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PubMed2003

Kainic acid-induced convulsions cause prolonged changes in the chondroitin sulfate proteoglycans neurocan and phosphacan in the limbic structures.

Systemic administration of kainic acid induces repeated convulsive seizures (KA convulsions) that result in neuropathological changes similar to temporal lobe epilepsy and the appearance of spontaneous recurrent seizures (SRS). The appearance of SRS is considered a result of the remodeling of neuronal networks following neuronal degeneration. We investigated the changes in chondroitin sulfate proteoglycans (CSPGs) in the limbic structures after KA convulsions in the rat using monoclonal antibodies 1G2, which recognizes full-length neurocan and the C-terminal half of neurocan, neurocan C, and 6B4, which recognize phosphacan and protein tyrosine phosphatase zeta. After KA convulsions, full-length neurocan appeared by 24 h and reached a peak by 48 to 72 h, whereas phosphacan decreased within 24 h in the hippocampus. In immunohistochemistry, neurocan increased in the limbic structures coincident with the appearance of reactive astrocytes. Phosphacan decreased coincident with pyramidal cell loss in the hippocampus, and the number of phosphacan-positive perineuronal nets around parvalbumin neurons decreased, whereas parvalbumin neurons were relatively conserved. In contrast, phosphacan increased in the entorhinal and piriform cortices in correlation with the severity of neuronal loss. Both neurocan and phosphacan recovered to the control level by 8 weeks after KA convulsions in some rats, but the changes in neurocan and phosphacan described above still persisted in more than half the rats. The results indicate that KA convulsions induce prolonged changes in neurocan and phosphacan similar to those in the developing rat brain and suggest a role of these CSPGs in the remodeling of neuronal networks related to the establishment or enhancement of epileptogenesis.

Animals↗
PubMed1999

Cortical neurons immunoreactive for the potassium channel Kv3.1b subunit are predominantly surrounded by perineuronal nets presumed as a buffering system for cations.

Perineuronal nets (PNs) are known as chondroitin sulphate-rich, lattice-like coatings of the extracellular matrix. In the cortex of mammalian species investigated so far, they were mainly found around GABAergic neurons, but to a lesser degree also around pyramidal cells. Previous investigations in the rat revealed similar distribution patterns of fast-firing neurons expressing both the Kv3.1b subunit of voltage-gated potassium channels and the calcium-binding protein parvalbumin. In the present study, triple fluorescence labelling was applied for the simultaneous demonstration of PNs with the N-acetylgalactosamine-specific Wisteria floribunda agglutinin (WFA), parvalbumin-immunoreactivity (ir) with a monoclonal antibody and of Kv3.1b-ir with several rabbit antibodies. Subsets of non-pyramidal neurons - enwrapped by PNs and expressing parvalbumin and Kv3.1b - were detected in the rat and monkey neocortex and hippocampus. In the rat, faintly stained PNs were additionally found around several layer II/III and V pyramidal cells immunonegative for Kv3.1b, but contacted by Kv3.1b-containing boutons. In the monkey, more intensely labelled PNs frequently occurred around pyramidal cells which themselves appeared to be Kv3. 1b-immunopositive. We also observed minor Kv3.1b-ir and parvalbumin-ir cortical cell populations which were devoid of PNs; occasionally, nets were detected around neurons lacking both immunoreactivities. By confocal laser scanning microscopy, Kv3.1b-ir and WFA-binding sites were found adjoining at the soma and proximal dendritic surface, while lectin-binding sites usually extended on more distal dendritic segments and the axon initial segments which failed to express detectable Kv3.1b-ir. This spatial relationship of both markers was also confirmed by combined WFA-gold labelling and Kv3.1b-immunoperoxidase staining at the electron microscopic level. The data are used for a critical examination of current hypotheses concerning the functional role of PNs. We conclude that PNs may serve as rapid local buffers of excess cation changes in the extracellular space. Somatic membranes of fast-spiking neurons seem to be a main, but not the only source of such changes.

Animals↗
PubMed1989

A net for extending the optic nerve at enucleation of the eyeball.

A long section of optic nerve can be obtained during enucleation, when the eyeball is caught in a net made specifically for this purpose. The net is knitted from surgical thread and is in the shape of a barrel with two openings: one wide, one narrow. Separate thread is wrapped around the edge of the wide opening. When the eyeball is freed from the extrinsic muscles and Tenon's capsule, it is drawn into the net, and the wide opening is closed round the optic nerve. At the narrow opening there are three slip-knots by which the net is pulled forward and out of the orbit. Then the optic nerve is exposed and the surgeon is able to cut it close to the apex of the orbit. The length of severed optic nerve amounts as a rule to about 15 mm or more, depending on the age of patient.

