PROACTIVE AND RETROACTIVE INHIBITION IN THE A-B, A-B' PARADIGM.
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Damage to the lateral nucleus of the septum in the rat resulted in atypical learning to a previously meaningless stimulus. Nonreinforced preexposure to a stimulus normally makes more difficult subsequent use of that stimulus for learning. The effect of this preexposure on learning is termed latent inhibition and was demonstrated in sham operated animals. Rats in which the lateral septum was damaged demonstrated a paradoxically smaller learning deficit in the presence of a conditioned stimulus that was previously presented without reinforcement, when compared to the performance of both septal lesioned rats no receiving nonreinforced preexposure and sham operates receiving preexposure. The interaction of nonreinforced preexposure and lateral septal lesions can be explained using a proposed sensitization hypothesis.
The present study tested the hypothesis that, unlike prosaccades, antisaccades require controlled processing, due to the prepotent response that needs to be inhibited. The effect of the Random time Interval Generation (RIG) task (Vandierendonck, A., De Vooght, G., & Van der Goten, K. (1998). European Journal of Cognitive Psychology, 10, 413-444) on these saccade latencies and errors was studied. This task has the advantage that it loads executive processes, with only minimal interference with verbal or visuo-spatial components. A first experiment compared saccade performance within the prosaccade and the antisaccade task, executed alone and in combination with the RIG task and fixed tapping (added to exclude possible motor component interference explanations). A second experiment investigated the influence of task characteristics on the effects found. Although it was shown that antisaccades are more prone to interference of an executive interference task, it seems that prosaccades are also vulnerable. Interference on prosaccades could originate from a controlled execution of these saccades. A third experiment confirmed that endogenously generated prosaccades are susceptible to dual-task interference and showed that controlled saccade execution, without the need to inhibit a prepotent response, is sufficient to produce interference.
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To evaluate the possible differences in memory dysfunction we analysed the episodic and semantic memory of patients with Alzheimer's disease (AD) and Parkinson's disease (PD) with dementia, and age-matched normal controls (NC). The memory was examined with story recall tests, list learning test with Buschke selective reminding method and category naming test. Both AD and PD groups committed more prior-story intrusion errors as compared with the NC subjects, but only the AD patients committed more extra-story intrusion errors. Both patient groups committed more extra-list intrusion errors than the NC group. Furthermore, the AD patients made more extra-list intrusion errors and recognized more false positive targets than the PD patients did. The results suggest that AD and PD patients have different patterns of memory dysfunction. The AD patients seem to perform poorly because of their inability to inhibit irrelevant information and because of increased sensitivity to interference, whereas the deficits of PD patients only reflect sensitivity to proactive interference.
PURPOSE: Temporal lobe epilepsy patients are well known to present deficits on explicit verbal memory procedures (e.g., recall, recognition). The integrity of implicit memory procedures in these patients is not established. Previous studies in this area used implicit memory measures contaminated by the effects of explicit memory. METHODS: We examined the integrity of verbal implicit and explicit memory in left temporal lobe epilepsy (LTLE) patients and hypothesized that a clear dissociation in performance would be found with a relative preservation of implicit memory. TLE patients (n = 15) and age- and education-matched healthy normal patients (n = 15) were shown a 40-word study list, followed by a test phase requiring completion of word stems based on the study words or new/unseen words. Experimental conditions involved instructions to provide either the old (study) words or novel/nonlist words when completing the stem. Measures of automaticity and recollection provided uncontaminated indices of implicit and explicit memory, respectively. RESULTS: The data showed a significant difference (p < 0.001) between the patients (Recollection, 0.12; SD, 0.18) and controls (0.50, SD, 0.15) on the measure of explicit memory. In contrast, the patients (Automaticity, 0.51; SD, 0.11) and controls (0.45, SD, 0.18) performed similarly on the implicit memory measure, with patient scores clearly at normative levels based on other Process Dissociation Procedure data. CONCLUSIONS: The data demonstrate the integrity of implicit memory in LTLE patients. Finding a dissociation between the two forms of verbal memory in LTLE patients provides evidence that they rely on different neuroanatomic systems.
