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

The post-training amnestic effect of ACTH, beta-endorphin, adrenaline or tyramine on a step-down inhibitory avoidance task in rats was reversed by the administration of the same drugs prior to testing. Each drug was more effective as an anti-amnestic agent when the amnesia was induced by post-training administration of the same drug than of one of the others. alpha 2-Adrenergic receptors were shown to be involved in the amnestic and anti-amnestic actions of all the drugs and alpha 1 receptors to be involved in the anti-amnestic action of adrenaline and tyramine. These findings support the concept that memory depends on the relationship between the neurohumoral and hormonal states both after training and at the time of testing. These drugs would have limited value as contextual cues, and the mechanisms sensitive to their influence should be those involved in the availability of stored information for retrieval.
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PMID:Endogenous state-dependency:memory regulation by post-training and pre-testing administration of ACTH, beta -endorphin, adrenaline and tyramine. 631 15

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

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

1. Post-training administration of the opiate receptor antagonist naloxone facilitates the memory consolidation of a wide variety of tasks by rats. 2. Post-training administration of subanalgesic doses of beta-endorphin causes retrograde amnesia. This effect is shared by other opiates and opioids and is competitively antagonized by naloxone. These other opiates and opioids probably act by the release of endogenous beta-endorphin. 3. During various forms of aversive and non-aversive training beta-endorphin (but not Met-enkephalin) is released in the rat brain in amounts compatible with amnestic doses of this substance. 4. A number of treatments that cause naloxone-reversible retrograde amnesia, i.e. high doses of ACTH or adrenaline, low doses of morphine or of opioids, electroconvulsive shock, release massive amounts of beta-endorphin and Met-enkephalin in the rat brain. 5. These findings point to the existence of a physiological amnesic mechanism mediated by beta-endorphin, and perhaps other opioids as well, that normally prevents memory from being as good as it could be, and when operating at an exaggerated level may cause complete amnesia. 6. This mechanism interacts with other systems that influence memory consolidation (central dopaminergic and noradrenergic pathways, ACTH, peripheral adrenaline) and is a powerful modulator of their activity. 7. One possible role of the amnesic mechanism during training is to cause the rapid forgetting of adventitious learning that may interfere with acquisition of the main tasks for which animals are being trained. 8. Either through this action, or by some direct effect, beta-endorphin facilitates retrieval of a variety of behaviors in the rat when given before a test session.
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PMID:The role of an endogenous amnesic mechanism mediated by brain beta-endorphin in memory modulation. 675 90

Histamine administered intraperitoneally increased, in a dose-dependent manner, AVP, OXT and PRL levels in plasma of rats, whereas alpha-MSH levels were not affected. Levels of AVP in plasma after histamine 20.0 mg/kg treatment were approximately 100-fold higher than those of controls, while OXT and PRL levels were approximately 7-fold higher after this treatment. CSF content of AVP, OXT, PRL and alpha-MSH was not influenced by histamine, indicating that a stimulated release of hormones from the pituitary into the blood is not accompanied by a concomitant increase of secretion of these hormones into the CSF. Convulsions induced by pentylenetetrazol were accompanied by a temporary increase in AVP levels and by strongly and consistently elevated OXT levels in plasma. PRL and alpha-MSH plasma levels were affected in a biphasic manner. A convulsion type 1 induced elevated PRL levels and diminished alpha-MSH levels, while a convulsion type 2 had no effect on plasma PRL concentration, but increased the concentration of alpha-MSH. Only the level of OXT in CSF was increased after a pentylenetetrazol-induced convulsion type 1. The present data suggest that histamine affects the release of AVP, while pentylenetetrazol might act more specifically on the OXT-releasing system. Furthermore, a possible relationship between the pentylenetetrazol-induced increase of OXT levels in the CSF and amnesia is suggested.
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PMID:Hypophyseal hormone levels in blood and cerebrospinal fluid in response to histamine and pentylenetetrazol. 715 99

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

Interleukin-1beta (IL-1beta) significantly influences memory consolidation. Treatments that raise the level of IL-1beta in the brain, given after training, impair contextual fear conditioning. The melanocortin alpha-MSH exerts potent anti-inflammatory actions by physiologically antagonizing the effect of pro-inflammatory cytokines. Five subtypes of melanocortin receptors (MC1R-MC5R) have been identified, with MC3R and MC4R predominating in the central nervous system. The present experiments show that injection of IL-1beta (5 ng/0.25 microl) in dorsal hippocampus up to 15 min after training decreased freezing during the contextual fear test. The treatment with IL-1beta (5 ng/0.25 microl) 12h after conditioning cause amnesia when animals were tested 7 days post training. Thus, our results also demonstrated that IL-1beta can influence persistence of long-term memory. We determined that animals previously injected with IL-1beta can acquire a new contextual fear memory, demonstrating that the hippocampus was not damaged. Treatment with alpha-MSH (0.05 microg/0.25 microl) blocked the effect of IL-1beta on contextual fear memory. Administration of the MC4 receptor antagonist HS014 (0.5 microg/0.25 microl) reversed the effect of alpha-MSH. However, treatment with gamma-MSH (0.5 microg/0.25 microl), an MC3 agonist, did not affect IL-1beta-induced impairment of memory consolidation. These results suggest that alpha-MSH, through central MC4R can inhibit the effect of IL-1beta on memory consolidation.
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PMID:Memory impairment induced by IL-1beta is reversed by alpha-MSH through central melanocortin-4 receptors. 1927 30

Previous exposure to the training context disrupts glutamatergic N-methyl-d-aspartate receptor (NMDAr) antagonist-induced amnesia, indicating that novelty is necessary for such an amnestic effect. While there are reports that novelty-related release of opioids cause amnesia, no study has addressed whether the amnestic effect of NMDAr antagonists involve opioid mechanisms. In this study we investigated whether pharmacological manipulation of the opioid system immediately after context pre-exposure alters the amnestic effect of arcaine, a NMDAr antagonist. Adult male Wistar rats were habituated (pre-exposed) to a fear conditioning training apparatus or to a different context (open field). Immediately after pre-exposure, animals were injected with saline or naloxone (0.5 mg/kg, i.p.) or anti-beta-endorphin antibody (1:500, i.c.v.). Forty eight hours after pre-exposure session, all animals were subjected to fear conditioning acquisition protocol and saline or arcaine (30 mg/kg, i.p.) was administered immediately after training. Testing was carried out 24 h later, and freezing responses due to re-exposure to the training apparatus were recorded. Pre-exposure to the training apparatus prevented the impairment of memory induced by post-training arcaine. Administration of naloxone or anti-beta-endorphin antibody, immediately after pre-exposure to the training apparatus, reinstated the amnesic effect of post-training arcaine. The results suggest that endogenous opioid mechanisms are involved in the pre-exposure-induced loss of the amnestic effect of arcaine.
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PMID:Opioid mechanisms are involved in the disruption of arcaine-induced amnesia by context pre-exposure. 2239 Aug 58


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