragments in the CNS.
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PMID:Time-dependency of neurohypophyseal peptide attenuation of puromycin amnesia in mice. 719 22

Vasopressin and oxytocin of hypothalamic neurosecretory origin affect both consolidation and retrieval of memory but in an opposite manner. Vasopressin facilitates these processes while oxytocin appears to be an amnesic neuropeptide. Additionally, vasopressin and a number of fragments of this peptide are able to prevent but also to reverse experimental amnesia. Structure activity studies suggest that the neurohypophyseal hormones may serve as mothermolecules for behaviorally active peptides which selectively affect consolidation or retrieval processes. The mechanism by which these neuropeptides modulate memory processes is likely an interaction with the impulse flow in aminergic systems in particular in the limbic-midbrain areas. It is suggested that experimental observations may be of predictive value for the clinical use of neuropeptides at memory disturbances.
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PMID:Vasopressin, oxytocin and memory: effects on consolidation and retrieval processes. 723 56

This paper attempts to take a broad view of investigations of brain mechanisms of motivated and emotional behavior in animals and humans. It examines the thesis that the same basic brain mechanisms are involved in physiological regulations, in various motivated behaviors and emotions, and in the hedonic experiences that can be reported by humans. It further suggests that reward and the reinforcement of learning depend on the same brain systems. Finally, it speculates on the possibility that these same brain systems play an important role in the selection of what is learned and in the consolidation, storage, and retrieval of memory. To present this conceptualization, selected experiments in thermoregulatory behavior, electrical self-stimulation of the brain, evoked approach and withdrawal behaviors, and the role of neuropeptides in thirst and hunger are reviewed. In addition, experiments will be discussed in which memory is blocked by puromycin, but in which puromycin-induced amnesia can be prevented by the administration of certain peptides such as vasopressin and some of its fragments. Speculation about the common underlying mechanism and its biological significance in the adaptation of the organism is discussed as are some of the experiments suggested by this line of thinking.
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PMID:Brain mechanisms and hedonic processes. 742 86

JTP-4819 ((S)-2-[[(S)-2-(hydroxyacetyl)-1-pyrrolidinyl]carbonyl]-N- phenylmethyl)-1-pyrrolidinecarboxamide) is a potent (IC50: 0.83 +/- 0.09 nM in rat brain supernatant; 5.43 +/- 0.81 nM in Flavobacterium meningosepticum) and specific inhibitor of prolyl endopeptidase (PEP). JTP-4819 (3 mg/kg p.o.) exhibited a strong and durable ex vivo inhibitory effect on PEP in various regions of the rat brain. In addition, JTP-4819 inhibited the degradation of substance P, arginine-vasopressin, thyrotropin-releasing hormone, neurotensin, oxytocin, bradykinin, and angiotensin II by purified PEP with IC50 values of 9.6, 13.9, 10.7, 14.0, 4.5, 7.6 and 10.6 nM, respectively. In the one-trial passive avoidance test in rats with scopolamine-induced amnesia, JTP-4819 significantly prolonged the retention time when administered orally at doses of 1 and 3 mg/kg 1 hr before acquisition or at 3 and 10 mg/kg 1 hr before retention. In addition, coadministration of JTP-4819 and substance P, arginine-vasopressin or thyrotropin-releasing hormone (at doses at which each drug alone did not prolong the retention time) improved the retention time of rats with scopolamine-induced amnesia. Microdialysis studies demonstrated that JTP-4819 caused a significant increase in ACh release in the frontal cortex and hippocampus of young rats at oral doses of 1 and 3 mg/kg, as well as in both brain regions of aged rats at a dose of 3 mg/kg. These results indicate that JTP-4819 potentiates neuropeptide functions inhibiting PEP, that it activates cholinergic transmission and that it enhances learning and memory.
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PMID:JTP-4819: a novel prolyl endopeptidase inhibitor with potential as a cognitive enhancer. 756 10

