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Marie-H Monfils

Publications and source records attributed to Marie-H Monfils.

10 recordsLinked to original sources

Induction of neocortical long-term depression results in smaller movement representations, fewer excitatory perforated synapses, and more inhibitory synapses.

Long-term depression (LTD) is one of the most widely investigated models of the synaptic mechanisms underlying learning and memory. Previous research has shown that induction of LTD in the neocortex decreases measures of pyramidal cell dendritic morphology in both layers III and V. Here, we investigated the effects of LTD induction on 1) the time course of recovery of synaptic efficacy, 2) movement representations, 3) cortical thickness and layer V neuron density, and 4) the density of excitatory and inhibitory synapses in layer V of sensorimotor neocortex. Rats carried a stimulating electrode in the midline corpus callosum and a recording electrode in the right sensorimotor neocortex. Each rat received either low-frequency stimulation composed of 900 pulses at 1 Hz or handling daily for a total of 20-25 days. Callosal-neocortical evoked potentials were recorded in the right hemisphere before and after stimulation or handling. Our results show that LTD induction lasts for 3 weeks and results in smaller motor maps of the caudal forelimb area. We did not observe any reduction in neocortical thickness or neuron density. There was a reduction in the density of excitatory perforated synapses and an increase in the density of inhibitory synapses in layer V of the sensorimotor neocortex, thereby providing a general mechanism for the reduction in motor map size. This study sheds light on the interaction between an artificial model of learning, receptive field characteristics, and synaptic number in the sensorimotor cortex.

Animals↗

Neocortical kindling is associated with opposing alterations in dendritic morphology in neocortical layer V and striatum from neocortical layer III.

Previous research has shown that seizures kindled in the corpus callosum result in a persistent enhancement of the callosal-neocortical evoked response but only a transient reduction in layer III pyramidal cell morphology. To date, there are no reports on the direct effects of repeated seizures on dendritic morphology in layer V, the pyramidal layer thought to mediate the kindling-induced enhanced evoked response. This experiment examined the effect of repeated seizures elicited from the corpus callosum, at the level of the frontal neocortex, on the morphology of sensorimotor frontal (Fr1) and occipital (OC1) neocortical layer V, as well as striatal and neuronal dendrites, in male rats. After 25 days of electrically elicited seizures or handling control, rats were sacrificed either 2 days or 3 weeks following the last seizure and processed for Golgi-Cox staining. Analysis of the impregnated pyramidal cell dendrites indicated a significant increase in the amount of dendritic length and branching in rats 2 days, but a decrease 3 weeks, following the last seizure. There was no effect at the distant occipital site. The differential effect between layer V pyramidal neurons and layer III pyramidal neurons suggests that these areas play different roles in the expression of seizures and the adaptation of the brain to the persistent effect of kindling.

Animals↗

FGF-2-induced cell proliferation stimulates anatomical, neurophysiological and functional recovery from neonatal motor cortex injury.

Infant rats treated with basic fibroblast growth factor-2 (FGF-2) after postnatal day (P)10 motor cortical injury, show functional improvement in adulthood relative to those that do not receive FGF-2. In this study we used a combination of behavioural, immunohistochemical, electrophysiological, electron microscopic and teratological approaches to investigate possible mechanisms by which FGF-2 may influence functional recovery. We show that subcutaneous injections of FGF-2 following bilateral lesions to the motor cortex at P10 in the rat leads to filling of the lesion area with migrating neuroblasts and cycling cells. We assessed the functionality of this tissue in adulthood, and show that cells from the filled region spontaneously fire and form synapses. Behavioural analysis shows enhanced motor performance in the FGF-2-treated lesion rats in comparison to vehicle-treated lesion rats, and this improvement is reversed by removal of the tissue from the previously lesioned area or by blocking cortical regeneration by embryonic treatment with bromodeoxyuridine (BrdU). The results show that FGF-2 stimulates filling of the lesion cavity with cells after neonatal motor cortex lesions, that the new tissue has anatomical and physiological properties similar to control tissue, and that the filled region supports motor behaviour.

Animals↗

A quantitative comparison of synaptic density following perfusion versus immersion fixation in the rat cerebral cortex.

The main objective of the present study was to perform an unbiased comparison of immersion vs. perfusion techniques to assess whether we could use the former to quantify synapses through electron microscopy (EM). Using the immersion technique is ideally suited for instances in which the specimen under study could not be perfused under the standard EM protocol. Our results suggest that, despite suboptimal qualitative results, fixation by immersion allows for adequate quantification of synapses.

Animals↗

In search of the motor engram: motor map plasticity as a mechanism for encoding motor experience.

Motor skill acquisition occurs through modification and organization of muscle synergies into effective movement sequences. The learning process is reflected neurophysiologically as a reorganization of movement representations within the primary motor cortex, suggesting that the motor map is a motor engram. However, the specific neural mechanisms underlying map plasticity are unknown. Here the authors review evidence that 1) motor map topography reflects the capacity for skilled movement, 2) motor skill learning induces reorganization of motor maps in a manner that reflects the kinematics of acquired skilled movement, 3) map plasticity is supported by a reorganization of cortical microcircuitry involving changes in synaptic efficacy, and 4) motor map integrity and topography are influenced by various neurochemical signals that coordinate changes in cortical circuitry to encode motor experience. Finally, the role of motor map plasticity in recovery of motor function after brain damage is discussed.

Animals↗

Long-term potentiation induces expanded movement representations and dendritic hypertrophy in layer V of rat sensorimotor neocortex.

