PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Avoidance Learning”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,405 records · Page 78Linked to original sources
PubMed1979

Facilitation of memory consolidation by vasopressin: mediation by terminals of the dorsal noradrenergic bundle?

Administration of arginine-vasopressin (AVP, 5 micrograms, s.c.) immediately after the learning trial results in a long-term facilitation of a one-trial learning passive avoidance response. This effect of AVP is absent in animals with prior destruction of the ascending dorsal noradrenergic bundle by bilateral microinjection of 6-hydroxydopamine (6-OHDA). Postlearning local microinjection of a minute amount of AVP via chronically implanted cannulae into the locus coeruleus did not influence passive avoidance behavior. Upon injection into the midbrain dorsal raphe nucleus, however AVP facilitated passive avoidance behavior. This effect, however, was absent in rats receiving previous microinjection of 5,6-dihydroxytryptamine (5,6-DHT) or of 6-OHDA into the dorsal raphe nucleus. Bilateral 6-OHDA-induced lesions of the nucleus accumbens or 5,6-DHT-induced destruction of the dorsal raphe nucleus did not prevent the effect of AVP administered subcutaneously. The data suggest that vasopressin facilitates memory consolidation processes by modulating noradrenergic neurotransmission in terminals of the dorsal noradrenergic bundle. The serotoninergic neuronal network originating from the dorsal raphe nucleus has a secondary--norepinephrine-mediated--influence upon these processes.

5,6-Dihydroxytryptamine↗
PubMed1979

Effect of oxytocin and vasopressin on memory consolidation: sites of action and catecholaminergic correlates after local microinjection into limbic-midbrain structures.

The effects of local postlearning microinjections of arginine-vasopressin (AVP) and oxytocin (OXT) on one-trial learning passive avoidance behavior and the influence of AVP on alpha-MPT-induced disappearance of norepinephrine (NE) and dopamine (DA) in discrete brain regions have been studied in the rat. OXT injected bilaterally in the hippocampal dentate gyrus (25-25 pg) or in the midbrain dorsal raphe nucleus (50 pg) significantly attenuated passive avoidance behavior. Facilitation of passive avoidance behavior was observed when the peptide was injected into the dorsal septal nucleus. AVP facilitated passive avoidance behavior when administered into the hippocampal dentate gyrus, dorsal raphe nucleus or dorsal septal nucleus. Injection of either neuropeptides into the central amygdaloid nucleus appeared to be ineffective. One week after the behavioral experiments a repeated injection of AVP into the hippocampal dentate gyrus increased the disappearance of NE in the dentate gyrus and in the nucleus ruber. An injection into the dorsal septal nuclei decreased the NE disappearance in the dorsal septal nucleus itself and increased it in the nucleus ruber. Injection in the dorsal raphe nucleus led to an increase in the disappearance of DA in the locus coeruleus and in the nucleus ruber. It is concluded that memory consolidation can be oppositely influenced by local application of minute amounts of either OXT or AVP into certain limbic-midbrain structures, suggesting an involvement of these brain regions in the memory effects of these peptides. Modulation of catecholamine turnover in specific brain areas after AVP administration may be related to this behavioral effect.

Animals↗
PubMed1987

Delayed memory dysfunction by transient hypoxia, and its prevention with forskolin.

Rats exposed to 40 min hypoxia 3 h before a one-trial learning passive avoidance task showed impaired memory retention 24 h later. this model was used to assess the ability of forskolin to restore the delayed memory dysfunction. Significant amelioration of memory retention was observed when forskolin (500 micrograms/kg, i.p.) was injected just after hypoxia. Forskolin is suggested to enhance cerebral blood flow and to facilitate memory function through the action of increased cyclic adenosine monophosphate (cAMP).

Animals↗
PubMed1988

Amygdala kindling effects on sleep and memory in rats.

