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PubMed2005

Functional interconnectivity between the globus pallidus and the subthalamic nucleus in the mouse brain slice.

In accordance with its central role in basal ganglia circuitry, changes in the rate of action potential firing and pattern of activity in the globus pallidus (GP)-subthalamic nucleus (STN) network are apparent in movement disorders. In this study we have developed a mouse brain slice preparation that maintains the functional connectivity between the GP and STN in order to assess its role in shaping and modulating bursting activity promoted by pharmacological manipulations. Fibre-tract tracing studies indicated that a parasagittal slice cut 20 deg to the midline best preserved connectivity between the GP and the STN. IPSCs and EPSCs elicited by electrical stimulation confirmed connectivity from GP to STN in 44/59 slices and from STN to GP in 22/33 slices, respectively. In control slices, 74/76 (97%) of STN cells fired tonically at a rate of 10.3 +/- 1.3 Hz. This rate and pattern of single spiking activity was unaffected by bath application of the GABA(A) antagonist picrotoxin (50 microM, n = 9) or the glutamate receptor antagonist (6-cyano-7-nitroquinoxaline-2, 3-dione (CNQX) 10 microM, n = 8). Bursting activity in STN neurones could be induced pharmacologically by application of NMDA alone (20 microm, 3/18 cells, 17%) but was more robust if NMDA was applied in conjunction with apamin (20-100 nM, 34/77 cells, 44%). Once again, neither picrotoxin (50 microM, n = 5) nor CNQX (10 microM, n = 5) had any effect on the frequency or pattern of the STN neurone activity while paired STN and GP recordings of tonic and bursting activity show no evidence of coherent activity. Thus, in a mouse brain slice preparation where functional GP-STN connectivity is preserved, no regenerative synaptically mediated activity indicative of a dynamic network is evident, either in the resting state or when neuronal bursting in both the GP and STN is generated by application of NMDA/apamin. This difference from the brain in Parkinson's disease may be attributed either to insufficient preservation of cortico-striato-pallidal or cortico-subthalamic circuitry, and/or an essential requirement for adaptive changes resulting from dopamine depletion for the expression of network activity within this tissue complex.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMedDate not supplied

[Electrophysiologic study of the ascending connections of the hippocampus with various neocortical zones in the rabbit].

In acute experiments on rabbits studies have been made on functional connections of hippocampal fields CA1 and CA3 with various zones of the neocortex. It was shown that these hippocampal structures are most closely connected with the limbic ancient associative cortex, as well as with the parietal and temporal regions. In the sensorimotor cortex, the EPs were rather irregular. Fields CA1 and CA3 exhibit different projections to the mentioned regions of the neocortex.

Afferent Pathways↗
PubMed1982

The giant neurone system in ophiuroids. III. The detailed connections of the circumoral nerve ring.

The morphology of the circumoral nerve ring of an ophiuroid, Ophiura texturata, is described. Particular attention is given to a system of fibres which are giant by echinoderm standards, and which occur both in the ectoneural and hyponeural parts of the nerve ring. The giant fibres in the ectoneurla tissue do not show the complicated pattern of distribution present in the segmental ganglia of the radial nerves. The main areas of neuropil in the ectoneural tissue are associated with small axon bundles which leave the nerve ring to innervate the gut and disc. The hyponeural tissue is exclusively motor and is involved in the innervation of the main radial and inter-radial muscles of the disc. Branches of the motor nerves are also associated with juxtaligamental tissue, the secretory products from which are thought to influence the plasticity of collagenous connective tissue. The structure of the circumoral nerve ring suggests that it serves as a functional connection between the nerve cords in adjacent radii. The ultrastructural evidence does not support the view that the circumoral nerve ring represents a central nervous system.

Animals↗
PubMed2004

Fos-tau-LacZ mice expose light-activated pathways in the visual system.

