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C Messier

Publications and source records attributed to C Messier.

At least 19 recordsLinked to original sources
PubMed2005

Glucose transporter plasticity during memory processing.

Various types of learning, including operant conditioning, induce an increase in cellular activation concomitant with an increase in local cerebral glucose utilization (LCGU). This increase is mediated by increased cerebral blood flow or changes in brain capillary density and diameter. Because glucose transporters are ultimately responsible for glucose uptake, we examined their plastic expression in response to cellular activation. In vitro and in vivo studies have demonstrated that cerebral glucose transporter 1 (GLUT1) expression consistently parallels changes in LCGU. The present study is the first to investigate the effect of memory processing on glucose transporters expression. Changes in GLUT expression produced by training in an operant conditioning task were measured in the brain of CD1 mice. Using semi-quantitative immunohistochemistry, Western blot and real time RT-PCR the cerebral GLUT1 and GLUT3 expression was quantified immediately, 220 min and 24 h following training. Relative to sham-trained and naive controls, operant conditioning training induced an immediate increase in GLUT1 immunoreactivity level in the hippocampus CA1 pyramidal cells as well as in the sensorimotor cortex. At longer post-learning delays, GLUT1 immunoreactivity decreased in the sensorimotor cortex and putamen. Parallel to the changes in protein levels, hippocampus GLUT1 mRNA level also increased immediately following learning. No effect of learning was found on hippocampal GLUT3 protein or mRNA expression. Measures of changes in glucose transporters expression present a link between cellular activation and glucose metabolism. The learning-induced localized increases in GLUT1 protein as well as mRNA levels observed in the present study confirm the previous findings that GLUT1 expression is plastic and respond to changes in cellular metabolic demands.

Animals↗
PubMed2002

Immunohistochemical localization and quantification of glucose transporters in the mouse brain.

A family of seven facilitative glucose transporters (Glut1-5, 7 and 8) mediates the cellular uptake of glucose. In the brain, Glut2, Glut5 and Glut8 are found at relatively low levels whereas Glut1, Glut3 and Glut4 were reported in abundance in several brain regions. Using immunofluorescence, this study investigated, compared and quantified the localization of the brain major glucose transporters, Glut1, Glut3 and Glut4, in the different cerebral areas of CD1 mice. Most of the staining of Glut1, Glut3 and Glut4 in the mouse brain coincides with observations made in rats. The results confirm the cortical neuropil distribution of Glut3, the prominence of this transporter in the mossy fiber field of the hippocampus and the Glut3 and Glut4 immunostaining of the hippocampal pyramidal cell layer. The present study also reports novel localizations of the transporters such as the presence of Glut3 in neuronal perikarya, Glut4-labeled neurons in the CA3 of the hippocampus and the subiculum. In the cerebellum, Glut3 shows subcellular localization to the base of the Purkinje cell bodies near the axon hillock. Furthermore, an important population of Golgi cells was found to be strongly immunostained for Glut4 in the granular cell layer of the cerebellum. The quantification results suggest that the relative abundance of Glut1 in the frontal and motor cortices coincides well with the high-energy demands of these brain regions. However, the Glut4-selective abundance in cerebral motor areas supports its suggested role in providing the energy needed for the control of the motor activity. The reported neuropil distribution of Glut3 seems to uphold its suggested role in synaptic energy provision and neurotransmitter synthesis. We conclude that the cellular and regional distributions of the glucose transporters in the rodent brain seem to be relevant to their corresponding functions.

Animals↗
PubMed2001

The hippocampal formation--orbitomedial prefrontal cortex circuit in the attentional control of active memory.

The long held view that the hippocampal formation is not only essential, but also solely responsible for declarative memory in humans (and by analogy non-human primates) has come into question. Based on extensive reciprocal connection patterns between the hippocampal formation and the orbitoventromedial prefrontal cortex in primates and rats, a central role for the hippocampal formation in the attentional control of behavior is emerging. In this paper, evidence is reviewed showing that the hippocampal-orbitomedial prefrontal cortex circuit may be involved in attentional monitoring of the internal sensorium. This attentional monitoring system, in a sense, is the working memory of viscero-emotional processing. The hippocampal formation can thus be viewed as a discrepancy detector with respect to the relative activational status of cognitive/emotional set in the orbitomedial prefrontal cortex. Discrepancies between the current representation of the internal milieu and the "just-prior" representation held "on-line" in orbitomedial prefrontal cortex associative working memory, are signaled from the hippocampus to the prefrontal cortex prospective attentional systems to activate, process, and reconcile internal (past) with external (present) environments, and finally to effectively alter active working emotional "sets" to exert cognitive-emotional control of behavior.

