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Showing papers by "Trevor W. Robbins published in 1993"


Journal ArticleDOI
01 Oct 1993-Brain
TL;DR: The results suggest that the gross set-shifting deficits reported in both frontal lobe patients and patients with Parkinson's disease may involve fundamentally different, though related, cognitive processes, and that these may be differentially affected by medication.
Abstract: Tests which assess the ability to shift cognitive set modelled after the Wisconsin Card Sorting Test are particularly sensitive to impairments in patients with Parkinson's disease as well as in patients with frontal lobe damage. However, the underlying mechanisms responsible for the similar deficits observed in the two patient groups are not well understood and may not be identical. For example, an apparent deficit in set-shifting ability may reflect either an impairment in the ability to shift from a perceptual dimension which has previously commanded attention (i.e. 'perseveration'), or in the ability to shift to an alternative perceptual dimension which has previously been irrelevant (i.e. 'learned irrelevance'). In this study, the performance of both medicated and non-medicated patients with Parkinson's disease were compared with a group of neurosurgical patients with localized excisions of the frontal lobes on a novel task designed to assess the relative contribution of 'perseveration' and 'learned irrelevance' to impaired set-shifting ability. Patients with frontal lobe damage were worse than controls in their ability to shift attention from a previously relevant stimulus dimension. Medicated patients with Parkinson's disease were worse at shifting to a previously irrelevant dimension. In contrast to both groups, nonmedicated patients with Parkinson's disease were impaired in both conditions. These results suggest that the gross set-shifting deficits reported in both frontal lobe patients and patients with Parkinson's disease may involve fundamentally different, though related, cognitive processes, and that these may be differentially affected by medication. Specifically, L-dopa therapy may protect Parkinson's disease patients from preservation of attention to a formerly relevant stimulus dimension.

658 citations


Journal ArticleDOI
TL;DR: Isolation rearing provides a nonpharmacological way to induce in rats a deficit in sensorimotor gating that is exhibited by schizophrenic patients, particularly when midrange 8 dB prepulses were used.

387 citations


Journal ArticleDOI
TL;DR: The results suggest a rather selective effect of amygdala-ventral striatal interactions on processes subserving conditioned reinforcement and a more fundamental influence of ventral subiculum- ventral Striatal interactions in mediating the psychomotor stimulant effects of D-amphetamine.

304 citations


Journal ArticleDOI
TL;DR: There are multiple memory impairments in PD which may differentially depend on the clinical severity of the disease, and significant impairments were found in both groups of medicated PD patients and particularly in those patients with more severe clinical symptoms.

243 citations


Journal ArticleDOI
TL;DR: Analysis suggests that many of the learning and memory impairments traditionally attributed to the cholinergic corticopetal system are due not to destruction of cholinergic neurons in the nbM, but instead result from the disruption of cortico-striatal outputs passing through the dorsal and ventral globus pallidus.

199 citations


Journal ArticleDOI
TL;DR: Results suggest that both D1 and D2 receptors in the nucleus accumbens are involved in mediating the effects of dopamine in potentiating the control over behaviour by conditioned reinforcers.
Abstract: Several experiments investigated the involvement of D1 and D2 dopamine receptors in the ventral striatum in the control over behaviour by a conditioned reinforcer using an acquisition of new response procedure. Intra-accumbens infusion of either the D1 receptor antagonist, SCH 23390, or the D2 receptor antagonist, raclopride, completely blocked the potentiative effects of intra-accumbensd-amphetamine on responding with conditioned reinforcement and reduced responding to control levels. SCH 23390 was more potent than raclopride. At higher doses in the absence ofd-amphetamine, both antagonists also blocked the preference for responding on the lever producing the conditioned reinforcer. Intra-accumbens infusions of either the D1 receptor agonist, SKF 38393, or the D2/3 receptor agonist, LY 171555 (quinpirole), selectively potentiated responding on the lever producing the conditioned reinforcer. Various combined infusions of the D1 and D2 agonists in specific low doses had additive, but not synergistic, effects on responding with conditioned reinforcement. None of the drugs affected the drinking of water in deprived subjects when infused intra-accumbens. These results suggest that both D1 and D2 receptors in the nucleus accumbens are involved in mediating the effects of dopamine in potentiating the control over behaviour by conditioned reinforcers.

