Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats were submitted to a normal (25% casein) or a low protein diet (8% casein) from the day of birth until the age of 110 to 120 days. Hypothalamic beta-endorphin-like immunoreactivity was lower in the animals raised and maintained with the low protein diet, and, in addition, it did not respond to training in a step-down inhibitory avoidance task with or without footshock with a depletion, as was the case with the normal diet animals. In the animals submitted to the normal protein diet posttraining ACTH (0.2 micrograms/kg) and beta-endorphin (1.0 micrograms/kg) caused retrograde amnesia of a step-down inhibitory avoidance task, and pretest administration of these substances had no effect of its own, but was able to reverse the amnesia induced by their previous posttraining administration. In the animals submitted to the low protein diet, results were similar except that pretest beta-endorphin caused amnesia on its own. On the basis of previous findings which suggest that pretest actions of ACTH and beta-endorphin depend on their endogenous release at the time of training, the present results are compatible with a malfunction of the brain beta-endorphin system in the undernourished animals.
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PMID:Effect of posttraining and pretest beta-endorphin and ACTH administration in normal and protein malnourished rats. 256 Jan 73

Pentylenetetrazol (PTZ, 45 mg/kg, ip) impaired retention of a one-trial step-through inhibitory avoidance task when injected into male Swiss mice 10 min after training, as indicated by retention performance 48 h later. The amnestic effect of PTZ was prevented by naltrexone (0.01 or 0.10 mg/kg, ip) administered after training, but prior to PTZ-treatment. On the contrary, neither naltrexone methyl bromide (0.01, 0.10, or 10.0 mg/kg, ip), a quaternarium analog of naltrexone, nor MR2266 (0.01 or 0.10 mg/kg, ip), a putative kappa opiate receptor antagonist, modified the behavioral effects of PTZ. On the other hand, the body seizures produced by PTZ were unaffected by any of the three opiate receptor antagonists that were given before the convulsant. Taken together, these results suggest that the effects of PTZ on retention are mediated, at least in part, by opioid peptides of central origin, and rules out a possible participation of opioid peptides derived from prodynorphin-precursor molecule. Administration of beta-endorphin (0.01 or 0.10 microgram/kg, ip) 10 min prior to testing attenuate the retrograde amnesia caused by PTZ. The effect of beta-endorphin was prevented by the simultaneous administration of naltrexone (0.10 mg/kg, ip) prior to testing. Naltrexone has no effect of its own upon retrieval. These results suggest that the impairment of retention induced by PTZ is probably due, at least in part, to a release of opioid peptides in the brain during the post-training period. PTZ given after training do not affect consolidation or memory storage, as mice thus treated may retrieve the learned information when they are submitted to an appropriate neurohumoral and/or hormonal state in the test session, that is, beta-endorphin injection. Therefore, the action of PTZ would be primarily at the level of the mechanism that make stored information available for late retrieval.
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PMID:The impairment of retention induced by pentylenetetrazol in mice may be mediated by a release of opioid peptides in the brain. 282 89

Posttraining administration of the opioid peptides, beta-endorphin or the enkephalins, is known to cause retrograde amnesia for a variety of tasks in rats. The present paper studies the effect of the posttraining administration of dynorphin 1-13 on retention of a step-down inhibitory avoidance task and of a shuttle avoidance task. For the purpose of comparison, the effect of human beta-endorphin was also studied. In confirmation of previous results, beta-endorphin (1.0 or 10.0 micrograms/kg, IP) caused retrograde amnesia for the two tasks. Dynorphin 1-13 had no effect at doses between 0.008-125.0 micrograms/kg IP or 1.25-125.0 ng/rat ICV in the inhibitory avoidance task, or at doses of 5.0, 25.0, or 125.0 micrograms/kg in the shuttle avoidance paradigm. These findings suggest that, in contrast to beta-endorphin, dynorphin 1-13 may not be involved in memory regulation at the posttraining period in rats.
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PMID:Unlike beta-endorphin, dynorphin 1-13 does not cause retrograde amnesia for shuttle avoidance or inhibitory avoidance learning in rats. 286 14