A same-different letter-matching task was used to examine the effects of stimulus intensity on negative priming, which is poorer performance when target letters have been presented as distractor letters on the immediately preceding trial. In Experiment 1, stimulus intensity was manipulated between-participants, whereas in Experiment 2, it varied randomly from trial-to-trial within-participants. In Experiment 1, negative priming was equivalent for both stimulus intensities. In Experiment 2, negative priming effects were larger for repeated intensity stimuli than for nonrepeated intensity stimuli, when stimulus intensity was dim. Furthermore, for repeated intensity stimuli, negative priming effects were enhanced when the overt response required to the stimulus was repeated from prime to probe trial. These results are consistent with the hypothesis that negative priming may be due to memory confusion, rather than to inhibition of the distractor stimuli.
This article introduces 2 new sources of bias in probability judgment, discrimination failure and inhibition failure, which are conceptualized as arising from an interaction between error prone memory processes and a support theory like comparison process. Both sources of bias stem from the influence of irrelevant information on participants' probability judgments, but they postulate different mechanisms for how irrelevant information affects judgment. The authors used an adaptation of the proactive interference (PI) and release from PI paradigm to test the effect of irrelevant information on judgment. The results of 2 experiments support the discrimination failure account of the effect of PI on probability judgment. In addition, the authors show that 2 commonly used measures of judgment accuracy, absolute and relative accuracy, can be dissociated. The results have broad implications for theories of judgment.
The substantia nigra pars reticulata (SNR) is one of the major output nuclei of the basal ganglia. It connects the dorsal and ventral striatum with the thalamus, superior colliculus and pontomedullary brainstem. The SNR is therefore in a strategic position to regulate sensorimotor behavior. We here assessed the effects of SNR lesions on prepulse inhibition (PPI) of the acoustic startle response (ASR), stereotypy and locomotion in drug-free rats, as well as after systemic administration of the dopamine agonist DL-amphetamine (2 mg/kg), and the NMDA receptor antagonists dizocilpine (0.16 mg/kg) and CGP 40116 (2 mg/kg). SNR lesions reduced PPI, enhanced spontaneous sniffing and potentiated the locomotor stimulation by dizocilpine and CGP 40116. PPI was impaired by dizocilpine and CGP 40116 in controls. The ASR was enhanced in controls by dizocilpine and amphetamine. SNR lesions prevented the enhancement of the ASR by amphetamine. A second experiment tested the hypothesis that the SNR mediates PPI via a GABAergic inhibition of the startle pathway. Infusion of the GABA(B) antagonist phaclofen but not the GABA(A) antagonist picrotoxin into the caudal pontine reticular nucleus reduced PPI. Hence, lesion of the SNR reduces sensorimotor gating possibly by elimination of a nigroreticular GABAergic projection interacting with GABA(B) receptors. Moreover, destruction of the SNR enhances the motor stimulatory effects of amphetamine and of the NMDA antagonists dizocilpine and CGP 40116. We conclude that the SNR exerts a tonic GABAergic inhibition on sensorimotor behavior that is regulated by the dorsal and the ventral striatum.
BACKGROUND: Schizophrenics show deficits in sensorimotor gating, as measured by prepulse inhibition of acoustic startle (PPI). The goal of this investigation is to further characterize PPI and habituation deficits in schizophrenia, and to examine whether differing subgroups of schizophrenics would show comparable PPI deficits. METHODS: PPI was measured in 24 male schizophrenic subjects (9 acutely decompensated inpatients and 15 stable outpatients) and in 20 age-matched normal control subjects. Schizophrenic subjects were rated for positive and negative symptoms at the time of testing. RESULTS: Schizophrenic subjects showed deficits in prepulse inhibition and habituation as compared to normal subjects. Similar latency facilitation was produced by the prepulse in both groups. Acutely decompensated inpatients and stable outpatients did not differ in percent PPI. PPI did not correlate with severity of positive or negative symptoms. CONCLUSIONS: These results suggest that schizophrenic subjects have impaired central inhibitory mechanisms as measured by PPI, and support the hypothesis that periods of relative clinical remission are not accompanied by normalization of sensorimotor gating.