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PubMedDate not supplied

Computation by ensemble synchronization in recurrent networks with synaptic depression.

While computation by ensemble synchronization is considered to be a robust and efficient way for information processing in the cortex (C. Von der Malsburg and W. Schneider (1986) Biol. Cybern. 54: 29-40; W. Singer (1994) Inter. Rev. Neuro. 37: 153-183; J.J. Hopfield (1995) Nature 376: 33-36; E. Vaadia et al. (1995) Nature 373: 515-518), the neuronal mechanisms that might be used to achieve it are yet to be uncovered. Here we analyze a neural network model in which the computations are performed by near coincident firing of neurons in response to external inputs. This near coincident firing is enabled by activity dependent depression of inter-neuron connections. We analyze the network behavior by using a mean-field approximation, which allows predicting the network response to various inputs. We demonstrate that the network is very sensitive to temporal aspects of the inputs. In particular, periodically applied inputs of increasing frequency result in different response profiles. Moreover, applying combinations of different stimuli lead to a complex response, which cannot be easily predicted from responses to individual components. These results demonstrate that networks with synaptic depression can perform complex computations on time-dependent inputs utilizing the ability to generate temporally synchronous firing of single neurons.

Action Potentials↗
PubMed2004

Gene expression profiling reveals multiple novel intrinsic and extrinsic factors associated with axonal regeneration failure.

In contrast to the regeneration-competent peripheral nervous system (PNS), lesions of nerve tracts within the central nervous system (CNS) lead to chronically impaired neuronal connections. We have analysed changes in gene expression patterns occurring as a consequence of postcommissural fornix transection at a time when spontaneous axonal growth has ceased at the lesion site. This was done in order to describe both extrinsic and intrinsic determinants of regeneration failure. Using a genomic approach we have identified a number of so far undetected factors such as bamacan and semaphorin 6B, which relate to chronic axonal growth arrest and therefore are promising candidates for lesion-induced axonal growth inhibitors. In addition, we observed that within the subiculum, where the fornix axons originate, neuronal Oct-6 was induced and NG2 was down-regulated, indicating that axotomized neurons as well as glial cells react at the level of gene expression to remote axotomy.

Animals↗
PubMed2003

Olfactory neurons expressing identified receptor genes project to subsets of glomeruli within the antennal lobe of Drosophila melanogaster.

We have used green fluorescent protein to trace the projection patterns of olfactory neurons expressing identified candidate odorant receptors to the brain of Drosophila. At the periphery, receptor expression correlates with specific sense-organ subtype, independent of location on the antennal surface. The majority of neurons expressing a given receptor converge onto one or two major glomeruli as described previously. However, we detected a few additional glomeruli, which are less intensely innervated and also tend to be somewhat variable. This means that functionally similar olfactory neurons connect to small subsets of glomeruli rather than to a single glomerulus as believed previously. This finding has important implications for our understanding of odor coding and the generation of olfactory behavior.

Animals↗
PubMed1980

Distribution and light microscopic features of granule cells in the cochlear nuclei of cat, rat, and mouse.

In the present study the cytology and the topography of the cochlear granule cell domain (a comprehensive term introduced here for all granule cell-containing regions of the cochlear nuclear complex) have been studied light microscopically in Nissl, Bielschowsky, and Golgi-Del Rio-Hortega material of cats, rats, and mice; in Golig rapid material of 0-14-day-old kittens; and in sections of 6-week-old kittens following HRP injections in the superficial dorsal cochlear nucleus (DCN). The domain has been parcellated in seven subdivisions which, in spite of some species' differences, are easily identifiable in all of the included animals. The cochlear granule cells are considered as a particular class of neuron, which is slightly different from, but nevertheless principally similar to the cerebellar granule cells in both shape and mode of neuronal connections. The digitiform terminals of the cochlear granule cells differentiate after the first two weeks of extrauterine life. In several respects these cells show larger variation among species than do the cerebellar granules, the similarity between the two classes of granule cells being most conspicuous in the rodent. The silver, Golgi rapid, and HRP material suggest that all, or at least the majority, of the granule cell axons project to the molecular layer of the DCN, forming parallel fibers similar to those of the cerebellar cortex. Also, the cochlear parallel fibers traverse the spiny apical dendrites of principal neurons (the pyramidal cells) and the smoother dendrites of molecular layer stellate cells.

Animals↗
PubMed2003

Gap junctions do not underlie changes in whole-cell conductance in anoxic turtle brain.