Sleep disturbances accompany the development of amygdaloid-kindled seizures in cats. Some of these sleep deficits resemble those seen in aged rats; these latter changes in sleep patterns are correlated with memory impairments in the aged animals. In the present study, we examined the hypothesis that sleep deficits after kindling may be related to memory impairments. Rats were kindled for 4 weeks (2-2.5 weeks after stage 5 seizures) and were then allowed a one week recovery period. Sleep patterns were assessed through-out the kindling and recovery periods. The animals were then trained on an inhibitory avoidance apparatus and tested for retention 24 h later. Only transient sleep changes occurred during the development of kindling (to stage 5 seizures). However, continued kindling resulted in significant reductions in several sleep measures which remained depressed for at least one week after the termination of the kindling trials. As a group, kindled rats were impaired in retention of the inhibitory avoidance learned response. In kindled animals, retention performance was significantly correlated with total paradoxical sleep, the ratio of paradoxical/total sleep, and paradoxical sleep, the ratio of paradoxical/total sleep, and paradoxical sleep bout duration. These correlations are consistent with the view that deficits in paradoxical sleep may be related to deficits in some forms of memory.

Amygdala↗
PubMed1989

Morris water task impairment and hypoactivity following cysteamine-induced reductions of somatostatin-like immunoreactivity.

The effects of cysteamine-induced reductions of somatostatin-like immunoreactivity (SLI) on spatial learning, passive avoidance, and locomotor activity were examined in adult Sprague-Dawley rats. Cysteamine hydrochloride (100 mg/kg, s.c.) produced 54% and 50% reductions in SLI in cortex and hippocampus, respectively, and impaired escape latencies and spatial probe behavior in the Morris water task. Although cysteamine-treated rats displayed hypoactivity in the activity boxes, their swim speed in the Morris water task was unaffected. Cysteamine did not impair passive avoidance retention when administered immediately following training or prior to daily retention testing. These results suggest a role for somatostatin in spatially-mediated behaviors in rats.

Animals↗
PubMed1990

Antinociception induced by stimulation of the habenular complex of the rat.

The changes in the tail-flick latency to noxious heat stimulation and in the threshold for defensive/affective reactions to noxious pressure of the skin were studied following electrical stimulation of the habenular complex (HbC) and adjacent brain structures in the male rat. Single brief (15 s), low intensity (53 microA r.m.s.) stimulation of the HbC caused no significant increase in the locomotor activity or motor deficit but induced a potent and short-lasting antinociception as revealed by both algesimetric tests. Animals stimulated in the HbC also displayed poor avoidance learning in a conditioned place preference paradigm, thus suggesting that aversion is unlikely to determine antinociception. Rats daily stimulated in the HbC became tolerant to the antinociception induced by HbC stimulation or to a high systemic dose of morphine (6 mg/kg i.p.). These results indicate that stimulation of the HbC may increase the thresholds of spinally and supraspinally integrated reflexes, thus supporting the hypothesis that this nucleus may play a role in pain control, probably involving an opioid-dependent mechanism.

Analgesia↗
PubMed1993

Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin.

The development of tolerance to morphine analgesia in amnesic model mice and the role of arginine vasopressin (AVP) in the underlying mechanism was examined. Hypoxia, brain ischemia, scopolamine and electroconvulsive shock (ECS) manipulation caused amnesia in the step-through type passive avoidance learning test performed at 24 h after the training trial. The amnesic state lasted for at least 3 days and recovered to naive control level on the 20th day after each manipulation. In all amnesic groups, radioimmunoassayable AVP content in hypothalamus was decreased, in particular, the reduction was significant in hypoxia and ischemic induced amnesic animals, then recovered to the control level by 20 days after each treatment. Daily morphine, 10 mg/kg, s.c. easily resulted in the development of tolerance to the analgesic effect in control animals; however, such treatment failed to develop tolerance in amnesic model animals, leaving the analgesic effect unchanged to the control levels. Daily pretreatment with i.c.v. AVP, dose-dependently reinstated the development of tolerance in amnesic model mice. When morphine injection was started from 20 days after the amnesia inducing treatment, tolerance developed as in a similar pattern as in control animals. Thus, amnesic model mice are deficient in brain AVP levels, and consequently, a certain level of AVP in the hypothalamus is required for maintaining the normal function such as the development of tolerance to morphine and the recovery from amnesia.

Amnesia↗
PubMed1983

Naltrexone-sensitive behavioral actions of the ACTH 4-9 analog (Org 2766).

