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)

Mice, partially trained to avoid footshock in a T-maze, showed enhanced retention relative to vehicle-injected mice when treated peripherally with arecoline, D-amphetamine, cholecystokinin octapeptide (CCK-8), epinephrine or naloxone. Both intra-amygdaloid and intraventricular injections of beta-endorphin resulted in amnesia. D-amphetamine and arecoline blocked the amnestic effect of beta-endorphin administered into the amygdala but it required higher doses for CCK-8, epinephrine and naloxone to block the amnestic effect of beta-endorphin. The effects of CCK-8, epinephrine and naloxone showed a differential ability to block amnesia induced by beta-endorphin intraventricularly with epinephrine and naloxone preventing amnesia but CCK-8 not improving retention. This data suggests that the memory enhancement produced by peripherally administered CCK-8 involves the amygdala and that both CCK-8 and epinephrine interact with opioid amnestic mechanisms within the amygdala to alter memory processing.
 ...
PMID:Evidence that cholecystokinin-enhanced retention is mediated by changes in opioid activity in the amygdala. 151 38

Alpha-MSH has a wide variety of putative biological activities in addition to its classical melanocyte dispersing activity. Since each of these activities appears to be mediated by a discrete receptor, this peptide is an excellent candidate for exploring conformational restrictions which determine the chemical-physical basis for hormone action on specific activities. Experiments One and Two evaluated several cyclic and linear analogs of alpha-MSH on retrieval of memory during the reactivation of memory for a passive avoidance response following hypothermia-induced amnesia. Three of the cyclic analogs appear to have enhanced the peptide's ability to serve as a reactivation agent. One of the linear Nle4,D-Phe7 analogs antagonized whereas three others enhanced reactivation. The D-Phe7 substitution in cyclic analogs did not affect reactivation. Another group of animals were trained on a step-through passive avoidance task and tested 25 days later. The cyclic analog enhanced memory whereas the D-Phe7 analog and alpha-MSH had no effect. Finally, two analogs were tested on a black-white discrimination. Although the cyclic analog had no effect on either acquisition or reversal of this learning, the Nle4,D-Phe7 analog significantly impaired reversal learning. The results from these preliminary studies suggest that structural modifications of alpha-MSH do alter its potency and pattern of actions in learning and memory situations.
 ...
PMID:The effects of structure-conformation modifications of melanotropin analogs on learning and memory: D-amino acid substituted linear and cyclic analogs. 254 4

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.
 ...
PMID:Effect of posttraining and pretest beta-endorphin and ACTH administration in normal and protein malnourished rats. 256 Jan 73

Adrenocorticotropic hormone (ACTH)1-24, ACTH4-10, corticosterone (CS) or arginine vasopressin (AVP) was administered subcutaneously to one day-old chicks immediately after learning a single trial passive avoidance task. Chicks were pretreated with 2 mM KC1 or 4 mM monosodium glutamate 5 min before learning. With KC1 or monosodium glutamate alone, no evidence of memory was observed on retention tests carried out as early as 5 min and as late as 24 h postlearning. However, the addition of ACTH1-24, ACTH4-10 or AVP to KC1-pretreated animals yielded normal retention levels up till 10 min, 10 min and 20 min after learning, respectively. Similar results were obtained with ACTH1-24 and AVP given to glutamate-pretreated birds. CS had no effect on KC1- or glutamate-induced amnesia. The calcium channel blocker, lanthanum chloride, also inhibited the formation of short-term memory, with amnesia still present as late as 24 h following learning. ACTH1-24, but not CS or AVP, yielded normal retention levels until 10 min postlearning in the presence of lanthanum chloride. Thus ACTH1-24 and AVP can overcome KC1 or glutamate inhibition of STM formation but will not prevent subsequent amnesia. The mechanisms underlying this action of ACTH1-24 and AVP are different. The possibility that the effect of ACTH1-24 is related to the role of calcium in STM formation is explored.
 ...
PMID:Effect of stress-related hormones on short term memory. 286 68

