Canadian journal of psychology最新文献

Global cerebral ischemia is well known to cause neuronal necrosis in selectively vulnerable sectors of the hippocampus. Since the hippocampus of the rat is involved in spatial navigation, learning, and memory, selective deficits in these abilities may arise from ischemic brain damage. Previous studies have shown (a) a detectable neurobehavioural deficit due to ischemic brain damage limited to half of the CA1 sector of the hippocampus and (b) a reduction of ischemic neuronal necrosis with the noncompetitive N-methyl-D-Aspartate (NMDA) antagonist MK-801. This study was designed to determine the relationship between the improvement in structural brain damage in postischemically treated rats and any improvement in neurobehavioural performance, using a learning-set water task. Seventeen male Wistar rats received 10.5 min of forebrain ischemia induced by carotid clamping and hypotension. Brain temperature was estimated with probes in the temporalis muscle. Ten of these animals received no therapy (controls), and seven animals received 5 mg/kg MK-801 iv, 20 min postischemia. Six additional rats underwent a sham operation. Postischemic hypothermia was prevented with heating lamps. Four controls and one MK-801 treated animal died. The survivors were then tested on a place learning-set task in a swimming pool paradigm, and quantitative histopathologic analysis of their entire brains was done. The learning-set task revealed defects in spatial navigation, reflected as increased errors and latency in the performance of the untreated control rats. The performance of the MK-801 treated group progressively approached that of sham-operated rats over the course of testing and was significantly better than controls. Importantly, no long-term detrimental effect of MK-801 on the learning-set task performance was seen. Quantitative neuropathology revealed significantly less damage in the MK-801 treated group in all major brain regions. In the hippocampus, MK-801 treated animals showed hippocampal damage limited to the vulnerable portion of the pyramidal cell band comprising 48.8% of the CA1 pyramidal cells, as opposed to 72.4% in untreated controls. Extra-hippocampal damage was evident only in untreated control animals. MK-801 totally prevented neuronal necrosis in both the cerebral cortex and striatum and also prevented infarction in the neocortex and thalamus. Three conclusions emerge from the study. First, postischemic MK-801 mitigates structural brain damage in several brain regions in the absence of concomitant hypothermia. Second, neurobehavioural performance appears to be improved by MK-801 when performance trends are examined, but is somewhat less sensitive than quantitated histopathology due to compounding interanimal variation in performance abilities.(ABSTRACT TRUNCATED AT 400 WORDS)

The goal of these experiments was to evaluate the effects of some drugs affecting noradrenergic (NE) synaptic transmission, commonly prescribed following stroke or traumatic brain injury, on functional recovery. Measurement of recovery from a transient hemiplegia produced by a traumatic unilateral focal contusion in sensorimotor cortex (SMCX) of rats was used to assess the effects of chronic haloperidol (HAL) treatment begun early (1 day) or late (18 days to recovered animals) after injury. Additionally, using the same model, the effects of a single administration of drugs with selective action at NE receptors were also evaluated early or late (30 days) after injury. These drugs were: phenoxybenzamine (PBZ), an alpha 1-NE antagonist; prazosin (PRAZ), an alpha 1-NE antagonist; yohimbine (YOH), an alpha 2-NE antagonist; propranolol (PROP), a beta 1- and 2-NE receptor antagonist; methoxymine (METHOX), an alpha 1-NE agonist; and clonidine (CLON), an alpha 2-NE agonist. The data indicate that drugs with antagonistic effects at alpha 1 NE receptors, including HAL and PRAZ but not PROP, administered early after SMCX contusion retard locomotor recovery. Beneficial effects of enhancing NE transmission by METHOX or YOH were not observed. In animals recovered from beam walk (BW) deficits, a single administration of PBZ or PRAZ (alpha 1 NE antagonists) or CLON (alpha 2 NE agonist) transiently reinstated hemiplegic symptoms. The nonspecific beta NE receptor antagonist PROP had no effect in recovered animals. A single dose of HAL had no effect in recovered animals, but a BW deficit transiently developed in some animals following chronic treatment. The data are discussed with reference to drug contraindications noted in clinical studies of recovery from poststroke aphasia and cognition in demented patients with degenerative brain disease.

The author, a clinical psychologist, sustained a serious head injury in 1977 when research on the rehabilitation of the head injured was in its early stages and advocacy/support organizations did not exist. Despite the total unavailability of formal rehabilitation and therapy, the author, with the help of his family, was eventually able to return to professional practice and attain a reasonable quality of life. In this account, the author describes his journey toward recovery and the ways in which, 12 years postinjury, he copes with the impairments that remain.

