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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neurophysins are neuropeptides (MW +/- 10,000) synthetized together with active nonapeptides vasopressin (AVP) and oxytocin (OT). The original description of the radioimmunoassay for neurophysins in 1969 allowed us to demonstrate the concomitant, equimolecular, release of them together with AVP and OT, thus bringing strong arguments in favour of neurohypophyseal exocytosis. Beside the use of those RIAs as direct indexes of neurohypophyseal release in various physiological and pathological conditions, we have been interested these last two years, to the putative use of neurophysins RIA as direct neuroendocrine markers in various neuropsychiatric diseases (depression, mania, schizophrenia) and paraneoplastic syndromes (SIADH).
Bull Mem Acad R Med Belg 1990
PMID:[Neurophysins]. 209 28

In three experiments, we examined the performance of patients with schizophrenia on implicit and explicit memory tests that have been shown to involve predominantly data-driven or predominantly conceptually driven processes. In Experiment 1, we compared the implicit tests of category production (conceptually driven) and word identification (data driven) and found that schizophrenic patients' performance on these tests did not differ from that of normal subjects. In Experiment 2, a comparison of the category-production and explicit cued-recall tests, both of which involve conceptual processes, showed that schizophrenic patients were impaired on the cued-recall test but not on the category-production test. In Experiment 3, a comparison of the word-identification and explicit graphemic cued-recall tests, both of which involve data-driven processes, showed that patients were impaired on the cued-recall test but not on the word-identification test. The results of both Experiments 2 and 3 revealed a dissociation between implicit and explicit test performance under conditions in which the two tests involve similar types of processes. These results support theoretical views that distinguish implicit from explicit modes of retrieval.
Mem Cognit 1993 Jan
PMID:Limits of the processing view in accounting for dissociations among memory measures in a clinical population. 843 49

The association between a conditioned stimulus (CS) and an unconditioned stimulus (US) in fear-conditioning depends on N-methyl-D-aspartate (NMDA) receptors in the basolateral amygdala complex (BLA). Latent inhibition (LI) is the retardation in learning due to nonreinforced presentation of the prospective CS before conditioning. Disruption of LI in rats is an animal model of schizophrenia, reflecting the deficits of schizophrenic patients in neglecting irrelevant information. We investigated whether the BLA is involved in LI of fear-potentiated startle. Infusions of the NMDA receptor antagonist D,L-2-amino-5-phosphonopentanoic acid (AP-5; 12.5 nmoles) into the BLA before preexposure of rats to the neutral stimulus prevent LI of fear-conditioning. We also demonstrated by the same method that a complex of thalamic nuclei, comprising the medial part of the medial geniculate nucleus, the posterior intralaminar nucleus, and the suprageniculate nucleus, is involved in fear-conditioning, but not in LI. This suggests that the presentation of an innocuous stimulus during preexposure leads to an NMDA receptor-dependent change of neurotransmission in the BLA, but not in the thalamus. Our data show that the BLA but not the thalamus regulates in LI of fear-potentiated startle. Furthermore, it supports the hypothesis that the inability of schizophrenic patients to ignore irrelevant stimuli may be caused by hypofunction of the glutamatergic transmission in the brain and suggests an involvement of the amygdala in the neuropathology of schizophrenia.
Learn Mem
PMID:Blockade of NMDA receptors in the amygdala prevents latent inhibition of fear-conditioning. 1111 98

Different forms of nondeclarative learning involve regionally specific striatal circuits. The motor circuit (involving the putamen) has been associated with motor-skill learning and the dorsolateral prefrontal cortex (DLPFC) circuit (involving the caudate) has been associated with cognitive-habit learning. Efforts to differentiate functional striatal circuits within patient samples have been limited. Previous studies have provided mixed results regarding striatal-dependent nondeclarative learning deficits in patients with schizophrenia. In this study, a cognitive-habit learning task (probabilistic weather prediction) was used to assess the DLPFC circuit and a motor-skill learning task (pursuit rotor) was used to assess the motor circuit in 35 patients with schizophrenia and 35 normal controls. Patients with schizophrenia displayed significant performance differences from controls on both nondeclarative tasks; however, cognitive-habit learning rate in patients did not differ from controls. There were performance and learning-rate differences on the motor-skill learning task between the whole sample of patients and controls, however, analysis of a subset of patients and controls matched on general intellectual level eliminated learning rate differences between groups. The abnormal performance offset between patients with schizophrenia and controls in the absence of learning rate differences suggests that abnormal cortical processing provides altered input to normal striatal circuitry.
Learn Mem
PMID:Habit and skill learning in schizophrenia: evidence of normal striatal processing with abnormal cortical input. 1246 3