We have employed fos-tau-LacZ (FTL) transgenic mice to examine functional activation in the visual areas of the nervous system. The FTL mice express the marker gene lacZ in neurons and their processes following many different stimuli, and allow the imaging of activation from the level of the entire brain surface through individual neurons and their projections. Analysis of FTL expression in the retinas of mice following diurnal exposure to light shows that bipolar cells, specific classes of amacrine cells, ganglion cells, and a dense network of processes in the inner plexiform layer are functionally activated. In animals deprived of light, there is almost no activity in the retina. In the lateral geniculate nucleus (LGN), light exposure appears responsible for FTL expression in dorsal nuclei, but not for expression in the ventral nuclei or the intergeniculate leaflet. In the superficial layers of the superior colliculus, FTL expression is highly dependent on light exposure. Similarly, light exposure is required for FTL expression in primary visual cortex (area 17), but some expression remains in area 18 of dark-adapted animals. Finally, using mice with one or both eyes missing, we have determined which parts of the visual system are dependent on the presence of a functional connectivity from the eye. These data demonstrate the usefulness of the FTL mice to map functional activation within the entire visual system. Furthermore, we can capture visual activation in a conscious animal. Our findings give an insight into the architecture of activity within the retina and throughout the visual system.

Animals↗
PubMed2003

Expression of connective tissue growth factor in bone: its role in osteoblast proliferation and differentiation in vitro and bone formation in vivo.

Connective tissue growth factor (CTGF) is a secreted, extracellular matrix-associated signaling protein that regulates diverse cellular functions. In vivo, CTGF is expressed in many tissues with highest levels in the kidney and brain. The purpose of this study was twofold; first, to localize CTGF in normal bone in vivo during growth and repair, and second, to examine CTGF expression and function in primary osteoblast cultures in vitro and test its effect on bone formation in vivo. Northern and Western blot analyses confirmed that CTGF is expressed in normal long bones during the period of growth or modeling. In situ hybridization and immunohistochemical analysis demonstrated intense staining for CTGF mRNA and protein in osteoblasts lining metaphyseal trabeculae. Examination of CTGF expression in the fracture callus demonstrated that it was primarily localized in osteoblasts lining active, osteogenic surfaces. In primary osteoblast cultures, CTGF mRNA levels demonstrated a bimodal pattern of expression, being high during the peak of the proliferative period, abating as the cells became confluent, and increasing to peak levels and remaining high during mineralization. This pattern suggests that CTGF may play a role in osteoblast proliferation and differentiation as previously demonstrated for fibroblasts and chondrocytes. Treatment of primary osteoblast cultures with anti-CTGF neutralizing antibody caused a dose-dependent inhibition of nodule formation and mineralization. Treatment of primary osteoblast cultures with recombinant CTGF (rCTGF) caused an increase in cell proliferation, alkaline phosphatase activity, and calcium deposition, thereby establishing a functional connection between CTGF and osteoblast differentiation. In vivo delivery of rCTGF into the femoral marrow cavity induced osteogenesis that was associated with increased angiogenesis. This study clearly shows that CTGF is important for osteoblast development and function both in vitro and in vivo.

Animals↗
PubMed1992

Interactions of mast cells with the nervous system--recent advances.

This article reviews recent advances in the understanding of mast cell-nervous system interactions. It is drawn largely from work published within the last ten years, and discusses the anatomical and biochemical evidence of a functional connection between mast cells and the nervous system, and the implications that such a relationship may have for normal and abnormal physiological functioning. Mast cells are found at varying levels of association with the nervous system; in CNS parenchyma (mainly thalamus), in connective tissue coverings (e.g. meninges, endoneurium), and in close apposition to peripheral nerve endings in a variety of tissues. There is, as yet, no clearly defined role for mast cells in nervous system function, or vice-versa, and it seems most likely that their interactions fulfil mutually modulatory roles. By extension, pathological situations where one of the partners in this relationship is overly stimulated may lead to a dysregulation of the other, and contribute to disease symptomatology.

Animals↗
PubMed2006

Conversion of atriopulmonary Fontan to extracardiac total cavopulmonary connection improves cardiopulmonary function.