Eye Enucleation↗
PubMed2004

Brain-derived neurotrophic factor controls functional differentiation and microcircuit formation of selectively isolated fast-spiking GABAergic interneurons.

GABAergic interneurons with high-frequency firing, fast-spiking (FS) cells, form synapses on perisomatic regions of principal cells in the neocortex and hippocampus to control the excitability of cortical networks. Brain-derived neurotrophic factor (BDNF) is essential for the differentiation of multiple interneuron subtypes and the formation of their synaptic contacts. Here, we examined whether BDNF, alone or in conjunction with sustained KCl-induced depolarization, drives functional FS cell differentiation and the formation of inhibitory microcircuits. Homogeneous FS cell cultures were established by target-specific isolation using the voltage-gated potassium channel 3.1b subunit as the selection marker. Isolated FS cells expressed parvalbumin, were surrounded by perineuronal nets, formed immature inhibitory connections and generated slow action potentials at 12 days in vitro. Brain-derived neurotrophic factor (BDNF) promoted FS cell differentiation by increasing the somatic diameter, dendritic branching and the frequency of action potential firing. In addition, BDNF treatment led to a significant up-regulation of synaptophysin and vesicular GABA transporter expression, components of the synaptic machinery critical for GABA release, which was paralleled by an increase in synaptic strength. Long-term membrane depolarization alone was detrimental to dendritic branching. However, we observed that BDNF and KCl exerted additive effects, as reflected by the significantly accelerated maturation of synaptic contacts and high discharge frequencies, and was required for the formation of reciprocal connections between FS cells. Our results show that BDNF, along with membrane depolarization, is critical for FS cells to establish inhibitory circuitries during corticogenesis.

Action Potentials↗
PubMed2006

Chondroitinase ABC digestion of the perineuronal net promotes functional collateral sprouting in the cuneate nucleus after cervical spinal cord injury.

Upregulation of extracellular chondroitin sulfate proteoglycans (CSPGs) after CNS injuries contributes to the impediment of functional recovery by restricting both axonal regeneration and synaptic plasticity. In the present study, the effect of degrading CSPGs with the application of the bacterial enzyme chondroitinase ABC (chABC) into the cuneate nucleus of rats partially denervated of forepaw dorsal column axons was examined. A dorsal column transection between the C6-C7 dorsal root entry zones was followed immediately by an ipsilateral brainstem injection of either chABC or a bacterial-derived control enzyme [penicillinase (P-ase)] and then subsequently (1 week later) followed with a second brainstem enzyme injection and cholera toxin B subunit (CTB) tracer injection into the ipsilateral forepaw digits and pads. After 1 additional week, the rats underwent electrophysiological receptive field mapping of the cuneate nucleus and/or anatomical evaluation. Examination of the brainstems of rats from each group revealed that CSPGs had been reduced after chABC treatment. Importantly, in the chABC-treated rats (but not in the P-ase controls), a significantly greater area of the cuneate nucleus was occupied by physiologically active CTB traced forepaw afferents that had been spared by the initial cord lesion. These results demonstrate, for the first time, a functional change directly linked to anatomical evidence of sprouting by spinal cord afferents after chABC treatment.

Afferent Pathways↗
PubMed2005

Loss of perineuronal net N-acetylgalactosamine in Alzheimer's disease.