Although subchronic phencyclidine (PCP) administration is recognized as a probative method to model schizophrenia-like symptoms in animals, only a few sets of data support the hypothesis of a cognitive prefrontal cortex (PFc) dysfunction in PCP-treated monkeys and rodents. Two experiments were here conducted to further test the integrity of prefrontal function in two versions of a memory for temporal order (MTO) task administered to rats. Original versions of this task elaborated by Kesner repeatedly yielded moderate to severe performance deficits in PFc lesioned rats. MTO assessment in an eight-arm radial maze consisted in a recency discrimination between two arms previously explored in the context of sequential forced choices. In Experiment 1, 16 naive Long-Evans rats were pre-trained on a variable version of the MTO task involving randomly re-mixed sequences until they reached a group criterion. Then, rats were treated daily for 21 days with PCP (10mg/kg) or saline vehicle and were tested on the same task approximately 20 h after an injection. The performance of the groups did not differ. In Experiment 2, 16 naive Long-Evans rats untrained prior to treatment received 27 daily injections of either PCP (10mg/kg) or saline vehicle and were tested, 20 h after each injection, on a constant version of the MTO task. This time, a fixed set of four sequences of successive arm entries was repeated within each daily session as well as across days. Again, prolonged PCP exposure failed to impair discrimination of temporal order despite the stability of sequential information over time. These negative results are not consistent with long-lasting hypofrontality, a major landmark of human schizophrenia, in the PCP rat model.
Neurobiol Learn Mem 2003 Sep
PMID:Schizophrenia-like syndrome inducing agent phencyclidine failed to impair memory for temporal order in rats. 1293 31

This study reviews the role of the serotonin 5-HT2A receptor in learning as measured by the acquisition of the rabbit's classically conditioning nictitating membrane response, a component of the eyeblink response. Agonists at the 5-HT2A receptor including LSD (d-lysergic acid diethylamide) enhanced associative learning at doses that produce cognitive effects in humans. Some antagonists such as BOL (d-bromolysergic acid diethylamide), LY53,857, and ketanserin acted as neutral antagonists in that they had no effect on learning, whereas others (MDL11,939, ritanserin, and mianserin) acted as inverse agonists in that they retarded learning through an action at the 5-HT2A receptor. These results were placed in the context of what is known concerning the anatomical distribution and electrophysiological effects of 5-HT2A receptor activation in frontal cortex and hippocampus, as well as the role of cortical 5-HT2A receptors in schizophrenia. It was concluded that the 5-HT2A receptor demonstrates constitutive activity, and that variations in this activity can produce profound alterations in cognitive states.
Learn Mem
PMID:Role of the serotonin 5-HT(2A) receptor in learning. 1455 8

Glia form a cellular network consisting mainly of astrocytes that nourish the neurons, oligodendrocytes that form myelin, and microglia that ensure the immunological defence of the nervous system. Experimental allergic encephalomyelitis is an animal model of multiple sclerosis, characterised by cellular infiltrates and demyelinisation in the central nervous system. It can be induced in susceptible rats (DA) by inoculation of foreign protein. Other, non-susceptible rats (AO) have infiltrates that disappear without functional signs of disease. We have found microglia and astrocytes in infiltrates 10 days after inoculation. At 14 days they are even more marked in the DA, but astrocytosis is less in the AO. Microglia have disappeared at 14 days in the DA, but persist in the AO. We suggest that the infiltrates are dispersed by microglial activity that persists in the AO and prevents astrocytosis. In the DA the loss of microglia allows gliosis to occur, with demyelination due to lesions of oligodendrocytes, and clinical signs. We have also studied astrocytes and microglia in the cerebral cortex of schizophrenics and control non-schizophrenics. The number of astrocytes does not vary between patients and controls, but microglia are more numerous in the patients. We conclude that there is a cortical microgliosis in schizophrenia that may be a response to an earlier lesion, perhaps protecting neighbouring neurons.
Bull Mem Acad R Med Belg 2003
PMID:[Role of neuroglia in central nervous system diseases]. 1513 3