161 citations


Journal ArticleDOI
TL;DR: The results replicated the abolition of LI found in previous studies, and demonstrated enhanced post-shock suppression in amphetamine-treated animals, and provided no evidence for the involvement of the mesolimbic dopamine system in LI.
Abstract: Latent inhibition (LI) is a phenomenon in which repeated, non-reinforced presentation of a stimulus retards subsequent conditioning to that stimulus. Several recent experiments have suggested that LI is abolished following acute, low doses of amphetamine given during pre-exposure and conditioning, and this effect has been attributed to amphetamine-induced changes in dopamine levels in the nucleus accumbens. Experiments 1 and 2 examined the effects of two doses of intra-accumbensd-amphetamine (10 µg/µl and 3 µg/µl) on LI in an on-baseline, within-subject conditioned suppression paradigm. There was no effect of either dose on LI, but a significant disinhibition of conditioned suppression resulted in a retardation of learning. In experiment 3 the effects of a low dose of systemicd-amphetamine (0.5 mg/kg) on latent inhibition were examined. The results replicated the abolition of LI found in previous studies, and demonstrated enhanced post-shock suppression in amphetamine-treated animals. These data provide no evidence for the involvement of the mesolimbic dopamine system in LI.

142 citations


Journal ArticleDOI
TL;DR: The results indicate that reward-related processes, as measured in the place preference conditioning paradigm, may depend upon ventral striatopallidal outflow that engages medial dorsal thalamus-frontal cortex mechanisms, in addition to the previously highlighted direct outflow to brainstem elements of the motor system.

141 citations


Journal ArticleDOI
TL;DR: This study tested the hypothesis that the hippocampus modulates dopamine-dependent function of the nucleus accumbens using behavioural and neurochemical evidence and functional interactions between the hippocampus and nucleus Accumbens involving the control of mesolimbic dopamine release.

116 citations


Journal ArticleDOI
TL;DR: It is concluded that additional cholinergic de-afferentation of the cingulate cortex produced by the septal/VDB lesion is of functional significance and may lead to deficits in conditional rule learning, which can contribute to spatial navigation performance under certain circumstances.

65 citations



Journal ArticleDOI
TL;DR: Statistical analysis of similarities in laminar distribution patterns of different receptors (co-distribution) reveals that L-glutamate binding sites are co-distributed with N-methyl-D-aspartate, GABAA, and muscarinic M1 and M2 receptors.

Journal ArticleDOI
TL;DR: The co-modulation by CCK and dopamine of the processing of reward-related stimuli within the NAS is discussed in terms of the co- modulation of the impact of D-amphetamine upon rates of response on the CR lever.

Journal ArticleDOI
TL;DR: The long-term neurobehavioural changes in a woman who, following the intake of an unidentified substance, sustained subtotal bilateral lesions of the globus pallidus and small lesions at selective sites adjacent to it are consistent with the view that it has important functions in mediating how internal representations of stimulus input are converted into various forms of action.
Abstract: This study has characterized the long-term neurobehavioural changes in a woman who, following the intake of an unidentified substance, sustained subtotal bilateral lesions of the globus pallidus and small lesions at selective sites adjacent to it. Associated with these lesions was a significantly reduced blood flow in multiple frontal cortical regions, most prominently in area 10, the anterior cingulate and the supplementary motor cortex. Her cognitive deficits were generally consistent with those found in patients with frontal lobe dysfunction but some deficits, i.e. in visual memory and learning, were more compatible with temporal lobe dysfunction. Incapacitating personality or obsessive compulsive changes as reported by others with similar lesions were absent and she could live independently. The cognitive changes are consistent with the view that the globus pallidus has important functions in mediating how internal representations of stimulus input are converted into various forms of action, for example, in planning solutions to problems and in working memory.

01 Jan 1993
TL;DR: The results indicate that Korsakoff but not non-KorsAKoff alcoholics have neuropsychological deficits on tests which have demonstrated medial temporal-lobe/diencephalic dysfunction in humans and non-human primates.
Abstract: It has been suggested that both Korsakoff and non-Korsakoff alcoholics share certain memory deficits following alcohol withdrawal. Since both groups have in common long-term alcohol abuse, this has been posited as evidence that alcohol per se can cause irreversible cognitive impairment. This hypothesis has been examined by comparing age and IQ matched groups of detoxified Korsakoff and non-Korsakoff alcoholics and normal controls on pencil and paper and computerised (CANTAB) memory tests. The results indicate that Korsakoff but not non-Korsakoff alcoholics have neuropsychological deficits on tests which have demonstrated medial temporal-lobe/diencephalic dysfunction in humans and non-human primates. Although non-Korsakoff alcoholics showed deficits on the Wechsler Memory Scale subtests these could not be related to damage of specific neuronal systems. Furthermore there was evidence that for the non-Korsakoff but not the Korsakoff alcoholics, superior performance on the Wechsler memory scale subtests was related to increased length of abstinence and independent of either age or duration of drinking.