In this article, mice were given a novel exploratory experience 1 hr prior to training on a one-trial inhibitory avoidance task or a Y-maze shock-motivated visual discrimination task. Half of the animals in each group received immediate posttraining electroconvulsive shock (ECS) delivered through implanted cortical screws. Retention was tested 24 hr later. In the inhibitory avoidance task, retention was assessed by the response latencies on Day 2. In the Y-maze, the discrimination was reversed on Day 2 and retention of the original discrimination was assessed by errors made on six reversal training trials. Comparable results were obtained in the two tasks: ECS impaired retention in controls not given the novel experience but did not affect retention in mice given the novel experience. These findings are interpreted in terms of previous evidence, which suggests that ECS-induced amnesia may be mediated by the release of brain beta-endorphin.
 ...
PMID:Novel experience prior to training attenuates the amnestic effects of posttraining ECS. 295 51

The effects of cholecystokinin octapeptide (CCK-8), cholecystokinin tetrapeptide amide (CCK-4), beta-endorphin, proglumide, and naloxone on passive avoidance behavior were studied in rats. Intracerebroventricular (i.c.v.) injection of beta-endorphin (1-10 micrograms) had no significant influence on the latency of the avoidance response in intact rats. Also, beta-endorphin (0.05-5 micrograms, i.c.v.) did not affect the response in rats treated with electroconvulsive shock (ECS). The preventive effect of CCK-8 (0.1-1.0 micrograms, i.c.v.) on ECS-induced amnesia was partly antagonized by beta-endorphin (0.05-10 micrograms, i.c.v.). Intraperitoneal (i.p.) injection of naloxone (1-10 mg/kg) could not prevent ECS-induced amnesia, but continuous subcutaneous infusion of this drug (2 mg/day, 7 days) completely abolished the amnesia. Naloxone (1 and 10 mg/kg, i.p.) also partly antagonized amnesia induced by proglumide (1 and 10 micrograms, i.c.v.) and prevented it when induced by CCK-4 (5 and 10 micrograms, i.c.v.). The results indicate the facilitating action of naloxone and the inhibitory effect of beta-endorphin on memory, suggesting that the endogenous opiate systems are involved in some way in the memory processes.
 ...
PMID:Interactions of cholecystokinin, beta-endorphin, and their antagonists on passive avoidance behavior in rats. 296 63

1. The effects of undernutrition during suckling and of post-training beta-endorphin administration on avoidance task were investigated in adult rats. 2. Young rats were undernourished from delivery until weaning (21 days) by feeding their mothers a diet containing 8% protein (w/w). Mothers of well-nourished rats were fed a 20% protein diet. After weaning, both groups of rats were fed a 20% protein diet until 90-120 days of age, when they were subjected to behavioral sessions. 3. Acquisition was measured in training sessions and retention in test sessions 24 h after training. Beta-endorphin or saline (control) was injected ip immediately after training. Rats were subjected to shuttle and step-down inhibitory avoidance sessions using footshock of 0.2 or 0.8 mA intensity. 4. Undernutrition during suckling caused hyperreactivity to 0.2 mA footshocks. Beta-endorphin caused amnesia to shuttle avoidance task only in normal rats trained with 0.8 mA footshocks. In the step-down inhibitory avoidance task, beta-endorphin was amnesic only for normal rats and only for 0.2 mA footshocks. Beta-endorphin was not amnesic in undernourished rats.
 ...
PMID:Effects of undernutrition during suckling and of post-training beta-endorphin administration on avoidance performances of adult rats. 297 Aug 75

