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)

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

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

A 43-year-old male patient with recurring impaired consciousness and retrograde amnesia was admitted to the department of neurology. During the neurological evaluation no pathological findings could initially be revealed but one day the patient was confused again and presented with inadequate behavior: at this time a blood glucose value of 40 mg/dl was measured. For further evaluation the patient was transferred to our department. As the reason for the impaired consciousness was suspected to be of neuroglucopenic origin a rapid adrenocorticotropic hormone (ACTH) stimulation test was first performed to rule out adrenal insufficiency. For further evaluation a fasting test was conducted: after 48 h an episode with neuroglucopenic symptoms occurred again which disappeared after intravenous administration of glucose. The laboratory results of glucose, insulin and c-peptide determined at this point in time led to the diagnosis of an insulinoma. By ultrasound examination a hypoechogenic lesion 1.5 cm in size could be shown in the head of the pancreas and was confirmed by magnetic resonance imaging (MRI). After duodenum-preserving partial pancreatic head resection with enucleation of the insulinoma no further neuroglucopenic symptoms occurred.
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PMID:[A 43-year-old patient with character changes, recurrent impaired consciousness and retrograde amnesia]. 2442 40


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