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At least 1,027 records · Page 57Linked to original sources
PubMed1998

CCK in anxiety and cognitive processes.

Extensive studies were carried out on the involvement of the CCKergic system in anxiety-, panic- and stress-related behaviour. The stimulation of CCK-A or CCK-B receptors is implicated in the physical and psychological responses of CCK to stress. Furthermore, several selective CCK-B agonists produce anxiogenic-like effects, while CCK-B antagonists induce anxiolytic-like responses in several models of anxiety. However, BC264 a highly selective CCK-B agonist, does not produce anxiogenic-like effects but increases attention and/or memory. These effects are dependent on the dopaminergic systems. Together with biochemical data, this led to the hypothesis of the existence of two CCK-B binding sites, CCK-B1 and CCK-B2, which could correspond to different activation states of a single molecular entity. Investigations into CCK-B1 and CCK-B2 systems might be of critical interest, since only one site, CCK-B1, appears to be responsible for the effects of anxiety. Furthermore, the improvement of attention and/or memory processes by CCK, through CCK-B2 receptors, could offer a new perspective in the treatment of attention and/or memory disorders.

Animals↗
PubMed1998

Immediate versus delayed visual memory task performance among schizophrenic patients and normal control subjects.

In an exploratory study, 10 schizophrenic patients and 10 normal control subjects performed immediate and delayed memory tasks, which were variants of previously developed continuous performance tests. Both tasks required participants to identify five-digit numbers which were repeated. Numbers were presented in series for 500 ms each and separated by a 500-ms time-out period. In the immediate memory task, subjects were to respond if a number was identical to the one that had immediately preceded it. The delayed memory task differed from the first task in that a longer delay (3.5 s) between stimuli was introduced, and during this delay distracter stimuli appeared. While normal control subjects performed accurately on both tasks (exceeding 80% correct detections), schizophrenic patients performed poorly, performing worse on the delayed memory task than on the immediate memory task. Rates of commission errors (responses made to similar, but not identical numbers) were nearly equal between groups on the immediate memory task, but on the delayed memory task normal control subjects made relatively more commission errors while schizophrenic patients made fewer commission errors. No differences in response latencies were observed between subject groups or tasks. This paradigm may prove useful in discriminating subtle differences in immediate and delayed memory capability among psychiatric populations and normal control subjects.

Adult↗
PubMed2002

Impairment of spatial memory in kaolin-induced hydrocephalic rats is associated with changes in the hippocampal cholinergic and noradrenergic contents.

We investigated the relationship between the degree of spatial memory impairment in an 8-arm radial maze and the changes in the contents of acetylcholine (ACh) and noradrenaline (NA) in the dorsal and ventral hippocampus and the frontal cortex, along with histological changes in kaolin-induced hydrocephalic rats. Kaolin-induced hydrocephalic rats were divided into three groups (non-impaired, impaired and severely impaired) according to the degree of impairment in a radial maze. Thirty percent of the hydrocephalic rats could not solve a radial maze (severely impaired group), while the remaining hydrocephalic rats could (non-impaired rats in the standard task). Forty percent of the non-impaired rats in the standard task failed to solve the delayed-response task (impaired group), whereas the remaining rats were able to solve it (non-impaired group). A positive correlation was observed between the impairment of spatial memory and ventricular dilatation. The ACh content in the dorsal and ventral hippocampus, and the NA content in the ventral hippocampus were decreased in the severely impaired group. Moreover, the NA content in the ventral hippocampus was decreased in the impaired group. These results suggest that the impairment of spatial memory in kaolin-induced hydrocephalic rats is associated with dysfunction of the hippocampal cholinergic and noradrenergic systems.

Acetylcholine↗
PubMed2003

Frontal cortex BDNF levels correlate with working memory in an animal model of Down syndrome.

Individuals with Down syndrome (DS) develop most neuropathological hallmarks of Alzheimer's disease early in life, including loss of cholinergic markers in the basal forebrain. Ts65Dn mice, an animal model of DS, perform poorly on tasks requiring spatial memory and also exhibit basal forebrain pathology beginning around 6 months of age. We evaluated memory as well as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) protein levels in basal forebrain, frontal cortex, hippocampus, and striatum in Ts65Dn mice at the age when cholinergic degeneration is first observed, and compared values to normosomic controls. Six-month-old Ts65Dn mice exhibited impairments in working and reference memory as assessed on a water radial-arm maze. The working memory deficit was related to the inability of Ts65Dn mice to successfully sustain performance as the working memory load increased. Coupled with cognitive performance deficiencies, Ts65Dn mice also exhibited lower frontal cortex BDNF protein levels than controls. Further, BDNF levels were negatively correlated with working memory errors during the latter portion of testing in Ts65Dn mice, thereby suggesting that lower BDNF protein levels in the frontal cortex may be associated with the observed working memory impairment.