Rats were trained and tested in an open field for habituation of rearing responses, for a water-finding task, or for both tasks simultaneously. Training-test interval was 24 hr. The water-finding task consisted of locating a metal tube in one of the walls of the box, which was attached to a water bottle on the outside; animals were water deprived between training and testing. Retention was estimated by measuring the latency to lick from the tube on the test session. Rats learned this task either with or without water deprivation, also prior to training. Habituation learning (reduction of the number of rearings between the training and test session) occurred either simultaneously with the water-finding task or in animals trained without the water tube, so that they could not learn the water-finding task. As happens with many other tasks, training in the open field was followed by a large decrease of hypothalamic beta-endorphin immunoreactivity, attributable to a release of this substance. Posttraining IP naloxone (1.6 mg/kg) administration facilitated, and posttraining beta-endorphin (2.0 micrograms/kg), leu-enkephalin (5.0 micrograms/kg), or electroconvulsive shock (15 mA, 60 Hz, 2 sec) depressed the retention of habituation; this occurred regardless of whether the animals were trained and/or tested with or without water deprivation, and whether the task was acquired alone or simultaneously with the water-finding task. By contrast, none of these treatments had any effect on retention of the water finding task, acquired either with or without prior water deprivation. Thus, habituation was, and water-finding was not, sensitive to posttraining treatments known to affect endogenous opioids: the opioids themselves, their antagonist, naloxone, and electroconvulsive shock which releases brain opioids and causes naloxone-reversible retrograde amnesia. Learning of the water-finding task was merely incidental to exploration of the open field; it took place even when the animals were trained without the water tube. This suggests that the posttraining treatments that affect endogenous opioid function affect memory only of the task(s) that actually cause the release of brain beta-endorphin (in this case, probably habituation), and not of others that may occur simultaneously but are merely incidental (water-finding). A feature apparently common to the former is that they must directly involve either the recognition of novelty, or the initiation of an interaction with a new environment, or perhaps the habituation of such interaction.
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PMID:Differential effect of posttraining naloxone, beta-endorphin, leu-enkephalin and electroconvulsive shock administration upon memory of an open-field habituation and of a water-finding task. 295 61

Beta-Endorphin-like immunoreactivity is reduced in the rat diencephalon after the animals are exposed for the first time to any of the following behavioral situations: 50 tones (habituation), 50 tone-footshock shuttle avoidance trials, one step-down inhibitory avoidance trial, simple exposure to the avoidance apparatus with no footshocks, or inescapable shock. The effect is not observed when animals are exposed to any of these situations for a second time. The reduction of brain beta-endorphin-like immunoreactivity is attributable to release and subsequent metabolism of the substance, and correlates with the novelty inherent in the diverse training or test situations. The role of beta-endorphin in behavior is discussed in the light of these and previous results which showed that it causes both retrograde amnesia and a facilitation of retrieval. The substance would appear to serve an adaptive function when animals are exposed to a new experience, by inducing a temporary forgetting of the experience together with (or leading to) a state of alertness or preparedness for what may happen next.
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PMID:Effect of various behavioral training and testing procedures on brain beta-endorphin-like immunoreactivity and the possible role of beta-endorphin in behavioral regulation. 609 11

The endogenous opiate peptide, beta-endorphin (0.4, 1.0, 2.0, and 10.0 microgram/kg) was injected IP into rats immediately after training in a shuttle avoidance task, and its effect on memory retention was evaluated in test sessions carried out 24 h later. The drug was found to cause retrograde amnesia, the ED50 being 1.0 microgram/kg. Beta-endorphin immunoreactivity was measured in the hypothalamus and rest of the brain of rats submitted to training, or test sessions of shuttle avoidance learning, pseudoconditioning in the shuttle-box, tones alone, or foot-shocks alone. After training in any of the four paradigms, there was a marked (46-60%) depletion of beta-endorphin immunoreactivity in the rest of the brain. No changes were detected in the hypothalamus or after test sessions. The loss of beta-endorphin immunoreactivity may be attributed to release of this substance caused by the stimuli used for training. From the present findings, as well as previous observations on the memory-facilitating influence of the opiate receptor antagonist, naloxone, it is concluded that there is a physiological amnesic mechanism mediated by beta-endorphin (and perhaps other opoid peptides as well), which is triggered by the non-associative factors present in the various forms of learning.
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PMID:Beta-endorphin causes retrograde amnesia and is released from the rat brain by various forms of training and stimulation. 625 5