Animals↗
PubMed2001

Infralimbic muscarinic M1 receptors modulate anxiety-like behaviour and spontaneous working memory in mice.

RATIONALE: Spontaneous working memory and anxiety-like behaviour can be concurrently influenced following kappa 1 opioid agonist or antagonist infusions in the infralimbic (IL) area of the ventromedial prefrontal cortex (vmPFC) in CD-1 mice. OBJECTIVE: The present study sought to evaluate whether acetylcholine (ACh) muscarinic (M) receptor drugs can similarly influence these cognitive-behavioural processes in the IL cortex. METHOD: Anxiety was evaluated in the elevated plusmaze and spontaneous working memory was evaluated in the Y-maze following scopolamine, pirenzepine or McN-A-343 infusion in the IL cortex. RESULTS: In experiment 1, the non-specific muscarinic receptor antagonist, scopolamine, was anxiogenic in trial 1 (5, 10 and 20 nmol), but did not influence behaviour in trial 2 (no-injection) in the elevated plus-maze 24 h later. In week 2, scopolamine disrupted spontaneous working memory in the Y-maze at the highest dose (20 nmol). In experiment 2, pretreatment with the M1 antagonist, pirenzepine, was anxiolytic in trial 1 (5 and 10 nmol), as well as in trial 2 (no-injection) in the elevated plus-maze 24 h later (0.25, 1.25, 2.5, 5 and 10 nmol). In week 2, pirenzepine disrupted spontaneous working memory in the Y-maze (2.5, 5 and 10 nmol). In experiment 3, pretreatment with the M1 agonist, McN-A-343, was anxiogenic in trial 1 (2.5, 5, 10 and 20 nmol), as well as in trial 2 (no-injection) in the elevated plus-maze 24 h later (2.5, 5, 10 and 20 nmol). In week 2, McN-A-343 enhanced spontaneous working memory in the Y-maze (2.5, 5, 10 and 20 nmol). CONCLUSIONS: (1) Enhanced ACh transmission in the vmPFC induces anxiety in challenging environments and enhances spontaneous working memory performance. (2) Blocking or activating postsynaptic M1 receptors in the vmPFC may truncate or exaggerate, respectively, afferent anxiety-relevant information. (3) IL pirenzepine and McN-A-343 exert long-term opposite effects on aversive learning during trial 1 in the elevated plus-maze.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed2001

Methodological and conceptual issues in the use of the elevated plus-maze as a psychological measurement instrument of animal anxiety-like behavior.

There has been some suggestion that 'risk assessment' defensive behaviors in rodents might resemble some of the behavioral/somatic symptoms of generalized anxiety in humans. Although the inclusion of some risk assessment behaviors enhanced the sensitivity of the elevated plus-maze to detect subtle changes in anxiety-like behavior, there is little evidence to support the inclusion of 15 or 20 indicator variables in an analysis. Several methodological, conceptual, complexity and interpretation problems associated with the factorial validity of recently published ethologically-derived large-scale principal components analyses of elevated plus-maze behavior are examined in this review. The utility of confirmatory factor analytic work currently being conducted in our laboratory to test structural hypotheses of anxiety-relevant elevated plus-maze behavior is then discussed with a view to address some of these issues. Finally, we propose that the growing number of measured behavioral indices in the elevated plus-maze test battery be reduced, and suggest that some of the underlying constructs thought to drive behavior in the apparatus are in need of re-evaluation.

Animals↗
PubMed2001

Glucose and glucoregulatory modulation of memory scanning, event-related potentials and EEG in elderly subjects.

