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At least 883 records · Page 49Linked to original sources
PubMed1981

Time discrimination with positional responses after selective prefrontal lesions in monkeys.

Monkeys with ablations of the cortex in the principal sulcus who were impaired on a spatial delayed reaction test were unimpaired on a time discrimination test in which length of time since the last trial signalled the spatial position of the correct foodwell. The finding undermines the view that the classical delayed reaction deficit after lateral prefrontal lesions reflects the loss of temporal structuring of the stream of sensory input. The result is consistent instead with the alternative view that the classical deficit reflects a spatial memory disorder. Monkeys with inferior prefrontal ablations were impaired on both spatial tasks, and on object discrimination reversal as well; analysis of their deficits indicated that they were instances of perseverative interference. Finally, monkeys with ablations of the cortex in the arcuate sulcus were not consistently impaired on any of the tasks. There is no evidence from these results that prefrontal cortex plays any role in time perception.

Animals↗
PubMed1993

Traumatic brain injury produces impairments in long-term and recent memory.

Traumatic brain injury (TBI) in humans typically produces neurological suppression and a longer lasting impairment of memory clinically defined as post-traumatic amnesia. An animal model that reliably reproduces the physiological changes associated with TBI was used to assess the memory deficits following brain injury. Prior to TBI, rats were trained to perform one of four tasks that assessed either motor performance, long-term or recent memory. Rats were randomly assigned to one of three groups (anesthesia only, sham operation or fluid percussion). Following fluid percussion, used to produce TBI, rats were tested for 6 test sessions. The first session occurred 1-2 min after the experimental manipulation. The next 5 sessions followed the training schedule maintained prior to experimental manipulation. Differences in long-term memory occurred only in the first post-operative test session. Differences in recent memory performance were found across all 6 test sessions. The memory deficits were clearly dissociated from motor deficits. The similar memory deficits observed following human head injury and the experimentally produced TBI injury demonstrate that fluid percussion is a useful approach to examine underlying neurobiological mechanisms involved in head injury and possible clinical interventions.

Animals↗
PubMed1992

Effects of benzodiazepine receptor inverse agonists on locomotor activity and exploration in mice.

This study investigates the effects of benzodiazepine receptor inverse agonists on the locomotor and exploratory behaviour of mice when tested in a familiar environment. The weak partial inverse agonist Ro 15-3505 (0.3, 1, 3 mg/kg i.p.) significantly increased locomotion and hole-dipping in habituated mice. However, the more efficacious partial inverse agonists Ro 15-4513 (0.3, 1, 3 mg/kg i.p.) and Ro 19-4603 (0.03, 0.1, 0.3 mg/kg i.p.) had no effect on these parameters. The benzodiazepine receptor antagonist flumazenil (3, 10, 20 mg/kg i.p.) also increased locomotion and hole-dipping in habituated mice, although like Ro 15-3505, these effects were of short duration occurring largely in the first 15 min following injection. Opposite effects were obtained with the partial benzodiazepine agonist Ro 17-1812 (1, 3, 10 mg/kg i.p.) which produced a longer-lasting significant decrease in hole-dipping behaviour in habituated mice without altering locomotion. Finally, in contrast to its effects in habituated animals, Ro 15-3505 (0.3, 1, 3 mg/kg i.p.) did not modify either locomotion or exploration in mice which were tested in a novel environment, showing that the effects of the inverse agonist were state-dependent. This demonstration that, under certain conditions, the weak benzodiazepine receptor inverse agonist Ro 15-3505 and the antagonist flumazenil, produce behavioural activation is in accordance with the work of others suggesting that these classes of compound may increase arousal and may therefore be of some value in treatment of memory disorders.

Animals↗
PubMed1993

Working memory deficits induced by intrahippocampal administration of 8-OH-DPAT, a 5-HT1A receptor agonist, in the rat.

In a test of working memory using a three-panel runway task, the 5-HT1A receptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), at 1.0 mg/kg i.p. significantly increased the number of errors (attempts to pass through two incorrect panels of the three panel gates at four choice points), but it had no effect on errors in a test of reference memory. Intrahippocampal injection of 8-OH-DPAT at 10 micrograms/side also significantly increased the number of working memory errors, without affecting that of reference memory errors. The effect of intrahippocampal 8-OH-DPAT (10 micrograms/side) on working memory was blocked by the 5-HT1A receptor antagonist, (-)-propranolol, at 5 mg/kg i.p. These results suggest that activation of hippocampal 5-HT1A receptors impairs working memory, but does not affect retention of reference memory.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

Spatial memory deficits following stimulation of hippocampal 5-HT1B receptors in the rat.

In this study we examined a possible contribution of serotonin (5-hydroxytryptamine, 5-HT) to spatial memory performance in the rat. Rats were trained to run in a radial maze in a manner that involved two kinds of memory function, i.e. working memory and reference memory. They received intrahippocampal microinjections of a 5-HT1A [8-hydroxy-2-(di-n-propylamino)tetralin or 8-OH-DPAT], or a 5-HT1B [3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one or CP-93,129] receptor agonist, and a muscarinic receptor antagonist (scopolamine). 8-OH-DPAT (5 micrograms/microliters), like injections of saline, induced no change in performance levels. In contrast, rats suffered an impairment in both reference and working memory following injection of scopolamine (10 micrograms/microliters). CP-93,129 induced a higher frequency of reference memory errors than of working memory errors at the intermediate (10 micrograms/microliters) and higher doses (16 micrograms/microliters). Thus, the stimulation of 5-HT1B receptors in the CA1 field of the dorsal hippocampus impairs the performance of rats in a spatial learning task.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Subchronic intraventricular infusion of quinolinic acid produces working memory impairment--a model of progressive excitotoxicity.

It has been proposed by Yamada et al. [Neurosci. Lett. 118: 128-131 (1990); J. Pharmacobiodyn. 14: 351-355 (1991)] that subchronic i.c.v. infusion of the NMDA receptor agonist quinolinic acid may serve as a model for some aspects of neurodegenerative dementia. In the present study, quinolinic acid (9 mM) was infused i.c.v. by ALZET osmotic minipumps for 2 weeks. This treatment produced a short-term working memory deficit in the T-maze (alternation) but no change in reversal learning in the same test. The working memory deficit in the T-maze was progressive i.e. seen after 14, but not 3 days of infusion and persisted for at least for 3 weeks after the termination of the infusion. Histological examination revealed a modest decrease in the number of cells in the nucleus basalis magnocellularis but not in the striatum, entorhinal cortex, or hippocampus. However, in most of the structures studied, morphological changes such as swollen somata and irregular shape were observed indicative of alterations in neuronal function. Autoradiography in the hippocampus revealed a decrease in [3H]hemicholinium and [3H]quinuclidinyl benzilate (QNB) binding to choline uptake sites and muscarinic receptors respectively. Surprisingly no change was observed in [3H]MK-801 binding to NMDA receptor channels in the hippocampus and cortex. The subchronic infusion of quinolinic acid may serve as a model of progressive deterioration of cognitive functions.

Alzheimer Disease↗