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)

The effect of beta-endorphin on spatial working memory was examined following microinfusions of beta-endorphin into the medial septal area and central amygdaloid nucleus in Long-Evans male rats. Working memory was assessed by spatial alternation in a T-maze. beta-Endorphin, 250 and 1000 ng/site, respectively, and muscimol, 20 ng/site, were infused into the medial septal area or central amygdaloid nucleus prior to behavioral testing. The hippocampal theta rhythm was examined following intraseptal infusions of beta-endorphin and muscimol. In the medial septal area, beta-endorphin and muscimol impaired choice accuracy and reduced the power of hippocampal theta rhythm. The degree of reduction in the power of hippocampal theta rhythm was correlated with the magnitude of behavioral impairment of choice accuracy in spatial alternation. In the central amygdaloid nucleus, beta-endorphin (1000 ng) and muscimol (20 ng) did not affect choice accuracy. The results suggest that septal, but not amygdaloid, opioid, and GABAergic activity modulate spatial working memory and hippocampal physiology.
Neurobiol Learn Mem 1995 Jan
PMID:Opioid modulation of working memory: intraseptal, but not intraamygdaloid, infusions of beta-endorphin impair performance in spatial alternation. 766 81

These experiments examined the effects on memory in two tasks, inhibitory avoidance and water-maze spatial learning, of intraamygdala injections of drugs affecting noradrenergic and opiate receptors. Male Sprague-Dawley rats (180 g, 50 days old on arrival) were given either a single training trial in an inhibitory avoidance task or eight trials in a water-maze task in which they were trained to swim to a platform submerged 1 cm below the water surface and located in a constant position. Intra-amygdala injections of beta-endorphin (0.03 or 0.1 ng), clenbuterol (10 or 30 ng), or propranolol (0.3 microgram) were given alone or concurrently: beta-endorphin (0.1 ng) + clenbuterol (10 or 30 ng) or beta-endorphin (0.03 ng) + propranolol (0.3 microgram). The injections (0.5 microliter) were administered immediately after inhibitory avoidance training and 5 min before water-maze training. Inhibitory avoidance retention was tested 48 h after training and water-maze retention was tested 24 h after training. In both tasks, clenbuterol attenuated the retention impairing effect of beta-endorphin. Also, in both tasks, low doses of beta-endorphin (0.03 ng) and propranolol (0.3 microgram), which did not affect retention when administered alone, impaired retention when administered concurrently. These results are consistent with extensive previous evidence suggesting that opioid and noradrenergic systems interact in modulating memory storage and provide additional support for the view that the interaction is due to opioid inhibition of noradrenergic activation within the amygdala.
Neurobiol Learn Mem 1995 Mar
PMID:Memory impairment induced by intraamygdala beta-endorphin is mediated by noradrenergic influences. 766 94

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.
Neurobiol Learn Mem 1997 Sep
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

Preterm birth is a major problem in clinical obstetrics, occurring in approximately 10% of all pregnancies, and leading to 75% of early neonatal mortality and morbidity. Studies in our laboratory have examined the neuroendocrine mechanisms by which the fetus, through activation of the hypothalamic-pituitary adrenal axis, provides the stimulus to the onset of parturition. Maturation of this axis occurs prematurely in response to stimuli such as stress. Stress induced activation of HPA function in human pregnancy, may lead to increased output of corticotropin-releasing hormone (CRH) from placenta and fetal membranes. CRH is one of the agonists that acts in concert with increased prostaglandin biosynthesis to provide the stimulus to myometrial contractility in late gestation. Recent studies have also recognized that approximately 15% of patients in idiopathic preterm labor present, with deficiency of the major prostaglandin metabolizing enzyme in the fetal membranes, particularly chorionic trophoblast. Understanding these processes may lead to new methods of managing the patient presenting in preterm labor.
Bull Mem Acad R Med Belg 1998
PMID:Molecular aspects of preterm labor. 998 33

It has been suggested that retrieval during a nonreinforced test induces reconsolidation instead of extinction of the mnemonic trace. Reconsolidation would preserve the original memory from the labilization induced by its nonreinforced recall through a hitherto uncharacterized mechanism requiring protein synthesis. Given the importance that such a process would have in terms of maintaining, as part of the animal behavioral repertoire, a learned response that has been devalued by experience, we analyzed its existence for the memory associated with a one-trial, step-down inhibitory avoidance task (IA), a memory whose consolidation and extinction require protein synthesis in the CA1 region of the dorsal hippocampus (CA1) and involve the participation of the basolateral amygdala (BLA) and entorhinal cortex (ENT). Rats were trained in IA, and 24 h later they were submitted either to a pure reactivation session (retrieval without stepping down), which was unable by itself to initiate extinction of the avoidance response, or to a second training session. Fifteen minutes before or 3 h after either the reactivation or the retraining sessions, animals were infused with the protein synthesis inhibitor anisomycin (ANI) into CA1, BLA, or ENT. Contrary to the prediction of the reconsolidation hypothesis, none of these treatments affected subsequent memory retention. Because reconsolidation is regarded to be a direct consequence of retrieval, one would expect that, when given before a retention test or a pure reactivation session, enhancers of memory expression should permanently improve retention and, therefore, facilitate retrieval both in that and in subsequent sessions. Using two well-known retrieval enhancers, noradrenaline and adrenocorticotropin(1-24), we could not find any evidence suggestive of reconsolidation. Hence, our results indicate that there is no retrieval-induced, protein synthesis-dependent process that would cause reconsolidation of IA memory.
Learn Mem
PMID:Retrieval does not induce reconsolidation of inhibitory avoidance memory. 1546 11

Hormones released in response to stress play important roles in cognition. In the present study, the effects of the stress peptide, corticotropin-releasing hormone (CRH), on spatial reference memory were assessed following post-training administration. Adult Long-Evans male rats were trained for 6 days on a standard water maze task of reference memory in which animals must learn and remember the fixed location of a hidden, submerged platform. Each day, immediately following three training trials, rats received bilateral infusions of CRH into the lateral ventricles over a range of doses (0.1, 0.33, 1.0, 3.3 microg) or a vehicle solution. Post-training infusions of CRH improved retention as indicated by significantly shorter latencies and path lengths to locate the hidden platform on the first training (retention) trial of days 2 and 3. Additionally, post-training administration of CRH increased spatial bias during probe trials as measured by proximity to the platform location. CRH did not enhance performance on retention or probe trials when administered 2h after daily training indicating that CRH facilitated consolidation specifically. The effects of CRH were attenuated by intraventricular co-administration of the beta-adrenergic antagonist, propanolol, at bilateral doses that had no effect on retention alone (0.1, 1.0 microg). Results indicate that post-training administration of CRH enhanced spatial memory as measured in a water maze, and this effect was mediated, at least partly, by a noradrenergic mechanism.
Neurobiol Learn Mem 2008 May
PMID:Post-training administration of corticotropin-releasing hormone (CRH) enhances retention of a spatial memory through a noradrenergic mechanism in male rats. 1808 39

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.
Neurobiol Learn Mem 2012 Mar
PMID:Opioid mechanisms are involved in the disruption of arcaine-induced amnesia by context pre-exposure. 2239 Aug 58