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PubMedDate not supplied

Age-related changes in calcium homeostatic mechanisms in synaptosomes in relation with working memory deficiency.

Aging is associated with alterations in different systems that govern neuronal calcium homeostasis. This study was designed to determine whether any of these alterations may contribute to the decline in spatial working memory that is observed in old rats. Several parameters [initial (5 s) and steady state (15 min) 45Ca2+ uptake, FCCP-releaseable 45Ca2+, [Ca2+]i levels, depolarization-induced phosphoprotein (P97, PP65, P42) dephosphorylation and acetylcholine levels and release) involved in calcium homeostasis/signaling were determined in whole brain synaptosomes derived from adult (9-month-old) and old (24-month-old) rats that were evaluated for spatial memory performance in the eight-arm radial maze. The neurochemical analysis indicated that both the 9- and 24-month-old rats were impaired with respect to 3-month-old animals. When learners (animals reaching criterion; RC) were compared to memory impaired rats (MI), it was found that the FCCP-releaseable 45Ca2+ of synaptosomes, that reflects mitochondrial calcium, was lower in the MI than the RC rats and was correlated with the behavioral performance of the rats in their first testing sessions. The results suggest that the loss of calcium uptake capacity in synaptic mitochondria during aging may be associated with impaired working memory in old animals.

Acetylcholine↗

PubMed1996

[Subcortical dementia].

Subcortical dementia, a concept introduced 20 years ago, is a clinical entity characterized by memory disorders, an impaired ability to manipulate acquired knowledge, important changes of personality (apathy, inertia or depression), slowed thought processes (or bradyphrenia). It is also marked by overwhelming signs of frontal dysfunction. Cognitive and behavioural disturbances are frequently combined to movement disorders (tremor, chorea, dystonia etc). Anatomical, clinical and scintigraphic data suggest that the frontal signs result from a disconnection of the frontal cortex from the basal ganglia. Therefore it is probably more accurate to use the term subcortico-frontal dementia. This pattern of dementia, clearly different from a cortical dementia as dementia of Alzheimer's disease, may be described in a wide range of diseases which mainly involve the subcortical areas: some cases of Parkinson's disease, Progressive Supranuclear Palsy, Huntington's disease, Wilson's disease, the état lacunaire, multiple sclerosis and so on. The concept of subcortical dementia has allowed a better understanding of the role of the basal ganglia and their cortical connections in cognition and behavior. Its neurochemical substrate remains poorly characterized, although the ascending dopaminergic and cholinergic pathways seem to be good candidates, at least in Parkinson's disease.

Brain Diseases↗

PubMed1984

Choline production from choline-containing phospholipids: a hypothetical role in Alzheimer's disease and aging.

Deficits in certain long-axon cholinergic brain neurons have been demonstrated both in senile dementia of the Alzheimer type (SDAT) and, to a lesser degree, in association with the cognitive and memory impairments sometimes seen with normal aging. Our studies support a hypothesis concerning the selective vulnerability of these neurons. In our superfused brain slice system, acetylcholine (ACh) release was dependent on the concentration of exogenous choline, at rest and during electrical stimulation. Decreases in intracellular levels of ACh and choline accounted for only a small fraction of the quantities of these compounds released into the superfusates, suggesting that some tissue pool of bound choline, such as the phospholipids (PL), might have liberated choline. In choline-free medium, the release and tissue content of ACh were sustained; thus, choline released from the putative endogenous pool can be utilized for ACh synthesis. We hypothesize that the use, by cholinergic neurons, of choline originating from the breakdown of membrane PL, may result in an impoverishment in certain PL. Since only cholinergic neurons use their membrane PL as a reservoir for their neurotransmitter's precursor, this relationship might explain the major deficits in long-axon cholinergic nerve terminals seen in SDAT and other age-related memory disorders.

Acetylcholine↗

PubMed1995

Rheoencephalographic and electroencephalographic measures of cognitive workload: analytical procedures.