The perineuronal net (PN), a specialised region of extracellular matrix, is interposed between the neuronal cell surface and astrocytic processes. It is involved in the buffering of ions, in the development, stabilisation and remodelling of synapses and in the regulating the neuronal microenvironment particularly around the parvalbumin-positive GABAergic neurons. We have investigated the relative preservation of Wisteria floribunda agglutinin (WFA)-positive PNs and parvalbumin-positive neurons in Alzheimer's disease (AD), and the relationship of WFA-positive PNs to parenchymal tau, amyloid beta-peptide (Abeta) and MHC class II antigen (a marker of activated microglia), in paraffin sections of 100 cases with AD and 45 controls. The density of PNs that could be labelled with WFA, which binds to the N-acetylgalactosamine (GalNAc) residues of chondroitin sulphate proteoglycans, was reduced by about 2/3 in AD (P<0.001). In contrast, the density of parvalbumin-positive neurons did not differ significantly between AD and controls. Combined fluorescence imaging showed granular disintegration of WFA labelling around some parvalbumin-positive neurons. There was no significant difference in the amount of phosphorylated tau, Abeta or MHC class II antigen in areas with and without WFA-positive PNs. In AD, there is marked loss of PN GalNAc that is not topographically related to neurofibrillary pathology, parenchymal Abeta load or activated microglia. Although the parvalbumin-positive neurons themselves are relatively spared, the loss of PN GalNAc, which maintains a polyanionic microenvironment around neurons, is likely to impair the function of these inhibitory interneurons. This could in turn lead to increased activity of the glutamatergic and other neurons onto which they synapse.

Acetylgalactosamine↗
PubMed1991

A learning network model of the neural integrator of the oculomotor system.

Certain premotor neurons of the oculomotor system fire at a rate proportional to desired eye velocity. Their output is integrated by a network of neurons to supply an eye position command to the motoneurons of the extraocular muscles. This network, known as the neural integrator, is calibrated during infancy and then maintained through development and trauma with remarkable precision. We have modeled this system with a self-organizing neural network that learns to integrate vestibular velocity commands to generate appropriate eye movements. It learns by using current eye movement on any given trial to calculate the amount of retinal image slip and this is used as the error signal. The synaptic weights are then changed using a straight-forward algorithm that is independent of the network configuration and does not necessitate backwards propagation of information. Minimization of the error in this fashion causes the network to develop multiple positive feedback loops that enable it to integrate a push-pull signal without integrating the background rate on which it rides. The network is also capable of recovering from various lesions and of generating more complicated signals to simulate induced post-saccadic drift and compensation for eye muscle mechanics.

Algorithms↗
PubMed1994

A neural-network system for control of eye movements: basic mechanisms.

This paper presents a neural-network-based system that can generate and control movements of the eyes. It was inspired by a number of experimental observations on the saccadic and gaze systems of monkeys and cats. Because of the generality of the approach undertaken, the system can be regarded as a demonstration of how parallel distributed processing principles, namely learning and attractor dynamics, can be integrated with experimental findings, as well as a biologically inspired controller for a dexterous robotic orientation device. The system is composed of three parts: a dynamic motor map, a push-pull circuitry, and a plant. The dynamics of the motor map is generated by a multi-layer network that was trained to compute a bidimensional temporal-spatial transformation. Simulation results indicate (1) that the system is able to reproduce some of the properties observed in the biological system at the neural and movement levels and (2) that the dynamics of the motor map remains stereotyped even when the motor map is subject to abnormal stimulation patterns. The latter result emphasizes the role of the topographic projection that connects the motor map to the push-pull circuitry in determining the features of the resulting movements.

Animals↗
PubMed2003

Remote activation of referred phantom sensation and cortical reorganization in human upper extremity amputees.

Phantom limb sensation, whether painful or not, frequently occurs after peripheral nerve lesions. It can be elicited by stimulating body parts adjacent to the amputation site (referred to as phantom sensation) and it is often similar in quality to the stimulation at the remote site. The present study induced referred phantom sensations in two upper limb amputees. Neuroelectric source imaging (ESI) as well as functional magnetic resonance imaging (fMRI) was used to assess reorganization in primary somatosensory cortex (SI). Whereas recent studies found mislocalization of sensation related to stimulation mainly in regions adjacent and ipsilateral to the amputation site, we report here the elicitation of phantom sensation in the arm by stimulation in the lower body part both ipsi- and contralateral to the amputation in two arm amputees. The fMRI evaluation of one patient showed no shift in the location of the foot whereas ESI revealed major reorganization of the mouth region in primary somatosensory cortex in both patients. These data suggest that cortical structures other than SI might be contributing to the phenomenon of referred sensation. Candidate structures are the thalamus, secondary somatosensory cortex, posterior parietal cortex and prefrontal cortex.

Adult↗
PubMed1991

Development of the human dorsal nucleus of vagus nerve: a morphometric study.

The development of the human dorsal nucleus of the vagus nerve was studied on serial sections of the brain of 10 fetuses at 16-40 weeks of gestation, an infant at 2 months of age and an adult of 63 years. A morphometric analysis revealed that the nucleus is divided into three subnuclei (caudal, dorsal and ventral) and that this subdivision is maintained from 16 weeks of gestation to adulthood. The early development of the nucleus is gradual between 16 and 40 weeks of gestation without the rapid growth phase apparent with the motor trigeminal, hypoglossal and facial nuclei.

