{"title":"α-和β-肾上腺素受体拮抗剂对试验后肾上腺素调节记忆的影响:与训练后脑去甲肾上腺素浓度的关系","authors":"Paul E. Gold, Roderick van Buskirk","doi":"10.1016/S0091-6773(78)93045-6","DOIUrl":null,"url":null,"abstract":"<div><p>Rats were trained in a one-trial inhibitory (passive) avoidance task. Each animal received a 30-min pretrial injection of saline, phenoxybenzamine, or propranolol and an immediate post-trial injection of saline or epinephrine. Animals were tested for retention 24 hr later. In the absence of pretreatment with either adrenergic blocking agent, epinephrine enhanced retention of training with low footshock and impaired retention of training with high footshock. Pretrial injections of propranolol, but not phenoxybenzamine, attenuated epinephrine-produced enhancement of retention performance. Conversely, pretrial treatment with phenoxybenzamine, but not propranolol, attenuated epinephrine-produced retention impairment. Post-training brain norepinephrine concentrations were sensitive to the training-treatment conditions; the extent of a transient decrease (maximal 10 min after training) predicted, in most cases, the retention performance observed in comparably trained and treated animals. These findings thus extend and corroborate our previous evidence suggesting that hormonally mediated central noradrenergic activity may underlie retrograde amnesia and enhancement of memory processes. In addition, these findings suggest that memory storage processing may be modulated by normal post-training hormonal and central aminergic responses to training.</p></div>","PeriodicalId":75577,"journal":{"name":"Behavioral biology","volume":"24 2","pages":"Pages 168-184"},"PeriodicalIF":0.0000,"publicationDate":"1978-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0091-6773(78)93045-6","citationCount":"116","resultStr":"{\"title\":\"Effects of α- and β-adrenergic receptor antagonists on post-trial epinephrine modulation of memory: Relationship to post-training brain norepinephrine concentrations\",\"authors\":\"Paul E. Gold, Roderick van Buskirk\",\"doi\":\"10.1016/S0091-6773(78)93045-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Rats were trained in a one-trial inhibitory (passive) avoidance task. Each animal received a 30-min pretrial injection of saline, phenoxybenzamine, or propranolol and an immediate post-trial injection of saline or epinephrine. Animals were tested for retention 24 hr later. In the absence of pretreatment with either adrenergic blocking agent, epinephrine enhanced retention of training with low footshock and impaired retention of training with high footshock. Pretrial injections of propranolol, but not phenoxybenzamine, attenuated epinephrine-produced enhancement of retention performance. Conversely, pretrial treatment with phenoxybenzamine, but not propranolol, attenuated epinephrine-produced retention impairment. Post-training brain norepinephrine concentrations were sensitive to the training-treatment conditions; the extent of a transient decrease (maximal 10 min after training) predicted, in most cases, the retention performance observed in comparably trained and treated animals. These findings thus extend and corroborate our previous evidence suggesting that hormonally mediated central noradrenergic activity may underlie retrograde amnesia and enhancement of memory processes. In addition, these findings suggest that memory storage processing may be modulated by normal post-training hormonal and central aminergic responses to training.</p></div>\",\"PeriodicalId\":75577,\"journal\":{\"name\":\"Behavioral biology\",\"volume\":\"24 2\",\"pages\":\"Pages 168-184\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1978-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S0091-6773(78)93045-6\",\"citationCount\":\"116\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Behavioral biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0091677378930456\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Behavioral biology","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0091677378930456","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Effects of α- and β-adrenergic receptor antagonists on post-trial epinephrine modulation of memory: Relationship to post-training brain norepinephrine concentrations
Rats were trained in a one-trial inhibitory (passive) avoidance task. Each animal received a 30-min pretrial injection of saline, phenoxybenzamine, or propranolol and an immediate post-trial injection of saline or epinephrine. Animals were tested for retention 24 hr later. In the absence of pretreatment with either adrenergic blocking agent, epinephrine enhanced retention of training with low footshock and impaired retention of training with high footshock. Pretrial injections of propranolol, but not phenoxybenzamine, attenuated epinephrine-produced enhancement of retention performance. Conversely, pretrial treatment with phenoxybenzamine, but not propranolol, attenuated epinephrine-produced retention impairment. Post-training brain norepinephrine concentrations were sensitive to the training-treatment conditions; the extent of a transient decrease (maximal 10 min after training) predicted, in most cases, the retention performance observed in comparably trained and treated animals. These findings thus extend and corroborate our previous evidence suggesting that hormonally mediated central noradrenergic activity may underlie retrograde amnesia and enhancement of memory processes. In addition, these findings suggest that memory storage processing may be modulated by normal post-training hormonal and central aminergic responses to training.