We investigated the effect of a single 2 micrograms dose of a vasopressin (AVP) analog, [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on processes of retrieval, consolidation and acquisition of conditioned reflexes in rats with experimentally induced amnesia. The investigated amnesia models were: long term ethanol intoxication, electroconvulsive shocks (ECS), and hypoxia. They all profoundly impaired the learning and memory processes in all tests used. The AVP analog-[d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP facilitated retrieval of passive avoidance in all amnesia models. It improved consolidation of active avoidance of rats previously treated with alcohol, but did not affect the acquisition of active avoidance. [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP lack antidiuretic properties.
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PMID:The effect of vasopressin analog: [d(CH2)(1)5,Tyr(Me)2,delta 3Pro7]AVP on learning and memory processes in rats with experimental amnesia. 840 55

We investigated the effect of a single 2 micrograms dose of vasopressin (AVP) analogue [(CH2)5(1),Tyr(Me)2]AVP on the processes of retrieval of conditioned reflexes in rats with experimentally induced amnesia. The models used were: electroconvulsive shock (ECS) and hypoxia. It severely impaired the memory processes. The AVP analogue [d(CH2)5(1),Tyr(Me)2]AVP facilitated retrieval of passive avoidance in all animals.
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PMID:The effect of vasopressin analogue [d(CH2)5(1),Tyr(Me)2]AVP on memory process in rats with experimental amnesia. 855 14

Prolyl oligopeptidase (EC 3.4.21.26), a widely distributed cytosolic enzyme, cleaves peptidylprolyl peptide and peptidylprolyl amino acid bonds in many neuropeptide substrates. Its action on vasopressin has been proposed as the underlying mechanism accounting for the ability of inhibitors of prolyl oligopeptidase to reverse scopolamine-induced amnesia in rats. Future behavioral studies would be facilitated by the availability of potent inhibitors readily synthesized from common intermediates. A series of Fmoc-aminoacylpyrrolidine-2-nitriles prepared by a simple two-step synthesis were found to be potent noncompetitive inhibitors of the rabbit brain enzyme. The most potent inhibitors, Fmoc-prolyl-pyrrolidine-2-nitrile and Fmoc-alanyl-pyrrolidine-2-nitrile, each have a Ki of 5 nM. The compounds are cell permeable and stable. They do not inhibit the related enzyme dipeptidyl peptidase IV (EC 3.4.14.5). When administered intraperitoneally to mice, Fmoc-alanyl-pyrrolidine-2-nitrile crosses the blood-brain barrier to inhibit brain prolyl oligopeptidase. The ease of synthesis, potency, efficacy in vivo, stability, and specificity of Fmoc-aminoacylpyrrolidine-2-nitriles may make them inhibitors of choice in studies probing the physiological significance of prolyl oligopeptidase.
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PMID:Inhibition of prolyl oligopeptidase by Fmoc-aminoacylpyrrolidine-2-nitriles. 878 42

Retrograde amnesia was induced in rats trained in step-down inhibitory avoidance by four different treatments: an ip injection of beta-endorphin (1.0 microgram kg), an electroconvulsive shock (ECS), an intrahippocampal infusion of the calcium/calmodulin protein kinase II inhibitor, KN62 (0.08 microgram/side), given 0 h after training, or an intrahippocampal infusion of the protein kinase A inhibitor, KT5720 (0.5 microgram/side), given 3 h after training. Pretest ip injections of ACTH (0.2 microgram/kg) or vasopressin (10.0 micrograms/kg), but not saline, reversed the amnesia caused by beta-endorphin and ECS but not that caused by the enzyme inhibitors. This suggests that the amnesia produced by intrahippocampal KN62 and KT5720 administration is stronger than that caused by ECS and beta-endorphin, possibly because the former interfere directly with specific steps of the core biochemical chain of events that underlies memory consolidation.
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PMID:Systemic administration of ACTH or vasopressin reverses the amnestic effect of posttraining beta-endorphin or electroconvulsive shock but not that of intrahippocampal infusion of protein kinase inhibitors. 932 61


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