Animals↗
PubMed1997

Characteristics of memory dysfunction in olfactory bulbectomized rats and the effects of cholinergic drugs.

The memory impairment of olfactory bulbs (OB)-lesioned rats was characterized using 4 different tasks of learning/memory, and the effects of certain cholinergic drugs on such memory impairment were examined. In reference memory and working memory tasks using a 3-panel runway apparatus, OB-lesioned rats showed a marked increase in errors. In the 3-lever operant task using delayed matching to a sample (DMTS) procedure, OB lesions significantly decreased the correct response in choice (test) trials without affecting the in sample (training) trials. An interesting finding is that impairment in the DMTS performance did not appear immediately after the OB lesion, but tended to appear after a delay. Based on this finding, it is unlikely that memory impairment in the OB-lesioned rats is due to the olfactory deficit itself. However, OB lesions significantly reduced the choice accuracy and delayed the choice reaction time during the 3-choice serial time task for assessing attentional function, using a 3-lever operant apparatus. These findings suggest that marked impairment of learning and memory in OB-lesioned rats may be caused by the attention deficit. Furthermore, the memory impairment in OB-lesioned rats was reduced by cholinesterase inhibitors, physostigmine and NIK-247. These finding suggest that dysfunction of the cholinergic system is involved, at least in part, in the memory impairment of OB-lesioned rats.

Animals↗
PubMed1997

Effects of the kappa-opioid dynorphin A(1-13) on learning and memory in mice.

The effects of intracerebroventricular administration of dynorphin A(1-13) on scopolamine- and pirenzepine-induced amnesia were investigated in mice by observing the step-down-type passive avoidance response and spontaneous alternation performance. The pre- or post-training, or preretention administration of dynorphin A(1-13) (0.3-10 micrograms) alone failed to affect the passive avoidance response, while scopolamine (1 mg/kg) significantly inhibited it. Dynorphin A(1-13) (1 microgram) given 15 min before training and retention tests, but not immediately after training, significantly improved the scopolamine (1 mg/kg)-induced impairment of passive avoidance response, indicating the anti-amnesic effects of dynorphin A(1-13). A lower dose (1 mg/kg) of the kappa-opioid receptor antagonist (-)-(1R,5R,9R)-5,9-diethyl-2-(3-furyl-methyl)-2'-hydroxy-6,7-benzomorpha n reversed the anti-amnesic effects of dynorphin A(1-13) (1 microgram). In contrast, although dynorphin A(1-13) (1, 3 and 10 micrograms) did not influence spontaneous alternation performance, scopolamine (1 mg/kg) and the muscarinic M1 receptor antagonist pirenzepine (3 micrograms) markedly decreased spontaneous alternation performance. Dynorphin A(1-13) (3, 5.6 and/or 10 micrograms) significantly improved the scopolamine (1 mg/kg)- and pirenzepine (3 micrograms)-induced impairment of spontaneous alternation performance. The improving effects of dynorphin A(1-13) (3 micrograms) were almost completely reversed by pretreatment with nor-binaltorphimine (4 micrograms), a kappa-selective opioid receptor antagonist. These results suggest that the stimulation of kappa-opioid receptors improves memory dysfunctions resulting from the blockade of muscarinic M1 receptors.

Analgesics, Opioid↗
PubMedDate not supplied

[Confirmation of cortical lesions of progressive prosopagnosia by cerebral SPECT].

We present the case of a 78 year old man admitted to the hospital with progressive memory disorder. Neuropsychological examination showed inability to recognize familiar faces (prosopagnosia). MRI documented cortical atrophy, which did not explain the neurological deficit. CT did not show abnormalities. Most patients with prosopagnosia present brain atrophy, as they are more than 65 years old. Scanning by SPECT revealed hypoperfusion in the right parietotemporal region, which was worse in a later examination.

Aged↗
PubMed1994

[Contribution of morphological imaging in the diagnosis of dementia. I--Alzheimer disease].

In patients with Alzheimer's disease, morphological neuroimaging techniques usually reveal signs of global cerebral atrophy which gradually worsen over time and depends on age and severity of the cognitive decline. Because of the lack of artifacts and of a more appropriate angle, magnetic resonance imaging scans may visualize a prominent atrophy of the medial temporal lobes, including hippocampal structures. Hippocampal atrophy is relatively specific of Alzheimer's disease before 65 and is related to the severity of memory disorders. White matter changes in patients without cerebrovascular risk factors are not more severe in patients with presenile Alzheimer's disease than in age-matched controls. They are, however, more severe in patients with senile onset than in age-matched controls. These findings suggest that white matter changes in patients with senile onset are consistent with a diagnosis of Alzheimer's disease.