An acute reduction in cell membrane permeability could provide an effective strategy to prolong anoxic survival. A previous study has shown that in the western painted turtle whole-cell neuronal conductance (G(w)) decreases during anoxia, which may be mediated by the activation of adenosine A(1) receptors and calcium. Reduction in G(w) is thought to be the result of ion channel closure, but closure of gap junctions could also be responsible for this phenomenon. In our study, antibody staining of connexin 32 and 43 (Cx32 and Cx43) suggested the presence of gap junctional components in the turtle cortex. To examine if gap junctions were involved in the previously measured anoxic decrease in G(w), neuronal connectivity was assessed through the measurement of whole-cell capacitance (C(w)). Turtle cortical sheets were perfused with normoxic (95%O(2)/5%CO(2)), anoxic (95%N(2)/5%CO(2)), high calcium (4 mM) and adenosine (200 microm) artificial cerebral spinal fluid (aCSF). No significant change in C(w) was observed under any of the above conditions. However, during hypo-osmotic aCSF perfusion C(w) decreased significantly, with the lowest value of 50+/-10.4 pF (P<0.05) occurring at 30 min. To visualize changes in gap junction permeability lucifer yellow was loaded into turtle neurons during normoxic, anoxic, 0 calcium, hypo-osmotic, cold shock, (+)-isoproterenol, nitric oxide donor S-nitoso-acetyl penicillamine, and 8-bromo-guanosine 3',5'-cyclic monophosphate aCSF perfusion. Dye propagation was only observed in 3 of 20 cold shock experiments (4 degrees C). We conclude that gap junctions are not involved in the acute reduction in G(w) previously observed during anoxia and that our results support the hypothesis that ion channel arrest is involved.

Animals↗
PubMed1993

Differential effects of MK-801 on brain-derived neurotrophic factor mRNA levels in different regions of the rat brain.

We have studied the effects of MK-801, a noncompetitive antagonist of N-methyl-D-aspartate-type glutamate receptors, on brain-derived neurotrophic factor (BDNF) mRNA levels in the rat brain. MK-801 decreased BDNF mRNA in the hippocampus and in the superficial layers of the cerebral cortex. However, in single cells of the middle layer of the cerebral cortex and the midline thalamic nuclei BDNF mRNA levels were markedly increased by MK-801. The highest density of these cells was found in the limbic cortex, especially in the retrosplenial and medial entorhinal cortex. Pentobarbital (an enhancer of gabaergic functions) and scopolamine (a muscarinic receptor antagonist) blocked the effects of MK-801 on BDNF mRNA levels in the retrosplenial cortex, but the nicotinic and dopaminergic receptor antagonists mecamylamine and haloperidol, respectively, were ineffective. Pilocarpine, a muscarinic cholinergic agonist increased BDNF mRNA in some, but not all, cortical areas, where MK-801 had elicited an increase in BDNF mRNA. Thus, the observations made with MK-801 demonstrate that depending on the neuronal connections and the transmitter systems involved, a given compound can elicit either a decrease or an increase in BDNF mRNA levels. This may open up pharmacological possibilities to a regionally more refined regulation of the neurotrophin synthesis.

Animals↗
PubMed1979

Tracing neural connections of human brain with selective silver impregnation. Observations on geniculocalcarine, spinothalamic, and entorhinal pathways.

In selected human brains, it is possible to study the efferent connections of a damaged site with the suppressive silver impregnation techniques described by Nauta and Gygax. Autopsy specimens with circumscribed lesions of recent origin ( one to five weeks before death) are suitable. However, the large size of the human brain and the lack of perfusion with fixative necessitates modifications in the methodology used on experimental animals. With these modifications, it has been possible to trace details of the spinothalamic tract, the geniculocalcarine pathway, and a projection into the entorhinal area in autopsied human brains. More frequent use of this methodology may substantially increase the information that is currently available on the neuronal connections of the human brain.

Aged↗
PubMed1998

The onset of parvalbumin-expression in interneurons of the rat parietal cortex depends upon extrinsic factor(s).