While long-term potentiation (LTP) is currently the most widely investigated model of the synaptic mechanisms underlying learning, there is a paucity of reports on the direct effects of LTP on cortical organization. Here we show that strengthening polysynaptic potentiation correlates with an expanded neocortical area that responds to intracortical microstimulation-induced movements of rat forelimb and increased dendritic material in layer V pyramidal cells. Rats carried a stimulating electrode in the corpus callosum (midline), and a recording electrode in the right caudal forelimb area (CFA). Each rat received 15 days of either high frequency stimulation (HFS) or handling. Evoked potentials of the transcallosal pathway were recorded in the right hemisphere before and after 15 days of stimulation or handling. Following the last stimulation, movement representations were determined in the left CFA using high-resolution intracortical microstimulation (ICMS) and then the brains were processed for Golgi-Cox staining. Our results show that synaptic modification results in a recruitment of more neocortical area into movement representations and increases in several measures of dendritic morphology in layers III and V. This study sheds light on the interaction between artificial models of learning, receptive field characteristics and dendritic morphology in the sensorimotor cortex.

Adaptation, Physiological↗

Induction of long-term depression is associated with decreased dendritic length and spine density in layers III and V of sensorimotor neocortex.

Long-term potentiation (LTP) and long-term depression (LTD) are currently the most widely investigated models of the synaptic mechanisms underlying learning and memory. Previous research has shown that induction of LTP increases measures of pyramidal cell dendritic morphology in the hippocampus and layers III and V of the neocortex. However, to date there are no reports on the direct effects of LTD induction on dendritic morphology. Here, we investigated the effects of LTD induction on sensorimotor pyramidal cell dendritic morphology. Rats carried a stimulating electrode in the corpus callosum (midline) and a recording electrode in the right sensorimotor cortex. Each rat received low-frequency stimulation composed of 900 pulses at 1 Hz or handling daily for a total 15 days. Evoked potentials (EPs) of the transcallosal pathway were recorded in the right hemisphere before and after the 15 days of stimulation or handling. The rats were then perfused with saline and the brains were immediately processed for Golgi-Cox staining. Our results show that LTD induction is related to decreases in dendritic length and spine density both in layers III and V as well as a decrease in dendritic branch complexity in layer V of the sensorimotor cortex. Thus, neuronal alterations following modifications in neocortical synaptic efficacy may provide a general mechanism for the physical instantiation of learning and memory.

Animals↗

Differential neuroplastic changes in neocortical movement representations and dendritic morphology in epilepsy-prone and epilepsy-resistant rat strains following high-frequency stimulation.

The epileptogenic-prone (FAST) and epileptogenic-resistant (SLOW) rat strains have become a valuable tool for investigating the neurochemical and neurophysiological basis of epilepsy. This study examined the two strains with respect to their neocortical movement representations and cortical layer III pyramidal cell dendritic morphology in both control and potentiated conditions. FAST and SLOW rats received high-frequency stimulation of the corpus callosum in order to induce long-term polysynaptic potentiation of the transcallosal pathway to the sensorimotor neocortex. Baseline-evoked potentials of this pathway were recorded in the left hemisphere before stimulation, and following 5, 10, 15 and 20 days of high-frequency stimulation. All rats then underwent high-resolution intracortical microstimulation (ICMS) in order to assess functional movement representations of the left caudal forelimb area of the sensorimotor cortex. Immediately following ICMS, the brains were stained with the Golgi-Cox method, and the length, branching and spine density of frontal and occipital neocortical layer III pyramidal neurons were measured. We observed that high-frequency stimulation induced similar increases in polysynaptic potentiation in both rat strains; however, only the FAST strain showed an increase (doubling) in the size of their motor maps. We also observed decreases in dendritic length and branching in the FAST rats, and the opposite profile in the SLOW rats. The potentiated FAST rats also showed an increase in spine density. Our results suggest that differences in susceptibility to epileptogenesis may result in a differential response to stimulation-induced plasticity.

Animals↗

Number-of-features effects and semantic processing.

Participants list many semantic features for some concrete nouns (e.g., lion) and fewer for others (e.g., lime; McRae, de Sa, & Seidenberg, 1997). Pexman, Lupker, and Hino (2002) reported faster lexical decision and naming responses for high number of features (NOF) words than for low-NOF words. In the present research, we investigated the impact of NOF on semantic processing. We observed NOF effects in a self-paced reading task when prior context was not congruent with the target word (Experiment 1) and in a semantic categorization task (concrete vs. abstract; Experiment 2A). When we narrowed our stimuli to include high- and low-NOF words from a single category (birds), we found substantial NOF effects that were modulated by the specificity of the categorization task (Experiments 3A, 3B, and 3C). We argue that these results provide support for distributed representation of word meaning.

Decision Making↗

Motor map expansion following repeated cortical and limbic seizures is related to synaptic potentiation.

The effect of experimentally induced seizure activity on the functional reorganization of motor maps has not previously been investigated. Furthermore, while the functional reorganization of motor maps has been thought to involve increases in synaptic communication, there has yet to be a test of this hypothesis. Here we show that repeated seizure activity (kindling), that is accompanied by increased synaptic strength within adult rat motor cortex, results in a doubling of the caudal forelimb motor area. We measured neo-cortical evoked potentials in the right hemisphere prior to 25 days of electrical kindling of the medial frontal corpus callosum or amygdala and re-measured them either 1 or 21 days following the last kindling session. Then, using high resolution intracortical microstimulation (ICMS), the caudal forelimb area in the left hemisphere was mapped. This is the first report of any procedure causing a motor representation to double in size. Furthermore, this expansion was related to the enhanced area of a neocortical polysynaptic field potential and not the motor convulsions per se. Moreover, both the motor map and field potential enhancements were persistent in nature and could be driven from either cortical or limbic sites. The data have implications for human populations with epilepsy.

Animals↗