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At least 577 records · Page 32Linked to original sources
PubMed1988

Enhanced inhibitory avoidance learning produced by post-trial injections of substance P into the basal forebrain.

The effects of injections of the neuropeptide substance P or the GABA agonist muscimol on performance of a step-down inhibitory avoidance task were examined. Immediately after the training trial, rats with chronically implanted cannulas were injected with 100 or 10 ng of substance P or 500 or 50 ng of muscimol into the region of the nucleus basalis magnocellularis. Control groups included vehicle-injected rats, a sham-operated group, a substance P 5-h delay group, and a substance P no-footshock group. Rats injected with 100 ng of substance P exhibited longer step-down latencies when tested 24 h later than did vehicle-injected rats. The retention latencies for rats in the substance P 5-h delay group did not differ from those of vehicle-injected animals, indicating that proactive effects on performance were not responsible for the effect. In contrast to injections of SP, injections of 500 or 50 ng of muscimol disrupted performance. However, in the absence of a delayed-injection control group, proactive effects cannot be ruled out.

Animals↗
PubMed1992

Effects of concurrent nicotinic antagonist and PCPA treatments on spatial and passive avoidance learning.

The present study investigates the effects of concurrent manipulations of nicotinic cholinergic receptors (mecamylamine 10 mg/kg, i.p.) and serotonin neurons (PCPA, 400 mg on each of 4 days) on spatial navigation (water maze, WM) and passive avoidance (PA) performance. PCPA treatment had no effect on WM navigation or PA performance of intact rats, but greatly aggravated mecamylamine induced performance deficit. Either single or combined treatments with hexamethonium (5.0 mg/kg, s.c.) and PCPA had no effect on WM or PA performance. These findings may suggest that nicotinic cholinergic receptors are also importantly involved in the cholinergic-serotonergic regulation of cognitive functioning.

Animals↗
PubMed1982

Mathematical modelling of the reaction latency. Part III: A model of avoidance reaction latency and avoidance learning.

The linear-dynamic-stochastic model of a reaction latency as applied to avoidance experiment is presented. Reactions are classified on the basis of the model into following classes: escape, avoidance, late avoidance, three types of inter-trial responses and "no reaction". The experimental latency distribution is split into latency distributions of the escape, avoidance and late avoidance responses, providing a new insight into latency distribution. The results of fitting the model to latency measurements obtained in the avoidance conditioning experiment are presented. The same processes of the parameter changes as in the escape conditioning are discovered, one causing a latency to decrease and the other causing a latency to increase during learning. The first process affects a latency stronger than the second and, consequently, the latency decreases during learning. The second process is responsible for a decay of inter trial-responses during experiment. The value of the correlation coefficient between the threshold of avoidance reaction and the threshold of escape reaction was also estimated. Negative values of this coefficient were obtained, therefore, on the average, the greater the avoidance reaction threshold the smaller the escape one. In the course of learning the correlation coefficient tends to be equal to - 1, i.e., as a result of training, both thresholds became dependent in a functional (non-random) way. This result may provide an objective index of the "state of learning". The model provides a new tool for analysis of results of latency-based experiments.

Animals↗
PubMed2001

Involvement of the sigma receptor in passive-avoidance learning in the day-old chick during the second wave of neuronal activity.

The specific sigma-receptor agonist (+)-SKF 10047 and antagonist BD 1047 were used to investigate whether this receptor was involved in passive-avoidance training in the day-old chick. We found 300 microM (+)-SKF 10047 to be amnesic when injected into the lobus parolfactorius 5 h after training (p < .01). Higher or lower concentrations of (+)-SKF 10047 did not disrupt memory formation. The amnesia produced by the efficacious dose of (+)-SKF 10047 was reversed by the specific antagonist, BD 1047. It is suggested that the sigma-receptor may exert its effect on passive-avoidance memory consolidation during the later stages of long-term memory formation by modulation of memory-related neurotransmission.

Amnesia↗
PubMed1960

Avoidance learning and relearning as a function of shuttlebox dimensions.

Rats in a low-ceiling shuttlebox initially show a lower level of learning than rats in a high-ceiling box. After an hour's interruption of conditioning the performance of animals in low-ceiling boxes improves and avoidance is slightly more efficient than in the unimproved performance of animals in high-ceiling boxes. Box height also interacts significantly with length of box.

Animals↗
PubMed1995

Reversible inactivation of the medial septal area impairs consolidation but not retrieval of passive avoidance learning in rats.

Involvement of the medial septal area (MSA) in consolidation and retrieval of passive avoidance response (PAR) was investigated with functional suppression of this area by tetrodotoxin (TTX). Rats carrying a chronically implanted cannula aimed at the MSA were trained on a step-through passive avoidance task and received intraseptal injection of 5 ng TTX dissolved in 1 microliter saline 5, 90 and 360 min after the acquisition trial or 60 min before the retrieval test. TTX injected 5 and 90 min after the acquisition trial significantly reduced avoidance of the dark compartment in comparison with the control group injected with saline. PAR was not impaired by septal TTX injected 360 min after acquisition or 60 min before the retrieval test. Step-through latency of naive rats was not affected by septal blockade. The results indicate that the MSA contributes to PAR consolidation at least 90 min after acquisition but its involvement in PAR retrieval is unlikely. It is concluded that functional ablation of the MSA may disrupt integrity of subcortical circuits participating in PAR learning.

Animals↗