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 505 records · Page 28Linked to original sources
PubMed1995

Impaired avoidance learning after closed-head injury: dissociation between two tasks due to classical conditioning.

Like controls, a Closed-Head Injury (CHI) group learned quickly to press a button during a 3-s warning stimulus in order to avoid a noxious buzzer. In a similar task, however, the CHI group had greater difficulty achieving the learning criterion compared to controls when required to prevent an innocuous visual display (i.e., a circle). The difficulty levels of these two avoidance tasks were identical. The major differences concerned the temporal contiguity of the warning cue with the stimulus to be avoided and the intrinsic aversiveness of the buzzer compared to the appearance of a circle on a computer screen. We hypothesize that, although both tasks were operant in essential character, the buzzer may have produced a degree of classical conditioning. These results suggest that CHI survivors may have some difficulty forming connections between arbitrary stimuli when performance depends almost entirely upon conscious, effortful processing. When a stimulus is sufficiently noxious to be capable of producing an affective or autonomic response, however, automatic processes may aid in the formation of associations.

Acoustic Stimulation↗
PubMed1985

Separation of the associative and non-associative effects of brain serotonin released by p-chloroamphetamine: dissociable serotoninergic involvement in avoidance learning, pain and motor function.

p-Chloramphetamine (PCA, 0.63-5 mg/kg IP) injected 30-60 min before testing produced a dose-related impairment of avoidance acquisition, prolonged reaction time in the hot-plate test and increased locomotor activity. Pretreatment with the selective serotonin (5-HT) uptake inhibitor zimeldine (10 mg/kg IP) blocked these behavioral effects. Degeneration of brain 5-HT neurons by a high neurotoxic dose of PCA (2 X 10 mg/kg IP) or inhibition of tryptophan hydroxylase by p-chlorophenylalanine (300 mg/kg IP) also blocked the behavioral effects of PCA. There was a complete blockade of the PCA-induced avoidance deficit following pretreatment with metergoline, a central 5-HT receptor blocking agent. On the other hand, metergoline failed to block the hot-plate analgesia and the increased locomotion caused by PCA. Depletion of brain NA and DA by the tyrosine hydroxylase inhibitor H44/68 did not counteract the PCA effect on avoidance or hot-plate performance, but reduced the locomotor stimulating effect. The selective NA neurotoxin DSP4 (50 mg/kg IP) or the opiate antagonist naloxone (1 mg/kg) failed to affect the PCA-induced modulations of the behaviours studied. In addition, PCA administration in doses that caused avoidance deficits, did not result in motor impairment as assessed by the tread mill test. The above results support the hypothesis that the PCA-induced impairment of active avoidance acquisition does not involve changes in nociception or altered locomotor activity. It is concluded that behavioural processes related to serotonergic neurotransmission can be independently modified, suggesting differences in the underlying 5-HT mechanisms.

Amphetamines↗
PubMed2001

Pharmacological differences between memory consolidation of habituation to an open field and inhibitory avoidance learning.

Rats implanted bilaterally with cannulae in the CA1 region of the dorsal hippocampus or the entorhinal cortex were submitted to either a one-trial inhibitory avoidance task, or to 5 min of habituation to an open field. Immediately after training, they received intrahippocampal or intraentorhinal 0.5-microl infusions of saline, of a vehicle (2% dimethylsulfoxide in saline), of the glutamatergic N-methyl-D-aspartate (NMDA) receptor antagonist 2-amino-5-phosphono pentanoic acid (AP5), of the protein kinase A inhibitor Rp-cAMPs (0.5 microg/side), of the calcium-calmodulin protein kinase II inhibitor KN-62, of the dopaminergic D1 antagonist SCH23390, or of the mitogen-activated protein kinase kinase inhibitor PD098059. Animals were tested in each task 24 h after training. Intrahippocampal KN-62 was amnestic for habituation; none of the other treatments had any effect on the retention of this task. In contrast, all of them strongly affected memory of the avoidance task. Intrahippocampal Rp-cAMPs, KN-62 and AP5, and intraentorhinal Rp-cAMPs, KN-62, PD098059 and SCH23390 caused retrograde amnesia. In view of the known actions of the treatments used, the present findings point to important biochemical differences in memory consolidation processes of the two tasks.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