BACKGROUND: Experimental studies showed that extracardiac total cavopulmonary connection provides superior hemodynamics than atriopulmonary Fontan. METHODS: We prospectively assessed the impact of conversion of atriopulmonary Fontan to extracardiac total cavopulmonary connection on exercise capacity and cardiac function in 6 consecutive patients. RESULTS: Six months after conversion to extracardiac total cavopulmonary connection, we observed an increase in peak oxygen uptake in all patients (p=0.01;+17%). This improvement was associated to an increase of peak O(2) pulse (p=0.01;+16%), but no change in peak heart rate, arterial oxygen saturation at peak exercise, and pulmonary function. Ventricular ejection fraction did not change significantly after surgery. Conversion was associated with an improvement in heart failure symptoms as assessed by the New York Heart Association classification. Patients who had undergone additional anti-arrhythmia surgery for atrial fibrillation had no recurrence of arrhythmia at follow-up. CONCLUSION: Data indicate that conversion to extracardiac total cavopulmonary connection is associated with an improvement of cardiopulmonary function and heart failure symptoms. Improved exercise capacity is due to an increase in O(2) pulse and may reflect an improved cardiac stroke volume after the operation.

Adolescent↗
PubMed1985

Nucleus accumbens and preoptic area stimulation: tuberoinfundibular single unit responses, modulation of electrical activity and gonadotrophin secretion.

Single unit activity was recorded from tuberoinfundibular neurones in urethane-anaesthetized pro-oestrous rats. Responses following single shock (0.2 Hz) stimulation of the preoptic area/anterior hypothalamus (PO/AH) or nucleus accumbens (ACB) were recorded and computed for 137 single units. More cells were shown, by antidromic activation, to project to ACB (4 of 77) than to PO/AH (1 of 60). Fewer units were responsive to stimulation of ACB (p less than 0.02), those that were responsive showing a longer latency to the onset of response compared to that following PO/AH stimulation. Significantly (p less than 0.02) more slowly firing cells were found in the group of animals tested with stimulation of PO/AH. Delivery of high frequency stimulation to PO/AH resulted in a 21/2 fold increase in plasma luteinizing hormone (LH) levels (p less than 0.05), whereas ACB-stimulated and control animals showed no increases in plasma LH concentrations. During delivery of the high frequency stimulation only one cell in the ACB group of animals was orthodromically affected (out of five tested). However, in the PO/AH group, five of the seven cells tested showed either excitation or inhibition during stimulation. The possibility that the functional connections demonstrated between ACB and the endocrine hypothalamus are involved in the expression of 'higher' brain functions, recognised during changing endocrine states, is discussed.

Animals↗
PubMed2001

[Changes in intracellular mechanisms in sensory neurons in experimental diabetes mellitus].

Here we summarises the results of experimental investigation of changes in intracellular calcium homeostasis in sensory neurones of rats with streptozotocin-induced diabetes mellitus. Decrease in the calcium-accumulating function of both inositol-trisphosphate- as well as caffeine-sensitive endoplasmic reticulum has been detected both in primary sensory neurones of dorsal root ganglia and in secondary neurones of the spinal cord dorsal horn. Predominant depression in the functioning of metabotropic receptors of ligand-gated channels compared with those of ionotropic ones has been demonstrated. Changes in the pharmacological sensitivity of potential-operated calcium channels (predominantly of L-type), linked, probably, with alterations of functional connections between membrane channels and endoplasmic reticulum, are described. A predominant role of changes in the functioning of intracellular Ca(2+)-accumulating structures, leading to prolongation of depolarisation-induced Ca2+ transients in primary and secondary sensory neurones and corresponding changes in the transmission of nociceptive signals during diabetic neuropathy are discussed.

Animals↗
PubMed1991

[The comparative characteristics of the neuronal activity in surviving slices of transplanted and intact neocortex].

The background single unit activity and single or multiunit responses to electrical stimulation of the rat's embryonic cortex, grafted into the somatosensory cortex of adult rats were investigated in a slice preparation. The same characteristics of the intact cortex neurons were observed as a control. The percentage of neurons with background activity within grafts was higher, than that within intact neocortex slices (23% and 6%, respectively). However the percentage of neurons responding to electrical stimulation of the recipient neocortex was lower in grafts. The mean latency of multiunit responses of graft neurons was longer, than that of neurons of the intact neocortex recorded at the same distance from the stimulating electrode (19.4 +/- 5.0 and 5.8 +/- 1.1 ms, respectively). Duration of the evoked population discharges was approximately ten times longer in grafts. It is concluded that there are local functional connections between a graft and the host brain and that inhibitory processes within grafts are weak. Functional integration of grafts with the host brain of the recipients after cranial trauma is shown.