Endogenous P300b event-related potential (ERP) and behavioral performance measures, extracted during a visual memory scanning task, and spectral indices of resting electroencephalographic (EEG) activity, were assessed in 12 healthy elderly adults before and after double-blind oral administration of a placebo or glucose (50 mg) beverage. Glucoregulation was estimated by deriving a recovery index to categorize subjects as having better (BR) or poorer (PR) blood glucose recovery. Although glucoregulatory status did not impact on EEG or task performance, PR subjects exhibited reduced P300b areas relative to BR subjects prior to beverage administration. Glucose did not alter P300b or memory scanning performance but, regardless of glucoregulatory status, it increased the EEG power in the slow alpha frequency band. The study results suggest that peripheral glucoregulation can influence neuroelectric measures of cognition and that the acute ingestion of glucose can modulate central arousal processes.

Aged↗
PubMed2000

U-69,593 microinjection in the infralimbic cortex reduces anxiety and enhances spontaneous alternation memory in mice.

The present report investigated the contributions of the ventromedial prefrontal cortex to the control of spontaneous alternation/working memory and anxiety-related behaviour. In Experiment 1, we examined the effects of microinjections of the selective kappa(1) receptor agonist, U-69,593, in the infralimbic cortex (IL) of CD-1 mice on several ethologically-derived anxiety indices in the elevated plus-maze (EPM) and defensive/withdrawal (D/W) anxiety in the open field, as well as on memory in the EPM transfer-latency (T-L) test and implicit spontaneous alternation memory (SAP) in the Y-maze. In week 1, pretreatment with one injection of vehicle, 1, 10 or 25 nmol/1.0 microliter U-69,593 in the IL dose-dependently prolonged T-L and produced a dose-dependent anxiolytic behavioural profile in the first EPM trial. Following a 24-h delay, the same mice were given a drug-free second trial in the EPM tests of T-L memory and anxiety. Whereas T-L memory was not disturbed, small but detectable carry-over effects were observed in trial-2 EPM behaviour relative to vehicle-treated animals. In week 2, the same groups of mice were again pretreated with one injection of the same doses of U-69,593 in the IL and given a D/W test in an open field, followed immediately by an 8-min SAP trial in the Y-maze. The smallest U-69,593 dose was anxiolytic in the D/W test, and SAP/working memory was dose-dependently enhanced in the Y-maze. In Experiment 2, we evaluated whether 0.5 microliter volume microinjections would produce comparable behavioural and carry-over effects in the IL of three new groups of CD-1 mice, in the event that the 1.0 microl volume injections used in Experiment 1 diffused beyond the IL and therefore may have confounded some effects. Experiment 2 procedures were carried out in the same manner as in Experiment 1, except the animals were tested in reverse order. Thus in week 1, SAP memory was tested in the Y-maze followed by D/W anxiety in the open field for half of the animals in each group, and the other half was tested in reverse order. In week 2, T/L memory and anxiety were tested in the EPM in 2 trials as described in Experiment 1. Pretreatment with one injection of vehicle, 10 or 25 nmol/0.5 microliter U-69,593 in the IL reduced D/W anxiety and enhanced SAP memory regardless of testing order in week 1. In week 2, the same groups of mice were again pretreated with one injection of the same doses of U-69,593 in 0.5 microliter volumes in the IL and tested in the EPM. In a similar fashion to Experiment 1, U-69,593 dose-dependently prolonged T/L and produced an anxiolytic behavioural profile in the first EPM trial. Following a 24-h delay, T/L recall memory was again not significantly influenced, but a robust anxiolytic behavioural profile was observed in the second drug-free anxiety trial in the EPM relative to vehicle-treated animals. Results are discussed relative to a) injection volumes and testing order, b) the possible influence kappa receptors may exert on neurochemical responsivity to anxiety-provoking environments in the IL area of the mPFC, c) the possibility that kappa-mediated anxiolysis from the IL in CD-1 mice results from interactions with neurochemical systems involved in the blunting of incoming anxiety-provoking information, d) evidence that SAP memory may be an implicit subtype of working memory, and e) the possibility that IL implicit working memory processes may modulate the induction and expression of anxiety-related behaviour.

Animals↗
PubMed2000

Ethological confirmatory factor analysis of anxiety-like behaviour in the murine elevated plus-maze.