The effects of the ACTH 4-9 analog (Org 2766) and the COOH-terminal tripeptide of Org 2766 (Phe-D-Lys-Phe; PDLP) on retrieval of one-trial learning passive avoidance behavior were compared with those of beta-endorphin, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin, des-Tyr1-[Met5]-enkephalin and des-enkephalin-gamma-endorphin (DE gamma E). Amounts of intracerebroventricularly administered Org 2766, PDLP, [Met5]-enkephalin, [D-Ala2,Met5]-enkephalin and DE gamma E, which induced a comparable attenuation of passive avoidance behavior were determined. Pretreatment with the opiate antagonist naltrexone prevented the attenuating effect of these peptides on passive avoidance behavior except that of DE gamma E. The attenuating effect of Org 2766 and of [Met5]-enkephalin was reversed to facilitation of passive avoidance behavior in the presence of naltrexone. Subcutaneous treatment with Org 2766 and [D-Phe7]-ACTH 4-10 decreased electrical self-stimulation behavior elicited from the medial septal area. Naltrexone prevented the inhibitory effect of Org 2766 on this behavior, but not that of [D-Phe7]-ACTH 4-10. Although the attenuating effect of PDLP on passive avoidance behavior was not reduced by pretreatment with [Met5]-enkephalin- or beta-endorphin-antiserum, and PDLP induced neither analgesia nor excessive grooming, the data suggest that the inhibitory effect of Org 2766 and PDLP on passive avoidance behavior and electrical self-stimulation are mediated by endorphin systems in the brain.

Adrenocorticotropic Hormone↗
PubMed1990

Effects of low doses of alcohol on delta-9-tetrahydrocannabinol's effects in pregnant rats.

Pregnant rats were intubated with 50 mg/kg of delta-9-tetrahydrocannabinol (THC) or with THC plus alcohol to determine if a low dose of alcohol (1 g/kg) would significantly increase blood levels of THC. On the basis of this study, a second study was conducted in which pregnant rats were intubated with THC (50, 25 or 0 mg/kg) plus alcohol (2, 1 or 0 g/kg) from gestation day six to parturition. THC reduced birth weights but did not significantly affect litter size or passive avoidance learning. Alcohol did not have a significant effect on offspring birth weight nor did it interact with THC to affect offspring.

Animals↗
PubMed1980

Learned aversion to soiled bedding in male mongolian gerbils.

This study was designed to determine whether the conditioned aversion paradigm could be extended to aversion to soiled bedding in the male Mongolian gerbil. In Experiment 1, sixty subjects were exposed to a glass petri dish filed with soiled bedding placed in the center of a one-meter-square open field for two 5-min sessions 48 hours apart. Half of the subjects received an injection of lithium chloride immediately after session 1, while the rest received saline. The LiCl subjects learned to avoid the soiled bedding in session 2, as indicated by significantly longer latency to first approach and lower frequency of approach to the stimulus. Experiment 2 examined conditioned aversion to specific to soiled bedding. The research results demonstrate olfactory aversion of this type is possible in gerbils, and suggest that it may have an important influence on their social behavior.

Animal Husbandry↗
PubMed1982

In utero taste/odor aversion conditioning in the rat.

Rat fetuses exposed to a taste-odor stimulus and an aversive stimulus in utero showed an aversion to the taste/odor stimulus when tested 16 days postnatally. Fetuses which received various control treatments in utero did not show an aversion. These data show that rat fetuses at 20 days of gestation are capable of associative learning which can be demonstrated more than two weeks postnatally.

Animals↗
PubMed1982

Delayed post hypoxic transient amnesia is not associated with electrical brain seizures.

Rats rendered hypoxic by brief exposure to N2 after learning an avoidance response go into convulsions and subsequently become amnestic. Overt convulsions can be avoided whilst yet producing delayed post-hypoxic transient amnesia (DPHTA) by using 2% O2 in N2 in place of pure N2. The experiments reported here show that with this gas mixture, the ECoG shows hardly any of the electrical activity associated with seizures which occurs with N2. It is concluded that electrical seizures are not associated with the mechanism responsible for DPHTA.

Animals↗