The intracerebroventricular (icv) administration of 5.0 or 25.0 ng of beta-endorphin or Met-enkephalin causes retrograde amnesia for a shuttle avoidance task ion rats. In both cases, the higher dose was more effective than the lower one. The present results confirm previous similar findings obtained using systemic administrations of these compounds, and suggest that the amnestic effect of beta-endorphin and Met-enkephalin is mediated centrally.
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PMID:Intracerebroventricular administration of nanogram amounts of beta-endorphin and Met-enkephalin causes retrograde amnesia in rats. 627 67

The ip administration of ACTH1-24 (0.2 microgram/kg) or adrenaline-HCl (5.0 micrograms/kg) immediately after training or 6 min prior to testing facilitated retrieval of a one-trial step-down inhibitory avoidance task in rats, acquired using a low intensity footshock. Post-training administration of beta-endorphin (0.1 micrograms/kg, ip) caused retrograde amnesia, but pre-test administration facilitated retrieval. The amnesia caused by post-training administration of beta-endorphin was prevented by ACTH, adrenaline or beta-endorphin given prior to testing. Memory facilitation was most pronounced when the same drug was administered both after the training session and prior to testing. These findings suggest that ACTH, adrenaline and beta-endorphin have at least two effects on memory processing: 1) during the post-training period on the entry of recently stored information into a system that makes it available for retrieval; and 2) both after training and during the test session, that makes learning dependent on states induced by the drugs.
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PMID:Memory modulation by the administration of ACTH, adrenaline or beta-endorphin after training or prior to testing in an inhibitory avoidance task in rats. 632 41

The post-training administration of ACTH1-24 (0.2 microgram/kg), human beta-endorphin (1.0 microgram/kg) or epinephrine HC1 (5.0 micrograms/kg), intraperitoneally, caused retrograde amnesia for a step-down inhibitory avoidance task in rats, and their pre-testing administration reversed this effect. The concomitant administration of the alpha 2-adrenergic receptor blocker, yohimbine HC1 (2.0 mg/kg), antagonized both the post-training amnestic and the pre-testing anti-amnestic effects of the three substances. The anti-amnestic effect of epinephrine, but not that of ACTH or beta-endorphin, was also antagonized by the alpha 1-adrenergic receptor blocker, prazosin HC1 (2.0 mg/kg). These findings suggest that alpha 2-adrenergic receptors are involved both in the amnestic and in the anti-amnestic effect of ACTH, beta-endorphin and epinephrine at the doses used, and that, in the case of the anti-amnestic effect of epinephrine, alpha 1 receptors also are involved. It seems likely that memory regulation by post-training and pre-testing ACTH and beta-endorphin requires the concomitant activity of alpha 2-adrenergic mechanisms, either central or peripheral.
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PMID:Involvement of alpha-adrenergic receptors in the amnestic and anti-amnestic action of ACTH, beta-endorphin and epinephrine. 633 Jul 84

Electroconvulsive shock (ECS) is used in the treatment of depression and causes antero- and retrograde amnesia as a side effect. One of the many neurochemical effects of ECS is depletion of brain beta-endorphin and Met-enkephalin. These two opioid peptides cause antero- and retrograde amnesia also. Naloxone antagonizes the amnestic effect of ECS and of the opioid peptides. Thus, it is possible that the amnestic effect of ECS is mediated by an endogenous release of the peptides. Surgical posterior hypothalamic deafferentation, but not anterior deafferentation or fornix transection, abolishes the amnestic effect of ECS. This suggests that the hyperactivation of endogenous opioid systems by ECS that leads to amnesia is mediated by posterior ascending fibers to the hypothalamus. The relevance of these considerations to the treatment of depression merits investigation.
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PMID:Amnesia as a major side effect of electroconvulsive shock: the possible involvement of hypothalamic opioid systems. 652 15


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