Verbal declarative memory is one of the most reliably impaired cognitive functions in schizophrenia. Important issues are whether the problem is reversible, and which brain regions underlie improvement. We showed previously that glucose administration improved declarative memory in patients with schizophrenia, and sought in this pilot study to identify whether glucose affects the location or degree of activation of brain regions involved in a verbal encoding task. Seven clinically stable and medicated patients with schizophrenia or schizoaffective disorder, who showed deficits on a clinical test of memory, participated in the study. Subjects served as their own controls in a double-blind, crossover protocol that consisted of two sessions about a week apart. In each session, subjects ingested a beverage flavored with lemonade that contained 50 g of glucose on one occasion, and saccharin on the other. Blood glucose was measured before and 15, 50, and 75 min after ingestion. After ingesting the beverage, they performed a verbal encoding task while undergoing brain functional magnetic resonance imaging. The results showed significantly greater activation of the left parahippocampus during novel sentence encoding in the glucose condition, compared to the saccharin condition, despite no change in memory performance. A trend towards greater activation of the left dorsolateral prefrontal cortex (p<.07) was also evident in the glucose condition. These pilot findings emphasize the sensitivity of both the medial temporal and prefrontal regions to effects of glucose administration during encoding, and are consistent with the hypothesis that these regions also participate in declarative memory improvements following glucose administration.
Neurobiol Learn Mem 2005 Jan
PMID:Medial temporal and prefrontal lobe activation during verbal encoding following glucose ingestion in schizophrenia: A pilot fMRI study. 1560 89

The well-known family of low-density lipoprotein receptors represents a collection of ancient membrane receptors that have been remarkably conserved throughout evolution. These multifunctional receptors, known to regulate cholesterol transport, are becoming increasingly interesting to the neuroscience community due to their ability to transduce a diversity of extracellular signals across the membrane in the adult CNS. Their roles in modulating synaptic plasticity and necessity in hippocampus-specific learning and memory have recently come to light. In addition, genetic, biochemical and behavioral studies have implicated these signaling systems in a number of human neurodegenerative and neuropsychiatric disorders involving loss of cognitive ability, such as Alzheimer's disease, schizophrenia and autism. This review describes the known functions of these receptors and discusses their potential role in processes of synaptic regulation and memory formation.
Neurobiol Learn Mem 2006 Jan
PMID:A fresh look at an ancient receptor family: emerging roles for low density lipoprotein receptors in synaptic plasticity and memory formation. 1619 8

Clozapine is an atypical antipsychotic drug that has been shown to improve spatial memory in some animal models; however its efficacy in reversing spatial memory impairment in rats with hippocampal lesions is unknown. To address this issue, we tested the effects of clozapine on delayed spatial alternation deficits in rats with hippocampal damage in three separate experiments. In each experiment, adult male rats received sham surgery or direct stereotaxic infusions of the excitotoxin, NMDA, into the hippocampus. In the first study, seven days after surgery, the sham control animals received daily saline injections while the lesioned animals were split into two groups that received daily saline or clozapine (2.0 mg/kg, sc) injections. During the fifth week of injections, all animals were tested in a food-motivated delayed spatial alternation task. Saline-treated rats with excitotoxic hippocampal damage displayed significant deficits in delayed spatial alternation. Daily clozapine injections completely reversed this deficit. In a second experiment, it was found that clozapine treatment limited to the testing days only did not improve alternation performance in lesioned rats. Finally, in a third experiment, chronic clozapine treatment did not improve alternation performance in lesioned rats that were pre-trained in the alternation task prior to surgery. These results suggest that chronic, but not acute, clozapine treatment enables rats with hippocampal damage to develop new spatial learning, but can not rescue old spatial learning established prior to damage. These results may have implications for the treatment of cognitive deficits caused by hippocampal dysfunction in disorders such as schizophrenia, Alzheimer's disease, and others.
Neurobiol Learn Mem 2006 Jan
PMID:The effects of clozapine on delayed spatial alternation deficits in rats with hippocampal damage. 1621 57


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