This investigation demonstrates the feasibility of mental workload assessment by rheoencephalographic (REG) and multichannel electroencephalographic (EEG) monitoring. During the performance of this research, unique testing, analytical and display procedures were developed for REG and EEG monitoring that extend the current state of the art and provide valuable tools for the study of cerebral circulatory and neural activity during cognition. REG records are analyzed to provide indices of the right and left hemisphere hemodynamic changes that take place during each test sequence. The EEG data are modeled using regression techniques and mathematically transformed to provide energy-density distributions of the scalp electrostatic field. These procedures permit concurrent REG/EEG cognitive testing not possible with current techniques. The introduction of a system for recording and analysis of cognitive REG/EEG test sequences facilitates the study of learning and memory disorders, dementia and other encephalopathies.

Adult↗

PubMed1995

Complete callosal disconnection after closed head injury.

We report a patient with complete callosal disconnection syndrome after severe closed head injury. MRI showed a complete destruction of the corpus callosum throughout its length. Although traumatic callosal lesions are a frequent finding in autopsy studies, as well as in some recent MRI studies, clinical signs of callosal disconnection are rarely observed after head injuries and a complete disconnection syndrome has not been reported yet. This case study and the review of other reported cases suggest that posttraumatic callosal disconnection is probably often overlooked. Our patient had also a severe memory disorder that might be partly related to the bilateral involvement of the fornix, as this structure is closely adjacent to the posterior corpus callosum, and was also shown by MRI to be very probably damaged.

Adult↗

PubMed1986

Kindling of the hippocampus induces spatial memory deficits in the rat.

Since kindling produces electrophysiological and morphological changes in the brain area stimulated, it may well affect behavioural functions dependent on the kindled area. Using an 8-arm maze, it was found that hippocampal kindling can induce specific memory deficits in spatial tasks. Reference (long-term) memory as well as working (short-term) memory were impaired. The largest impairment was observed during the period in which generalized convulsions occurred. Working memory but not reference memory impairment was reversible. Hippocampal kindling may be a useful experimental model for investigating behavioural deficits correlated with epileptogenesis.

Animals↗

PubMed1990

Cholinergic stimulation enhances long-term potentiation in the CA1 region of rat hippocampus.

The effect of the cholinergic agonist carbachol on a putative substrate for memory (long-term potentiation; LTP) was investigated in slices of rat hippocampus (CA1 region). Carbachol (5 microM) increased LTP when the presynaptic depression of the EPSP was controlled. The results indicate that carbachol enhances the effectiveness of the tetanus, probably through postsynaptic mechanisms. This effect may have implications for the role of acetylcholine in memory and the use of cholinergics in memory disorders.

Animals↗

PubMed1993

Deficits in working but not reference memory in adult rats in which limbic seizures had been induced before weaning: implications for early brain injuries.

Male adult rats that displayed limbic seizures between postnatal days 18 and 21 after a single s.c. injection of Li followed 4 h later by a muscarinic agent were trained in a radial arm maze; they were compared with rats that had received the Li-pilocarpine (but had not displayed overt seizures) and to nonhandled controls. Only the rats that had displayed the (preweaned) seizures displayed significant impairment for working memory but not for reference memory. Light microscopy demonstrated histological evidence of earlier damage only within select thalamic structures that are directly associated with the amygdaloid-hippocampal complex. The results are compatible with the hypothesis that early seizures during the time of CA1 hippocampal maturation can produce long-term changes in the efficacy of short-term memory.

Animals↗

PubMed1994

The activity of synaptosomal calcium channels is inversely correlated with working memory performance in memory impaired, aged rats.

Aged, memory-impaired rats do not learn an 8-arm radial maze task but differ in their performance along testing. The aim of this study was to determine whether any of the systems that govern calcium homeostasis in synaptosomes may be related to that difference in performance. A negative correlation between initial (5 s) K(+)-stimulated 45Ca2+ uptake and the behavioral scores from the last testing sessions was obtained K(+)-stimulated 45Ca2+ uptake showed also a negative correlation with an improvement score that evaluates the progress made by the rat along testing. The results support the notion that calcium inflow through synaptosomal voltage gated calcium channels in old rats is inversely correlated with their behavior. This may explain the beneficial effects of organic calcium channel blockers on behavioral performance in aged animals.