Brain↗
PubMed1994

Analysis of synchrony (correlations) in neural populations by means of unit-to-aggregate coherence computations.

This paper presents a general outline of the mathematical basis of an approach for analysis of population synchrony by means of coherence computations, a demonstration of the use of this approach, and a discussion of the potential utility and limitations of the approach. The coherence function for the pair single-unit activity and population-aggregate activity is studied in the light of theoretical considerations on the superposition of partially correlated unitary activities. The theoretical analysis, as well as computer simulations, indicate that when a subset of units in a population are correlated around some frequency, the unit-to-aggregate coherence function for members of this subset shows, in a wide range of conditions, a clear peak around that frequency (and possibly harmonic peaks), being very low at other frequencies where there is no synchrony. Specifically, the value of the peak coherence at the frequency of synchrony reflects the strength of the unitary correlations and their extent within the population, the numerical size of the population, and the degree of phase concentration for the units of the correlated subset. This value remains substantial, or at least significant, for wide ranges of values of these parameters. In contrast, the unit-to-aggregate coherence function for the remaining uncorrelated units has very low values at all frequencies, and tends to zero in the case of a large population. On the basis of these properties, an approach is presented for analysis of synchrony (correlations) in a neural population, which is simple and efficient, particularly when the population is large in numerical size. This approach utilizes unit-to-aggregate coherence computations for a sample of recorded unitary activities as a means for detecting population synchrony and estimating the extent of synchrony. In addition, this analysis can provide useful information on other characteristics of synchrony, such as the strengths of the unitary correlations. The use of the approach is demonstrated with an example from a study of fast rhythms in inspiratory activities, and other applications are also briefly described. The main advantage of unit-to-aggregate coherence analysis is that by using readily recorded activities, it efficiently identifies correlated units in a population and provides information on characteristics of synchrony, at every frequency within the range of interest.

Animals↗
PubMed2005

Brain activation during antisaccades in unaffected relatives of schizophrenic patients.

BACKGROUND: Schizophrenia patients have difficulty inhibiting automatic saccades. Many studies have failed to resolve whether healthy first-degree relatives share the same deficit. Measures of brain activity may be more sensitive than behavioral measures. In patients, the saccadic inhibition deficit has been related to impaired frontostriatal functioning. This study attempts to establish whether this abnormality is also present in unaffected relatives of patients. METHODS: Functional brain images were acquired during prosaccades and antisaccades in 16 control subjects and 16 unaffected siblings of schizophrenia patients using an event-related functional magnetic resonance imaging design. Eye movements were measured during scanning. RESULTS: The task activated a network of regions corresponding to the oculomotor system. Siblings and control subjects did not differ during execution of prosaccades. During antisaccades, siblings did not activate the caudate nucleus. Siblings and control subjects did not differ on the percentage of antisaccade errors. CONCLUSIONS: Siblings did not appropriately activate the striatum during antisaccades, similar to what has been reported in patients. Siblings, however, did not make significantly more errors during antisaccades, indicating that they were able to compensate for the inactive caudate. Future research is needed to assess the potential of this striatal deficit as (genetic) risk factor for schizophrenia.

Adult↗
PubMed2006

The role of vagal function in the risk for cardiovascular disease and mortality.

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. The understanding of the risk factors for CVD may yield important insights into the prevention, etiology, course, and treatment of this major public health concern. We review the evidence for the role of vagal function in the risk for cardiovascular disease and mortality. Using a broad range of indicators of vagal function including resting heart rate, heart rate recovery, heart rate variability, and baroreflex sensitivity we show that decreased vagal function is associated with an increased risk for morbidity and mortality. These effects are independent of traditional risk factors. Moreover, we show that decreased vagal function is associated with both traditional and emerging risk factors as well as modifiable and non-modifiable risk factors. Most importantly, we provide evidence to support the notion that decreased vagal function precedes the development of a number of risk factors and that modification of risk profiles in the direction of lower risk is associated with increased vagal function. We close with a brief overview of the neural concomitants of vagal function and suggest that a model of neurovisceral integration may provide a unifying framework within which to investigate the impact of risk factors, including psychosocial factors, on cardiovascular disease.