This paper presents evidence from microdialysis experiments that three different behavioural outcomes of depletion of striatal dopamine (DA) by either 6-hydroxydopamine or methamphetamine (sparing of function, recovery of function, and loss of function) may be related to differences in the ability of residual DA neurons to maintain extracellular concentrations of DA. It is shown that when up to 80% of the mesostriatal DA system is destroyed, the remaining DA terminals maintain normal extracellular dopamine concentrations. Following a lesion in the 80-95% range, most animals maintain a relatively normal extracellular concentration of DA, but the ability to respond to increased demand is reduced in some animals. When over 95% of the normal DA input to the striatum is destroyed, there is a sharp drop in the extracellular concentration of DA and a nearly complete loss in the ability to increase DA release upon demand. Thus, this new method of sampling extracellular DA and its metabolites in freely moving animals provides insights into the behavioural capacities of animals and into the neural mechanisms that underlie recovery of function following brain damage.

The fuzzy judgement model of Ward (1979) predicts an inverse relation between the amount of stimulus information available to subjects and the magnitude of sequential dependencies on previous stimuli and responses in psychophysical scaling tasks. Ward confirmed this prediction for magnitude estimations of interdot distance for previous responses but not for previous stimuli, although the inverse relation has been repeatedly reported for both the previous stimuli and responses in absolute identification (e.g., Mori, 1989). This paper further explores this seemingly puzzling contradiction. A magnitude estimation of loudness experiment was conducted in which the amount of stimulus information available to subjects was manipulated by a modified version of informational masking (Watson, 1987). An absolute-identification-with-feedback experiment was also conducted to check the effectiveness of the informational masking in reducing the amount of stimulus information. The results of the magnitude estimation experiment show a striking similarity with those of Ward and generalize the failure of sequential dependencies on previous stimuli to vary inversely with stimulus information. An additional assumption that judgement strategies are altered under low-information conditions is necessary to explain this result.

Forty-eight congenitally blind children aged 6 to 14 were asked to discriminate and recognize Braille characters unimanually and to perform unimanual motor tasks which tested tapping ability and grip-strength. Haptic and motor efficiency scores increased with age, but no specific relationships were found between ipsilateral haptic and motor scores. Exploring Braille characters was faster in bimanual than unimanual conditions, but right-hand scores did not differ from left-hand scores. The role of blindness in manual functional asymmetry is discussed.

In a previous study, Earhard and Walker (1985) showed that outer details of forms were more accurately reported than inner details. Although they suggested that this pattern might reflect a routinely applied outside-in processing strategy, their ability to generalize was limited by a reliance on small, single forms which occupied a fixed position in the visual field. To provide a more adequate assessment of generality of outside-in processing, a series of five experiments examined the discriminability of inner- and outer-line detail under a wide variety of conditions. Support for a general outside-in processing routine was obtained. More accurate reporting of outer detail was evident with large as well as small forms, with long and short exposure durations, and with trial-by-trial variations in the size and orientation of forms. Outer lines were also reported more accurately when a number of forms were presented simultaneously for inspection and under circumstances where error rates were low and reaction time procedures were employed. Evidence was presented to support the view that the more accurate discrimination of outer detail reflected the deployment of an attentional strategy.

Previous research has indicated that men who stutter transcribe rapidly presented sequences of letters more slowly and less accurately than nonstutterer controls. Experiment 1 demonstrated that the transcription deficit is not limited to task conditions that demand concurrent monitoring and responding. This was evidenced by comparable deficits on a successive response condition that required subjects to write letters after the presentation was complete. The results of Experiment 2 indicated that the deficit is not due to a difficulty by stutterers in parsing streams of stimulus information internally. Their performance did not differentially improve when letters were grouped with brief pauses, nor with experience in transcribing preparsed letter sequences. This experiment also demonstrated that the phenomenon is generalizable to women. In related testing, stutterers were slower than controls in writing internally generated sequences of letters, those of the alphabet forwards and backwards, but not in writing the same two letters, A and B, repetitively nor in the cognitively more demanding task of writing numbers backwards by three's. These results parallel those obtained with finger tapping of same versus unique sequences by stutterers and were interpreted as being consistent with the idea that while stutterers are not generally slower motorically than nonstutterers, they experience difficulty when required to organize and carry out tasks with new multiple response transitions. The two experiments have replicated and extended, under different conditions, the earlier findings of a letter sequence transcription deficit in stutterers, but the nature of the interference still remains to be clarified.

Priming effects were examined in two experiments using either a pronunciation or lexical decision task. The prime, either a strong associate of the target, an unrelated word, or a neutral prime, was presented for 200 ms. After an SOA of 200, 400, or 800 ms, a masked target was presented for 33.3, 50, or 66.7 ms. Attention was manipulated by varying the probability that prime and target would be strongly associated. Both experiments showed significant interference in the low attention condition and at the 200-ms SOA, presumably before the onset of consciously directed processing. Two subsequent experiments using a short SOA and the low attention condition attempted to determine the conditions under which this interference will occur by varying the interstimulus interval, target duration, and the mask. It was found that interference occurred only when targets were brief and masked. These results are discussed in terms of a model involving lateral inhibition between nodes in semantic memory. It is suggested that when the target is brief and masked, the node in memory corresponding to the target is much less strongly activated and therefore more susceptible to the inhibitory effects of other activated nodes.