The elevated plus-maze has been used in animal research to measure anxiety since 1985 and is currently the most widely used animal model of anxiety. Since this paradigm has been the subject of several principal components analyses, it is well qualified for confirmatory factor analysis research. The current report builds on the substantial theoretical knowledge and empirical data obtained from these structural analyses with a view to obtain further progress in the evolution of our understanding of animal anxiety in the elevated plus-maze. The purpose of the present report was two-fold: (a) to test if the a piori imposition of a 3-factor model, or a competing 2-factor elevated plus-maze model, would fit our sample (n=200 CD-1 mice) data in each of two trials within an inferential confirmatory factor analytic framework; (b) provide a well-fitting model that confers indicator variables that can most effectively and parsimoniously measure underlying constructs of elevated plus-maze behaviour. Multiple model-fitting criteria were used, and issues related to data non-normality, outliers, replicability of the model, sampling error and error of approximation in the estimation of final model fit were addressed. The final 2-factor model, with estimated error covariance between two different pairs of indicator variables, was a good fit on the trial-1 data, although it was necessary to allow unprotected stretch attends to non-significantly cross-load on factor-2. A 2-factor model also fit the trial-2 data from the present analysis, although it was necessary to allow closed arm time ratio to negatively cross-load on factor-1. These results indicate that inferential hypothesis testing and model building procedures within a confirmatory factor analysis framework produces interpretable animal anxiety indices in the elevated plus-maze. Moreover, a 2-factor, rather than a 3-factor model, parsimoniously and unambiguously explained the underlying constructs of anxiety-like mouse behaviour in the elevated plus-maze in the present study. Taken together, a reduction in the growing number of behavioural indices reported in elevated plus-maze pharmacological studies is suggested.

Animals↗
PubMed2000

Concurrent modulation of anxiety and memory.

We have previously shown that the ventromedial prefrontal cortex (vmPFC) is involved in spontaneous working memory and anxiety-related behaviour in CD-1 mice. Specifically, pretrial microinjection of the kappa(1) agonist, U-69,593, in the infralimbic (IL) area of the vmPFC produced a robust anxiolytic behavioural profile in the elevated plus-maze and enhanced spontaneous working memory in the Y-maze. In the present study we sought to determine whether these effects were specific to IL kappa receptors. We hypothesized that microinjection of the kappa antagonist, norBNI, in the IL cortex would influence anxiety and spontaneous memory in an opposite direction to the effects produced by the kappa(1) agonist. In week 1, transfer-latency reference memory and anxiety were tested in the elevated plus-maze in two separate trials with an intertrial interval of 24 h. In week 2, spontaneous working memory was tested in the Y-maze followed immediately by defensive/withdrawal anxiety in the open field for one half of the animals in each group, and the other half was tested in reverse order. Pretreatment with one injection of vehicle, 1, 5 or 10 nmol/0.5 microl norBNI in the IL cortex dose-dependently reduced transfer-latencies and produced an anxiogenic behavioural profile in the first elevated plus-maze trial. Following a 24 h delay, transfer-latency reference memory was not influenced, but a robust anxiogenic behavioural profile was observed in the second no-injection anxiety trial in the elevated plus-maze relative to control animals. In week 2, the same groups of mice were again pretreated with one injection of the same doses of norBNI in the IL cortex and tested in the open field and Y-maze. NorBNI pretreatment was anxiogenic in the defensive/withdrawal anxiety test and disrupted spontaneous working memory regardless of testing order. The present results show the influence of kappa receptor modulation on anxiety induction and spontaneous working memory. These results also support the hypothesis that immediate memory processing may modulate the induction of anxiety-related behaviours.

Animals↗
PubMed2000

Spatial and temporal distribution of chloroplast DNA polymorphism in a tropical tree species.