Animals↗
PubMed2026

Childhood Trauma and Frontoparietal Network Connectivity During Working Memory Task Performance in Individuals With Schizophrenia and Healthy Participants.

Schizophrenia is associated with altered frontoparietal connectivity, which supports higher-order cognition, including working memory. Childhood trauma has been linked to altered functional connectivity and reduced cognitive performance in individuals with schizophrenia and controls. Prior evidence suggests that trauma-related default mode dysconnectivity mediates the association between trauma and cognition. We hypothesised that childhood trauma would be associated with altered frontoparietal connectivity during a working memory task and that such connectivity changes would mediate the relationship between trauma and working memory. Childhood trauma, working memory and fMRI data were collected from individuals with schizophrenia or schizoaffective disorder (n = 38) and controls (n = 128). fMRI data were preprocessed in CONN, and seed-based connectivity analyses were performed for four frontoparietal seeds (bilateral dorsolateral prefrontal and posterior parietal cortices). Connectivity was contrasted across (a) diagnosis and (b) trauma severity. Moderated mediation analyses tested the associations between trauma, connectivity and working memory, with diagnosis as a moderator. Across all participants, higher physical neglect severity predicted poorer working memory performance. Stronger inverse connectivity between left dorsolateral prefrontal and frontal medial cortices predicted better working memory performance. As expected, patients showed widespread frontoparietal dysconnectivity relative to controls, but no differences in frontoparietal connectivity were observed across trauma severity groups. Frontoparietal connectivity did not mediate the association between trauma and working memory, although diagnosis moderated both the trauma-connectivity and connectivity-cognition associations. We conclude that, unlike previous evidence suggesting a mediating role for the default mode network, frontoparietal connectivity did not mediate the trauma-cognition association, possibly suggesting the unique significance of default mode network dysconnectivity in linking trauma to cognition in psychosis.

Humans↗
PubMed1987

Evidence for a threshold in experience-dependent long-term changes of kitten visual cortex.

In order to determine the role of unstructured and of spontaneous activity in the developmental plasticity of the visual cortex, we blocked in 7 kittens the retinal activity of one eye completely by intraocular injections of tetrodotoxin (TTX) while the other eye was left open. Littermates of these kittens were monocularly deprived by lid suture and served as controls. In 3 additional kittens one eye was inactivated with TTX and the other closed by lid suture to assess whether mere asymmetries in the activation levels of the two eyes were sufficient to induce ocular dominance changes. Despite some variability between the matched pairs, the ocular dominance shift towards the normal eye did not differ significantly in the kittens with monocular lid suture and monocular TTX injection (P greater than 0.3/chi 2). In the TTX-treated kittens there was a trend for neurones to be less sharply tuned for orientation but it was not significant (P greater than 0.08/chi 2). In the kittens which had one eye injected with TTX and the other sutured closed no shift of ocular dominance was apparent. Separate analysis of both hemispheres revealed only a small bias towards the respective contralateral eye. We conclude that the process mediating activity-dependent long-term changes of ocular dominance has a threshold. Afferent activity that fails to excite the postsynaptic neuron above this threshold plays neither a significant role in the stabilization nor in the disruption of functional connections.

Animals↗
PubMed1996

Responses of the superficial entorhinal cortex in vitro in slices from naive and chronically epileptic rats.