Aging↗

PubMed1996

Administration of amyloid beta-peptides in the rat medial septum causes memory deficits: reversal by SR 57746A, a non-peptide neurotrophic compound.

Different putative toxic amyloid beta (A beta) peptides, beta (1-42), beta (1-40) and beta (25-35), were infused (0.75, 1.5 or 3 nmol) in the rat medial septum. Memory deficits were then investigated using the social recognition test. A significant amnesia was observed 4, 7 and 14 days after intraseptal injection of 3 nmol of beta (1-42), beta-(1-40)- and beta (25-35). Lower amounts of beta (1-42) were inactive except 1.5 nmol that disrupted memory 7 days post-treatment. Used as control, the inverted peptide beta (40-1) and the scrambled beta (25-35) were inactive. Using the prolongation procedure, rats infused with 3 nmol of beta (1-40) were still able to recognize the same juvenile. Finally, a daily treatment with the non-peptide neurotrophic compound SR 57746A (10 mg/kg p.o.) over 21 days, prevented the deficits in short-term memory induced by the intraseptal infusion of 3 nmol of either beta (1-40) or beta (25-35). These findings suggest that A beta fragments could impair short-term memory when infused in the rat medial septum, an effect that is prevented by SR 57746A.

Amyloid beta-Peptides↗

PubMed1996

Effect of cholinergic activation by physostigmine on working memory failure caused in rats by pharmacological manipulation of hippocampal glutamatergic and 5-HTergic neurotransmission.

The muscarinic receptor antagonist scopolamine significantly increased the number of errors in the working memory task with a three-panel runway setup, when injected bilaterally at 3.2 micrograms/side into the dorsal hippocampus. The increase in working memory errors induced by intrahippocampal 3.2 micrograms/side scopolamine was reduced by concurrent injection of the cholinesterase inhibitor physostigmine (1.0 and 3.2 micrograms/side. However, physostigmine (3.2 micrograms/side) did not affect an increase in working memory errors induced by intrahippocampal injection of the competitive N-methyl-D-aspartate (NMDA) receptor antagonist (+/)-3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) at 32 ng/side. Likewise, physostigmine (3.2 micrograms/side) was ineffective in reducing an increase in working memory errors caused by intrahippocampal administration of the 5-hydroxytryptamine1A (5-HT1A) receptor agonist (+/-)-8-hydroxy-2-(di-n-pro-pylamino)tetralin (8-OH-DPAT) at 10 micrograms/side. These results suggest that the septohippocampal cholinergic activity is necessary for normal working memory processes, but that cholinergic activation neither compensates loss of hippocampal NMDA receptor-mediated neurotransmission nor counteracts the overstimulation of hippocampal 5-HT1A receptors in terms of working memory function.

Acetylcholine↗

PubMed1996

Reduction of regional brain glucose metabolism following different durations of chronic ethanol consumption in mice: a selective effect on diencephalic structures.

The effects of chronic alcohol consumption on regional brain glucose metabolism were examined in Balb/c mice using the [14C]2-deoxyglucose autoradiographic technique. Animals were given a solution of 12% v/v ethanol as their only source of fluid for either 6, 12 or 18 months and compared to control groups receiving either an isocaloric solution or saccharose or tap water. Alterations of cerebral brain glucose metabolism were assessed in mice who were returned to a non-alcoholic diet and allowed to freely explore a T-maze. The results showed that chronic ethanol consumption induced reductions of regional metabolic activity which were functions both of the duration of alcohol treatment and of the structure studied. Whereas a six month period of alcoholization did not induce any significant effects on metabolic activity, 12 months of treatment were necessary to induce the first observable and significant reductions in [14C]2-deoxyglucose labelling. These effects were mainly limited to diencephalic structures such as the lateral mammillary nuclei and the anterodorsal thalamic nuclei. The cerebellum was also affected but to a lesser degree. After 18 months of alcoholization, a generalized spread of the metabolic reduction to the entire mammillary complex (lateral, medial and posterior nuclei) and to the thalamic nuclei was observed. This same duration of treatment was necessary to induce the first detectable decrease of metabolic activity in the hippocampus. In agreement with data from human neuropathology, these findings confirm the particular vulnerability of diencephalic structures to ethanol and suggest that damage limited to diencephalic regions rather than to hippocampal or cortical areas could be primarily responsible for the memory disorders observed in Korsakoff's syndrome.