The level and the spatial organization of chloroplast DNA polymorphism were investigated in Dicorynia guianensis Hamshoff (Caesalpiniaceae) at different spatial and temporal scales. D. guianensis is a canopy tree of the rain forest that is distributed throughout the Guiana plateau in small aggregates. Twelve different haplotypes were identified using restriction analysis of polymerase chain reaction (PCR) amplified fragments of the chloroplast genome. When populations from different areas of French Guiana were compared, a clear geographical pattern of haplotype frequencies was identified along the Atlantic coast. This pattern is most likely the result of the restriction-expansion dynamics of the tropical forest during the Quaternary. At the local level, D. guianensis was characterized by a high level of within population diversity. Maintenance of within population diversity results from the dynamics of the aggregates; stochastic demography associated with the turnover of aggregates generates genetic differentiation among them. At the stand level, a strong spatial aggregation of haplotypes persisted from the adult to the seedling cohort indicating limited seed flow. There was also a strong difference in levels of diversity between the cohorts which suggested that recruitment over several years is needed in order to maintain genetic diversity during regeneration.

DNA, Chloroplast↗
PubMed2000

Glucose regulation and brain aging.

Blood glucose regulation is not only a complex phenomenon but glucose regulatory levels also vary significantly across individuals. Thus, whereas individuals compromised with moderately elevated blood glucose levels are diagnosed as having impaired glucose tolerance, excessive blood glucose levels render a Type II diabetes diagnosis. Type II diabetes prevalence rates in the adult population have been estimated to be between 6 and 10 percent. Although Type II diabetes has been typically associated with older people, the disease has become much more common among young adults and children. It has become increasingly evident that protracted glucose tolerance impairment usually precedes a type II diabetes diagnosis, although impaired glucose tolerance will not necessarily progress to a diabetic state. Furthermore, a number of studies have shown that impaired glucose tolerance or type II diabetes is associated with impaired cognitive function in older subjects. In addition, we recently found that cognitive deficits are also associated with moderately impaired glucose regulation in young healthy volunteers. These data, although in need of confirmation and extension, suggest that impaired glucose tolerance is associated with impaired cognition, independent of age. Moreover, since impaired glucose tolerance is more prevalent than diabetes across all ages, then our finding lead to the implication that impaired cognitive function may be more prevalent in the general population than previously estimated. Finally, the dysfunction of glucoregulatory mechanisms may be an important intervening factor when studying the evolution of cognitive function through the aging process.

Aged↗
PubMed1999

Contribution of cholinergic and gabaergic functions to memory processes in BALB/cANnCrlBR mice.

Several lines of evidence indicate that glucose influences on memory depend on interactions between glucose, glucoregulation and hippocampal cholinergic function. We previously demonstrated that glucose and scopolamine differentially affected memory consolidation for an operant bar pressing task in two closely-related BALB/c mouse strains. Whereas glucose normally improves memory in several animal strains, memory consolidation was not effected by systemic glucose injections in BALB/cANnCrlBR mice. Moreover, these mice were relatively insensitive to the normally observed amnestic effects of scopolamine. We therefore sought to determine whether cholinergic mechanisms in the dorsal hippocampus were involved in such atypical drug effects on memory processing in that strain of mice. In Experiment 1, we examined whether post-training oxotremorine would also atypically influence memory consolidation for an appetitively reinforced operant bar pressing task following microinjection in the dorsal hippocampus. In Experiment 2, we examined the effects of intrahippocampal GABAA drugs on memory consolidation. The non-selective muscarinic agonist, oxotremorine, dose-dependently impaired memory and the GABAA antagonist, bicuculline, improved retention in BALB/cANnCrlBR mice. It was concluded that GABA-mediated influences on hippocampal pyramidal output in BALB/cANnCrlBR mice and other strains are similar; but the amnestic effects of oxotremorine from the dorsal hippocampus were opposite to facilitating effects normally observed in other animal strains. Results are discussed relative to possible altered septo-hippocampal cholinergic neurotransmission in BALB/cANnCrlBR mice.

Acetylcholine↗
PubMed1999

New techniques in stereotaxic surgery and anesthesia in the mouse.

Mice are used in increasing numbers in neuroscience research. This increase is linked to the availability of numerous pure genetic lines and the advent of transgenic animals. Many neuroscience techniques can be used in the mouse with success, including stereotaxic placement of cannulae and electrodes. With the recent publication of a mouse brain atlas by Franklin and Paxinos and improvements in surgical procedures for the mouse, stereotaxic surgery in mice can be performed routinely and with accuracy. In the present article, we describe techniques and apparatuses for the surgical implantation of cannulae in the mouse brain. We also present new developments in anesthesia, pain management, and postoperative care that improve survival and recovery times of mice. Using these new techniques, we have gained shorter training time for students, lower mortality rates following surgery, and faster recovery.