1. The main purposes of this study are to characterize the intracellular and extracellular responses of cells in superficial layers of entorhinal cortex (EC) in chronically epileptic animals, determine whether their altered physiology is dependent on being connected to hippocampus, and investigate whether there is evidence of augmented excitation and inhibitory interneuron disconnection. 2. Functional connectivity was maintained between the hippocampal area and the EC in vitro in a combined rat hippocampal-parahippocampal slice preparation by slicing with a vibratome at a 30-deg angle to the base of the brain. Three groups of animals were studied: naive animals, animals that had experienced a previous episode of (nonconvulsive) self-sustaining limbic system status epilepticus (SSLSE) induced by electrical stimulation resulting in a chronically epileptic state, and animals in an electrode control group. In chronically epileptic rats and the electrode control group, studies were done on tissue contralateral to the side of electrode implantation. 3. Extracellular and intracellular recordings were made from the superficial layers of EC. Neurons in the superficial layers of the EC were activated by stimulation of the deep layers within the EC or the angular bundle adjacent to the EC, which contains axons from EC neurons. Responses could be elicited by antidromic and synaptic mechanisms by stimulation at either site. In addition, a monosynaptic protocol was used that involved direct activation of interneurons with a stimulating electrode placed near the recording electrode in the presence of the ionotropic glutamate blockers D(-)-2-amino-5-phosphonovaleric acid (APV) and 6,7-dinitroquinoxaline-2-3-dione (DNQX). 4. Responses were collected over a range of stimulus intensities, from very low to high intensities, to construct input/output function (I/O) curves. Amplitudes and durations were measured at the lowest stimulus intensity that elicited a maximum responses. 5. Extracellular field potential responses from electrode controls did not differ from naives qualitatively with respect to morphology of field potential responses or quantitatively with respect to response duration and amplitude. Field potential responses in tissue from post-SSLSE rats differed markedly in morphology from naive and electrode controls, being more complex, significantly longer in duration, and decreased in amplitude. These epileptiform responses were shortened markedly by blockade of N-methyl-D-aspartate (NMDA) receptors with APV, but this manipulation did not convert responses to a normal morphology. These responses were abolished by blockade of non-NMDA mediated ionotropic glutamate receptors with DNQX. 6. During intracellular recordings of neurons in slices from both control and epileptic animals, neurons were quiescent under resting conditions in the absence of electrical stimulation. 7. Intracellular responses in electrode controls were identical to naive, and together were considered "controls." In control tissue, evoked intracellular responses were similar to those previously described and most commonly consisted of an excitatory postsynaptic potential (EPSP) that was blocked partially by the NMDA-receptor antagonist APV, followed by hyperpolarizing potentials, which were identified electrophysiologically and pharmacologically as gamma-aminobuturic acid-A (GABAA)- and GABAB-receptor-mediated inhibitory postsynaptic potentials (IPSPs). EPSPs were blocked completely by DNQX. 8. In chronically epileptic tissue, evoked intracellular responses differed markedly from responses in control animals, exhibiting all-or-none prolonged paroxysmal depolarizing events with multiple superimposed action potentials in response to a single shock. These depolarizing events were reduced in duration and amplitude, but not abolished, in APV. IPSPs were not seen or markedly reduced at all stimulus intensities. These intracellular responses never resembled control responses. Intracellur responss correlated precisely in morphology and duration with extracellular field potentials. (ABSTRACT TRUNCATED)

Animals↗
PubMed2005

Fusing EEG and fMRI based on a bottom-up model: inferring activation and effective connectivity in neural masses.

The elucidation of the complex machinery used by the human brain to segregate and integrate information while performing high cognitive functions is a subject of imminent future consequences. The most significant contributions to date in this field, known as cognitive neuroscience, have been achieved by using innovative neuroimaging techniques, such as electroencephalogram (EEG) and functional magnetic resonance imaging (fMRI), which measure variations in both the time and the space of some interpretable physical magnitudes. Extraordinary maps of cerebral activation involving function-restricted brain areas, as well as graphs of the functional connectivity between them, have been obtained from EEG and fMRI data by solving some spatio-temporal inverse problems, which constitutes a top-down approach. However, in many cases, a natural bridge between these maps/graphs and the causal physiological processes is lacking, leading to some misunderstandings in their interpretation. Recent advances in the comprehension of the underlying physiological mechanisms associated with different cerebral scales have provided researchers with an excellent scenario to develop sophisticated biophysical models that permit an integration of these neuroimage modalities, which must share a common aetiology. This paper proposes a bottom-up approach, involving physiological parameters in a specific mesoscopic dynamic equations system. Further observation equations encapsulating the relationship between the mesostates and the EEG/fMRI data are obtained on the basis of the physical foundations of these techniques. A methodology for the estimation of parameters from fused EEG/fMRI data is also presented. In this context, the concepts of activation and effective connectivity are carefully revised. This new approach permits us to examine and discuss some future prospects for the integration of multimodal neuroimages.