Alzheimer Disease↗
PubMed2004

Protection against beta-amyloid peptide-induced memory impairment with long-term administration of extract of Angelica gigas or decursinol in mice.

We investigated the effect of long-term oral administration of ethanolic extract of Angelica gigas Nakai (Umbelliferae) (EAG) or decursinol, a coumarin isolated from A. gigas, on beta-amyloid peptide 1-42 (Abeta(1-42))-induced memory impairment in mice. Mice were allowed free access to drinking water (control) or water containing different concentrations of EAG. After 4 weeks, Abeta(1-42) (410 pmol) was administered via intracerebroventricular injection. Pretreatment of mice with EAG (0.1%) for 4 weeks significantly blocked the Abeta(1-42)-induced impairment in passive avoidance performance. Next, mice were fed with chow mixed with various doses of decursinol for 4 weeks before intracerebroventricular injection of Abeta(1-42) (410 pmol). Pretreatment of mice with decursinol (0.001%, 0.002%, and 0.004%) for 4 weeks significantly attenuated the Abeta(1-42)-induced impairment in passive avoidance performance. Decursinol (0.004%) also significantly blunted the Abeta(1-42)-induced decrease in alternation behavior (spatial working memory) in the Y-maze test without change in general locomotor activity. These findings suggest that EAG or decursinol may have preventive effect against memory impairment related with Abeta of Alzheimer's disease.

Amyloid beta-Peptides↗
PubMed1997

Microdialysis-coupled place cell detection in the hippocampus: a new strategy for the search for cognition enhancer drugs.

1. The MPCD method in freely moving rats is a new neuroscience technique. It is able to detect the location-specific firing of hippocampal place cells, and to deliver, via microdialysis, various drug solutions into the extracellular environment of the detected neurons. Place cells are critical elements of the neural system in brain which governs cognitive processes. It is emphasized in this article that effective cognition enhancer drugs must selectively and significantly affect the firing of these cells. 2. By using MPCD, it is possible to recognize drug combinations which can increase the location-specific firing of place cells to an optimal level. This paper proposes that such pharmacological action facilitates engram-creation in extrahippocampal cortical areas, improving cognitive functions. Thus, an MPCD-based research strategy may lead to the rational development of a new generation of cognition enhancer drugs for the treatment of learning and memory disorders, including Alzheimer's disease (AD).

Animals↗
PubMed2003

In-hospital cardiac arrest leads to chronic memory impairment.

OBJECTIVE: To assess the prevalence and severity of memory deficits in a group of patients who survived an in-hospital cardiac arrest (IHCA) in comparison with patients resuscitated after cardiac arrest outside hospital (OHCA) and patients with acute myocardial infarction (MI). SUBJECTS: Thirty-five IHCA survivors, 35 OHCA survivors, and 35 patients who had suffered MI uncomplicated by cardiac arrest. PROCEDURE: Participants were assessed 8.2 (4.5) months after the event for current affective state (Hospital anxiety and depression scale (HADS)), pre-morbid intelligence (National adult reading test (NART)), short-term memory (digit span test) and long-term episodic memory (Rivermead behavioural memory test-RBMT). RESULTS: IHCA patients scored lower on the RBMT than MI controls but did not score significantly differently OHCA patients. Moderate or severe memory impairment was found in 26% of the IHCA group and 38% of the OHCA group. None of the MI group was found to have this degree of impairment. This difference in prevalence of memory impairment between the two cardiac arrest groups was not statistically significant. However, both arrest groups had significantly greater memory impairment than the MI control group. CONCLUSIONS: Clinically important memory impairment was found in one in four patients surviving IHCA. The shorter arrest durations that are thought to be associated with IHCA may not be sufficient to protect patients from memory impairment associated with cerebral hypoxia.

Adolescent↗
PubMed2001

Effect of vagal autotransplantation on quantitative [3H]-vesamicol binding image in rats with unilateral lesions of nucleus baslis magnocellularis.

It is considered that nodosal ganglion grafting improves learning and memory disorder in nucleus basalis magnocellularis lesioned rats, and that [3H]-vesamicol is one of the mapping agents for presynaptic cholinergic neurons. Quantitative autoradiography was performed using high sensitive imaging plate system to evaluate the effect of neurotransplantation on [3H]-vesamicol binding. The affected-side to unaffected-side ratio of [3H]-vesamicol in the nucleus basalis magnocellularis lesioned group was significantly lower than that in the sham-operated group at 1, 2 and 4weeks (P<0.01). In the transplanted group, the ratio was significantly higher than that in the untreated group at 4weeks (P<0.05). [3H]-vesamicol binding is one of the most sensitive indicators of nucleus basalis magnocellularis lesions and the effect of the nodosal ganglion grafting.