Acetylcholine↗
PubMed2005

Spontaneous crossed phrenic activity in the neonatal respiratory network.

Hemisection of the cervical spinal cord causes paralysis of the ipsilateral hemidiaphragm in adult rats. Activation of a latent crossed phrenic motor pathway can restore diaphragmatic function, although structural changes take place before the pathway can be activated. Since mechanisms are employed to eliminate non-functional projections during development, we predicted that this latent neural pathway might be active during development. Therefore, we examined the effect of spinal hemisection (C2) on respiratory-like activity bilaterally using the brainstem--spinal cord preparation from neonatal rats (0-4 days). Spontaneous crossed phrenic activity (respiratory-like activity recorded from the ipsilateral C4 or C5 ventral roots following C2 hemisection) was observed in an age-dependent manner; younger preparations exhibited more than older preparations. Increasing drive (increasing [K+] or superfusion of theophylline) either increased or induced crossed phrenic activity. Hemisection caused no change in the frequency, the burst area, duration or peak amplitude contralateral to hemisection. Unlike adult rats, this study shows that crossed phrenic activity is present in the in vitro respiratory network of neonatal rats suggesting that a crossed neural pathway may be functionally active in neonates.

Action Potentials↗
PubMed2005

Functional representation of the finger and face in the human somatosensory cortex: intraoperative intrinsic optical imaging.

We applied the intrinsic optical imaging technique to the human primary somatosensory cortex during brain tumor/epilepsy surgery for nine patients. The cortical surface was illuminated with a Xenon light through an operating microscope, and the reflected light, which passed through a 605 nm bandpass filter, was detected by a CCD camera-based optical imaging system. Individual electrical stimulation of five digits induced changes in the reflected light intensities. Visualizing the intrinsic optical responses, we constructed maps of finger representation in Brodmann's area 1. In the maps, response areas of Digits I to V were sequentially aligned along the central sulcus in the crown of the postcentral gyrus from the latero-inferior region (Digit I) to the medio-superior region (Digit V). The neighboring response areas partially overlapped each other, as previously described in the monkey somatosensory cortex. Similar results were obtained in the face region with stimulation of the three branches of the trigeminal nerve. These results suggest that the overlap of the response areas is a common feature in the somatosensory cortex not only in monkeys, but also in humans.

Adult↗
PubMed2004

Functional MRI mapping of brain activation during visually guided saccades and antisaccades: cortical and subcortical networks.

Antisaccade tasks require a subject to inhibit a saccade toward a briefly appearing peripheral target and instead to immediately generate a saccade to an equivalent point in the opposite hemifield. Using functional magnetic resonance imaging (fMRI), we investigated the neural networks required to inhibit reflexive saccades and to voluntarily generate saccades. The results demonstrated that saccade and antisaccade tasks often bilaterally activate frontal, parietal and supplementary eye fields, lenticular nuclei and occipital cortex. Additional activation of bilateral dorsolateral prefrontal cortices, supramarginal gyri, anterior cingulate cortices and thalamus was observed during antisaccade tasks. These results indicate that fronto-parietal and fronto-striato-thalamo-cortical circuits are involved in antisaccade tasks. The fronto-parietal circuit is thought to be related to the planning of saccadic eye movements that involve attentional control, while the fronto-striato-thalamo-cortical circuits connect to cortical region as a feedback network. We speculate that the abnormalities in spatial attention and eye movement control observed in schizophrenia stem from dysfunctions in the fronto-parietal and fronto-striato-thalamo-cortical circuits.

Adult↗
PubMed2004

Role of pontile mechanisms in the neurogenesis of eupnea.

We have proposed a "switching concept" for the neurogenesis of ventilatory activity. Eupnea reflects the output of a pontomedullary neuronal circuit, whereas gasping is generated by medullary pacemaker mechanisms. Pontile mechanisms, then, are hypothesized to play a fundamental role in the neurogenesis of eupnea. If pontile mechanisms do play such a critical role, several criteria must be fulfilled. First, perturbations of pontile regions must alter eupnea under all experimental conditions. Second, neuronal activities that are consistent with generating the eupneic rhythm must be recorded in pons. Finally, medullary mechanisms alone cannot fully explain the neurogenesis of eupnea. Evidence from previous studies that support the validity of these criteria is presented herein. We conclude that pontile mechanisms play a critical role in the neurogenesis of eupnea.

Animals↗