Brain↗
PubMed2001

Theory of FID NMR signal dephasing induced by mesoscopic magnetic field inhomogeneities in biological systems.

A theory of the NMR signal dephasing due to the presence of tissue-specific magnetic field inhomogeneities is developed for a two-compartment model. Randomly distributed magnetized objects of finite size embedded in a given media are modeled by ellipsoids of revolution (prolate and oblate spheroids). The model can be applied for describing blood vessels in a tissue, red blood cells in the blood, marrow within trabecular bones, etc. The time dependence of the dephasing function connected with the spins inside of the objects, s(i), is shown to be expressed by Fresnel functions and creates a powder-type signal in the frequency domain. The short-time regime of the dephasing function for spins outside the objects, s(e), is always characterized by Gaussian time dependence, s(e) approximately exp[-zeta(k)(t/tc)2], with zeta being a volume fraction occupied by the objects, t(c) being a characteristic dephasing time, and the coefficient k depending on the ellipsoid's shape through the aspect ratio of its axes (a/c). The long-time asymptotic behavior of s(e) is always "quasispherical"-linear exponential in time, s(e) approximately exp(-zetaCt/tc), with the same "spherical" decay rate for any ellipsoidal shape. For long prolate spheroids (a/c)<<1, there exists an intermediate characteristic regime with a linear exponential time behavior and an aspect-ratio-dependent decay rate smaller than (zetaC/tc).

Algorithms↗
PubMed1989

Expression of acetylcholinesterase during visual system development in Drosophila.

As in other insects acetylcholine (ACh) and acetylcholinesterase (AChE) function in synaptic transmission in the central nervous system of Drosophila. Studies on flies mutant for AChE indicate that in addition to its synaptic function of inactivating acetylcholine, this neural enzyme is required for normal development of the nervous system (J.C. Hall, S.N. Alahiotis, D.A. Strumpf, and K. White, 1980, Genetics 96, 939-965; R.J. Greenspan, J.A. Finn, and J.C. Hall, 1980, J. Comp. Neurol. 189, 741-774). In order to understand what role AChE may play in neural development, it is necessary to know, in detail, where and when the enzyme appears. The use of monoclonal antibodies to localize AChE in the developing visual system of wild type Drosophila has yielded the novel observation that AChE appears in photoreceptor (retinula) cells 4-6 hr after they differentiate and 3 to 4 days before they are functional. Three days later the staining in the cell body of these cells is reduced. Because retinula cells have no functional connections at the time when AChE is first detected, AChE can not be performing its standard synaptic function. Subsequent to the reduction of AChE in the retinula cells, midway through the pupal stage, the enzyme accumulates rapidly in the neuropils of the optic lobes of the brain. Thus, there is a biphasic accumulation of AChE in the developing visual system with the enzyme initially being expressed in the retinula cells and accumulating later in the optic lobes.

Acetylcholinesterase↗
PubMed2003

The evolution of the cortico-cerebellar complex in primates: anatomical connections predict patterns of correlated evolution.

Investigations into the evolution of the primate brain have tended to neglect the role of connectivity in determining which brain structures have changed in size, focusing instead on changes in the size of the whole brain or of individual brain structures, such as the neocortex, in isolation. We show that the primate cerebellum, neocortex, vestibular nuclei and relays between them exhibit correlated volumetric evolution, even after removing the effects of change in other structures. The patterns of correlated evolution among individual nuclei correspond to their known patterns of connectivity. These results support the idea that the brain evolved by mosaic size change in arrays of functionally connected structures. Furthermore, they suggest that the much discussed expansion of the primate neocortex should be re-evaluated in the light of conjoint cerebellar expansion.

Anatomy, Comparative↗