Anesthesia↗
PubMed1999

Effect of glucose, glucose regulation, and word imagery value on human memory.

Changes in memory performance were examined after intake of a glucose (50 g) or saccharin (50 mg) solution in fasted men and women. Glucoregulation was estimated by using a recovery index to categorize participants within each gender as having poor or good recovery. Memory was assessed with word-learning tasks in which the imagery-evoking value of the words was systematically manipulated to yield high- and low-imagery lists. The results showed that men and women characterized as having poor glucose regulation had significantly worse memory performance under the saccharin condition. This decrement was reversed by glucose ingestion. These effects were observed for both low- and high-imagery words. This study supports the hypothesis that poor glucoregulation is associated with poor memory performance even in young healthy participants and that the ingestion of glucose can improve their memory.

Adult↗
PubMed1998

The absence of effect of glucose on memory is associated with low susceptibility to the amnestic effects of scopolamine in a strain of mice.

In this series of experiments, we examined the ability of post-training glucose injections to improve memory of the Balb/cAnNCrlBR strain of mice for a bar-pressing task. We could not replicate this effect which has been demonstrated in many other strains of mice including Balb/cbyJ, a related strain. We found that the Balb/cAnNCrlBR strain of mice is also much less sensitive to the disrupting effects produced by pre- or post-training injections of the competitive cholinergic antagonist scopolamine. This strain also shows altered glucoregulation compared to the Balb/cbyJ strain. The absence of glucose effects on memory in Balb/cAnNCrlBR mice appears to be associated with decreased sensitivity to cholinergic antagonists. These results can be contrasted with previous ones obtained in a related strain, the Balb/cbyJ, in which glucose was shown to improve memory while scopolamine could easily disrupt memory processes. Taken together, these data provide additional indirect support for the hypothesis that glucose improvement of memory is closely linked to a functional interaction with central cholinergic systems. The comparison of these two strains could be the basis for a useful animal model to investigate the relationship between age-related changes in memory and central cholinergic function.

Amnesia↗
PubMed1998

Dose-dependent action of glucose on memory processes in women: effect on serial position and recall priority.

Previous research has shown that glucose can enhance memory in animals and humans. In humans, the facilitative effect of glucose is best observed with declarative memory tasks in older subjects. While the memory-enhancing action of glucose is well established, the underlying physiological mechanisms and the specific aspects of memory that are modulated by glucose in humans are not well understood. The present study sought to examine the effects of glucose on memory in young women using a memory paradigm sensitive to specific encoding and retrieval strategies. The glucose dose was adjusted for the weight of each participant in order to generate a dose response curve covering most doses used in previous studies. The results showed that 300 mg/kg glucose enhanced the primacy effect as defined by the recall of the first five items of the lists. However, none of the doses of glucose produced changes in the recall priority given to primacy items. The effect of glucose appears to be localized on the recall primacy effect, suggesting that glucose acts on precise memory operations. This improvement, however, is independent of the order in which subjects recalled the words. Cholinergic drugs have been shown to alter the recall of the primacy part of word lists and this observation is consistent with the hypothesis that glucose acts on memory through an interaction with brain cholinergic systems.

Acetylcholine↗
PubMed1997

Object recognition in mice: improvement of memory by glucose.

In most of the demonstrations of the memory-improving action of glucose in animals, training conditions have included electric shocks, food deprivation, or food rewards, all of which produce changes in blood glucose. In these experiments, training conditions may interact with the exogenous injection of glucose and make it more difficult to interpret results. To circumvent this problem, the ability of glucose to improve memory in an object-recognition task was examined. Animals were first habituated to an open field. The next day, they were placed in the same open field together with two identical objects and the time spent observing and exploring the objects was recorded. The animals were then given either a saline or an immediate or delayed (1 and 5 h) glucose (500 mg/kg) injection or no treatment. On the final day, animals were placed in the open field with a previously observed object and a new object. Exploration time was recorded. Results showed that the animals that received the immediate glucose injection spent significantly more time exploring the new object, suggesting that glucose retroactively and noncontingently improved the memory for the previously observed object.

Animals↗