Animals↗
PubMed2002

Spatial memory testing decreases hippocampal amyloid precursor protein in young, but not aged, female rats.

Using young and aged rats, we investigated relationships between amyloid precursor protein (APP) and working or reference memory, as well as assessed whether cognitive testing altered APP levels. In young rats, higher APP levels were related to more working memory errors as a linear function. Aged rats exhibited a curvilinear relationship between APP and working memory, with moderate APP levels associated with better relative performance. A comparison of rats that received cognitive testing with those that did not showed that testing decreased APP levels in young, but not aged, rats. Collectively, the data suggest that young and aged rats exhibit different relationships between APP and working memory, and that aged rats do not maintain the capacity to decrease APP in response to cognitive testing.

Aging↗
PubMed1998

Impaired short- and long-term memory in Ts65Dn mice, a model for Down syndrome.

Ts65Dn (TS), control littermates (CO) and Swiss (SW) male mice were tested in the elevated plus-maze and in the Morris water maze (MWM) for memory evaluation. In the plus-maze, each mouse was placed at the end of an open arm and initial freezing and the time to enter into an enclosed arm (transfer latency) were measured. SW mice decreased both measures over repeated trials, whereas no decrease of freezing was observed in CO mice, thus suggesting increased emotionality in this group. Compared to CO mice, TS mice showed less initial freezing, shorter transfer latencies, and spent less time in enclosed arms, suggesting a reduced ability to habituate or to inhibit behaviour. Animals were also submitted to a learning-set paradigm consisting of reaching a new platform position each day in the MWM. Two training phases (separated by a resting period of 6 weeks), each including eight acquisition and four cued sessions, were performed (each session consisting of four pairs of trials). CO and SW mice already reached an asymptotic performance by the second day of the first phase whereas TS mice did not achieve that level until the second training phase. The progression over trials indicated that CO and SW animals learned the new platform position between trials 1 and 2 of each session, whereas TS animals failed to do it and had more difficulties to find the platform when it was placed in the centre of the pool as compared to the other positions (SW, NE, E). The results suggest that TS mice show working memory impairments in addition to long-term memory deficits, although extensive training appeared to facilitate TS mice to achieve a level of performance similar to their control littermates. This represents another aspect of the cognitive deficits shown by TS mice: a mouse model of the human Down syndrome.

Animals↗
PubMed2003

Single intracerebroventricular administration of amyloid-beta (25-35) peptide induces impairment in short-term rather than long-term memory in rats.

Ample experimental evidence indicates that intracerebral injection or infusion of amyloid-beta peptides (Abeta) to rodents induces learning and memory impairments as well as neurodegeneration in brain areas related to cognitive function. In the present study, we assessed the effects of a single intracerebroventricular (i.c.v.) injection of aggregated Abeta fragment (25-35) at a dose of 15nmol/rat on short-term and long-term memory in rats during the 6-month post-surgery period. The results demonstrate that Abeta(25-35)-induced memory impairments in spontaneous alternation behavior in a Y-maze at 17, 36, and 180 days after the surgery as well as in a social recognition task 110 days post-surgery. Abeta(25-35) also impaired spatial memory in an 8-arm radial maze, but did not influence performance of the step-down passive avoidance task. These results suggest that Abeta(25-35) preferably induces impairments of spatial and non-spatial short-term (working) memory rather than long-term memory in rats.

Amyloid beta-Peptides↗
PubMed2004

Comparison of Predicted-difference, Simple-difference, and Premorbid-estimation methodologies for evaluating IQ and memory score discrepancies.

Discrepancies between WAIS-III and WMS-III scores for a group of 39 males and 48 females with a history of TBI were examined using three methodologies: Predicted-difference, Simple-difference, and Premorbid-estimation methods. Overall, the Predicted-difference method tended to classify the fewest individuals as impaired based on statistical rarity of discrepancies (11-16% classified as impaired), while the regression-based Premorbid method tended to classify the fewest individuals as impaired based on clinical rarity of discrepancies (4-8% classified as impaired). Degree of agreement is reported and was substantial. The only comparison between methods to reach statistical significance was the Predicted-difference method classifying subjects as impaired at a higher rate than other methods for Auditory Delayed memory index (Cochran's Q = 7.00, P < .05). Findings suggest a combination of estimates of premorbid functioning and regression-based predicted scores is optimal for interpreting IQ/memory score discrepancies. Clinical implications are discussed.

Adult↗