Parvalbumin (PV) belongs to the large family of EF-hand calcium-binding proteins and is an excellent marker for a subpopulation of GABAergic neocortical interneurons. During cortical development, PV first appears on postnatal day (P)8, in the infragranular layers; after P14, it also becomes apparent within the supragranular layers. However, nothing is known about the factors controlling its expression, which could involve functional activity, neuronal connectivity and/or neurotrophic factors. It being difficult to manipulate these parameters in vivo, their role may be more readily assessed in organotypic cultures, which are deprived of their subcortical afferents and efferents, and hence of subcortically derived neurotrophic factors and extrinsic functional activity. We prepared slices of the rat brain on P3, P5, P7 and P9, maintained them in culture for 2-5 weeks, and compared the temporal and spatial distribution pattern of PV-immunoreactivity within these slices with the in vivo situation. We found, first, that during late postnatal in vivo development and ageing, the number of PV-immunoreactive neurons in the parietal cortex decreases significantly, and second, that the expression of PV-immunoreactivity in the parietal cortex was markedly influenced by the phase of postnatal development at which slice cultures were explanted. In those removed on P7 and P9, the number of PV-immunoreactive cells, as well as the temporal and spatial distribution pattern of PV-immunoreactivity corresponded to the in vivo situation, but in explants obtained on P3 or P5, PV-immunoreactivity remained confined to layer V of the cortex, reminiscent of the expression profile manifested at the end of the second postnatal week in vivo. Also, the number of PV-immunoreactive cells in these cultures was significantly lower than in explants at the later stages. Our results indicate that the onset of PV-expression in the parietal cortex depends upon extrinsic cortical factors subsisting prior to P7. Once the production of this protein has been initiated, such influences are no longer required.

Animals↗
PubMed2006

Cochlear damage induces GAP-43 expression in cholinergic synapses of the cochlear nucleus in the adult rat: a light and electron microscopic study.

Recent studies suggest a potential for activity-dependent reconstruction in the adult mammalian brainstem that exceeds previous expectations. We found that a unilateral cochlear lesion led within 1 week to a rise of choline acetyltransferase (ChAT) immunoreactivity in the ventral cochlear nucleus of the affected side, matching the lesion-induced expression of growth-associated protein 43 (GAP-43) previously described. The rise of both ChAT and GAP-43 immunoreactivity was reflected in the average density of the staining. Moreover, the number of light-microscopically identifiable boutons increased in both stains. GAP-43-positive boutons could, by distinct ultrastructural features, regularly be identified as presynaptic endings. However, GAP-43 immunoreactivity was not only found in presynaptic endings with a classical morphology, but also in profiles that suggest morphological dynamic structures by showing filopodia, assemblages of pleomorphic vesicles, large vesicles (diameter up to 200 nm) fusing with the presynaptic plasma membrane close to synaptic contacts, small dense-core vesicles (diameter about 80 nm) and presynaptic ribosomes. Moreover, we observed perforated synapses as well as GAP-43 immunoreactivity condensed in rafts, both indicative of growing or changing neuronal connections. Classical and untypical ultrastructural profiles that contained GAP-43 also contained ChAT. We conclude that there is extensive deafness-induced GAP-43-mediated synaptic plasticity in the cochlear nucleus, and that this plasticity is predominantly, if not exclusively, based on cholinergic afferents.

Acetylcholine↗
PubMed1977

Evidence for selective axon-terminal uptake and retrograde transport of label in cortico- and rubrospinal systems after injection of 3H-proline.

In tracing the macaque's ascending spinal connections by anterograde axonal flow, perikaryal labelling was also observed within the n. ruber pars magnocellularis as well as in the sensorimotor cortex. While neuropil labelling was demonstrated after single injections of leucine or proline, labelling of perikarya was only evident following proline injections. Perikaryal labelling is most likely to be due to uptake of label by axons and/or axons terminals within the injection field and subsequent retrograde axonal transport of radioactive compound to the parent cell bodies. Advantages and disadvantages of the uptake of label by axon terminals are discussed in relation to the use of 3H-proline for tracing neuronal connections. The selectively of this event and its relationship to the suggested inhibitory functional role of proline and its metabolites is not clear and needs further investigation.

Afferent Pathways↗
PubMed2006

Dynamic switching of neural codes in networks with gap junctions.

Population rate coding and temporal coding are common neural codes. Recent studies suggest that these two codes may be alternatively used in one neural system. Based on the fact that there are massive gap junctions in the brain, we explore how this switching behavior may be related to neural codes in networks of neurons connected by gap junctions. First, we show that under time-varying inputs, such neural networks show switching between synchronous and asynchronous states. Then, we quantify network dynamics by three mutual information measures to show that population rate coding carries more information in asynchronous states and temporal coding does so in synchronous states.

Action Potentials↗
PubMed1998

Functional connections between medial prefrontal cortex and caudate-putamen in brain-stimulation reward of rats.