1. Recent evidence suggests that treatments given after training may influence memory in two ways: by becoming themselves incorporated to the experience, or by altering post-training mechanisms involved in the storage of the experience. The two processes may be called consolidation. 2. Some endogenous substances that are normally released during or after training (brain beta-endorphin; the peripheral stress hormones, ACTH, epinephrine and vasopressin) appear to be of particular importance. Their effect may become incorporated to the experiences as a conditioned stimulus (CS), generating state dependency. The effect of beta-endorphin appears to be physiological, since the substance is released by novel experiences. 3. Post-event information provided by other training experiences, in rats, or by comments or leading words, in humans, may also incorporate to the experiences, altering their content qualitatively or quantitatively. 4. A variety of substances including the stress hormones at low doses and analeptic drugs may facilitate retention when given after training. In this case, the effect is best explained by an enhancement of the post-training strengthening of memory traces. 5. The reiteration of part of the experiences at the time of testing facilitates retrieval. This may be viewed as a reconstruction of consolidation at the time of retrieval, and may be obtained using cognitive material ("priming"), or neurohumoral stimuli (a beta-endorphin injection, or a presumable release of brain beta-endorphin by an interpolated novel experience). The effect can be seen in animals rendered amnestic by electroconvulsive shock, and in humans with amnesia of organic and non-organic nature. 6. The human amnesic syndrome seems, thus, largely explainable by a deficit of retrieval. It is possible that the stimulation of retrieval by priming, or by drugs, through the "reconstruction" of consolidation, may be useful for the relief or treatment of the human amnesic syndrome.
 ...
PMID:Construction and reconstruction of memories. 297 33

Mice were trained in a 1-trial inhibitory avoidance task (0.7 mA FS) and tested for retention at 1, 3, or 6 h following training. Posttraining beta-endorphin (0.1 micrograms/mouse i.p.) administration impaired retention at 6 h, but not 1 or 3 h after training. Propranolol (0.3 mg/mouse i.p.), but not naloxone (0.1 mg/mouse i.p.) administered prior to retention testing at 1 or 3 h accelerated the onset of amnesia in mice given posttraining beta-endorphin. Neither propranolol nor naloxone affected retention when given alone. These findings suggest that the delayed onset of the amnesia produced by posttraining beta-endorphin is due to the activation of a beta-adrenergic system.
 ...
PMID:Delayed onset of the amnestic effect of posttraining beta-endorphin: effects of propranolol administered prior to retention testing. 299 52

The effect on retention of the post-training intraperitoneal administration of ACTH1-24 (0.2 or 2.0 micrograms/kg), epinephrine HCl (5.0 or 50.0 micrograms/kg), human beta-endorphin (0.1 or 1.0 microgram/kg), naloxone (0.4 mg/kg), and of the combination of naloxone or beta-endorphin with ACTH or epinephrine was studied in two different but closely related step-down inhibitory avoidance tasks in rats: task 1 (5 cm high 25 X 25 cm platform; 0.5 mA continuous footshock) and task 2 (7 X 25 cm platform, 0.3 mA discontinuous footshock). In task 1, saline control animals showed good retention in a test session carried out 24 hr later; beta-endorphin, ACTH and epinephrine caused amnesia; beta-endorphin potentiated the amnesic effect of ACTH and epinephrine; and naloxone caused memory facilitation and reversed the amnesic effect of ACTH and epinephrine. In task 2, control animals showed poor retention; beta-endorphin caused amnesia at the dose of 0.1 but not 1.0 microgram/kg; the other three drugs caused memory facilitation; naloxone potentiated the facilitatory effect of ACTH and epinephrine; and beta-endorphin reversed it and transformed it into a deep amnesia. These findings suggest that an opioid-mediated amnesic mechanism modulates the effect of ACTH and epinephrine on memory consolidation, either by dampening that effect when training parameters tend to make it facilitatory, or by enhancing it when training conditions tend to make it amnesic. On the basis of these and previous data it seems likely that the amnesic effect of ACTH and epinephrine could be mediated by endogenous beta-endorphin release.
 ...
PMID:Effect of ACTH, epinephrine, beta-endorphin, naloxone, and of the combination of naloxone or beta-endorphin with ACTH or epinephrine on memory consolidation. 630 1


1 2 Next >>