Alcohol Drinking↗

PubMed1991

MRI of the normal hippocampus.

Before it is possible to use MR imaging to investigate changes in the hippocampus in disease processes such as epilepsy and memory disorders, it is imperative that normal variations are defined. Using specific anatomic locations, we evaluated the hippocampi of 29 normal volunteers with coronal MR studies. Mild variations occur with regard to hippocampal size and shape, and hippocampal fissure visualization. Hippocampal signal intensity is isointense to cortical gray matter. Recognition of normally occurring variations should help prevent over-interpretation of hippocampal changes in pathologic disorders.

Amygdala↗

PubMedDate not supplied

Acute short-term memory loss from trimethyltin exposure.

We report a case of organic tin exposure in a graduate chemistry student. The inhalational and transcutaneous exposure occurred following a laboratory explosion. The patient initially presented with first and second degree burns of the face and chest, and developed an acute loss of short-term memory 72 hours after exposure. The memory loss gradually improved over the course of several months.

Acute Disease↗

PubMed1989

Psychiatrists and Alzheimer's disease.

Psychiatric symptoms in Alzheimer's disease are not specific: anxiety, agitation, depression, memory disorders, mental confusion. Of these disorders, depression is the most accessible of these to pharmacological treatment; agitation, however, raises the institutional problem. Throughout the inexorable evolution of the disease, the psychiatrist has to pay attention to the global situation: medical, social and legal.

Alzheimer Disease↗

PubMed2006

Controlled processes account for age-related decrease in episodic memory.

A decrease in controlled processes has been proposed to be responsible for age-related episodic memory decline. We used the Process Dissociation Procedure, a method that attempts to estimate the contribution of controlled and automatic processes to cognitive performance, and entered both estimates in regression analyses. Results indicate that only controlled processes explained a great part of the age-related variance in a word recall task, especially when little environmental support was offered.

Adult↗

PubMed2006

Cross-task repetition amnesia: Impaired recall of RSVP targets held in memory for a secondary task.

People often fail to select and encode the second of two targets presented within less than 500ms in rapid serial visual presentation (RSVP), an effect known as the attentional blink. We investigated how report of the two targets is affected when one of them is maintained in working memory for a secondary, memory-search task. The results showed that report of either target was impaired when it was a member of the memory set relative to when it was not. This effect was independent of both the temporal interval separating the RSVP target from the presentation of the memory set and the interval separating the targets. We propose that the deficit in recall occurs because the association between a target and the memory-search task interferes with the formation of a new association between that target and the following RSVP task, with the result that observers may be biased to ascribe the target only to the memory set.

Analysis of Variance↗

PubMed2006

Evidence for a double dissociation between spatial-simultaneous and spatial-sequential working memory in visuospatial (nonverbal) learning disabled children.

The paper describes the performance of three children with specific visuospatial working memory (VSWM) impairments (Study 1) and three children with visuospatial (nonverbal) learning disabilities (Study 2) assessed with a battery of working memory (WM) tests and with a number of school achievement tasks. Overall, performance on WM tests provides evidence of a double dissociation between spatial-simultaneous processes, underpinning the memorization item positioning in a spatial configuration, and spatial-sequential processes, which allow memorization of the presentation order. In both groups of children of the two studies, a selective impairment either on spatial-sequential or on spatial-simultaneous working memory tasks was observed. These data support the existence of -simultaneous and -sequential modality-dependent processes in visuospatial working memory and confirm the importance of distinguishing between different subtypes of visuospatial (nonverbal) learning-disabled children.

Child↗