Rats were trained to self-stimulate for trains of cathodal pulses delivered via electrodes placed in the medial prefrontal cortex (MPFC) and caudate-putamen (CPu). When the pulses were delivered via 9 ipsilateral MPFC and CPu sites alternately, summation varied from 13% to 40%. However, the overall summation for 2 contralateral MPFC-CPu pairs was 5%, thus indicating a greater integration of ipsilateral than contralateral reward signals. When the interval between alternate pulses decreased in 4 of the 9 ipsilateral pairs, the summation also decreased, an outcome consistent with collision of action potentials passing between the MPFC and CPu sites. The size of the collision effect ranged from 15% to 33%. Estimates of conduction velocity varied between 0.4 to 5.4 m/s, with a 1.7 m/s average. According to these values, the neurons connecting the MPFC and CPu self-stimulation sites appear to be slower than the ones that have been shown to link reward fibers that course between posterior brain regions.

Animals↗
PubMed1978

Vagal glucoreceptors in the small intestine of the cat.

1. In anaesthetized cats, the unitary activity of seventy-eight sensory vagal neurones was recorded in nodose ganglia by means of extracellular glass microelectrodes. 2. These neurones were stimulated by perfusion of the small intestine (duodenum and first part of jejunum) with glucose or other different carbohydrates at concentrations of 1--20 g/l. (i.e. 55--1100 m-osmole/l.). 3. The neurones were slowly adapting to stimulation and their discharge frequency was always low (1--30 Hz). 4. The activity of these neurones depended on the particular carbohydrate used and on its concentration: the discharge frequency generally increased when the concentration rose. 5. The neurones were of the C type (conduction velocities: 0.8--1.4 m/sec; mean, 1.1 m/sec). 6. In contrast with the known neurones connected to the gastro-intestinal tension receptors, they were not obviously activated by intestinal contractions or distensions. 7. In the same way, the stimuli which produced the response of other known endings, i.e. the mucosal receptors, were not effective; these stimuli included in particular stroking of the mucosa, over-distension of the bowel, intestinal perfusion with alkaline or acid solutions. On the other hand, the use of substances other than glucose (KCl and NaCl of the same osmolarity) showed that the osmotic pressure was not directly related to the receptor activation. 8. Therefore it is proposed to call the endings corresponding to these neurones 'glucoreceptors'. 9. The effect of glycaemia and intestinal motility were also studied. These variables acted presumably by changing the intestinal absorption rate. 10. The functional characteristics of the glucoreceptors (in particular the short latency of their response) strongly suggested that they were located close to the intestinal epithelium. 11. An ultrastructural study was performed in an attempt to identify the histological site of the receptors. Many non-medullated fibres were observed in the villi, especially beneath the epithelial layer. They gave complex branchings with abundant swellings. Some of them, at least, belonged to the vagal sensory component, because they were less numerous after unilateral selective sensory vagotomy. Therefore these complex endings could serve as the vagal glucoreceptors. 12. The roles of vagal intestinal glucoreceptors are discussed. Their functional characteristics as well as the clinical and experimental data suggest that they may be involved in the regulation of different types of alimentary behaviour (hunger, thirst, alliesthesia) and energy balance.

Action Potentials↗
PubMedDate not supplied

Transneuronal retrograde transport of attenuated pseudorabies viruses within central visual pathways.

Pseudorabies virus (PRV) has been shown to be an effective transneuronal tracer within both the peripheral and the central nervous system. The only investigations of this virus in the visual system have examined anterograde transport of PRV from injection sites in the retina. In the present study, we injected attenuated forms of PRV into the primary visual cortex of both rats and cats to determine whether transneuronal retrograde infection would occur back to the retina. In rats, we made small injections into visual cortex of a strain of PRV (Bartha Blu) that contained a beta-galactosidase promoter insert. In cats, we injected PRV-M201 into area V1 of visual cortex. After a 2- to 4-day incubation period, we examined tissue from these animals for the presence of the beta-galactosidase marker (rats) or the virus itself (cats). Cortical PRV injections resulted in transneuronal retrograde infection of the lateral geniculate nucleus (LGN), thalamic reticular nucleus (TRN), and retina. PRV was retinotopically distributed in the pathway. In addition, double-labeling experiments in cats using an antibody against gamma-aminobutyric acid (GABA) were conducted to reveal PRV-labeled interneurons within the LGN and TRN. All TRN neurons were GABA+, as was a subset of LGN neurons. Only the subset of TRN neurons adjacent to the PRV-labeled sector of LGN was labeled with PRV. In addition, a subset of GABA+ interneurons in LGN was also labeled with PRV. We processed some tissue for electron microscopy to examine the morphology of the virus at various replication stages. No mature virions were detected in terminals from efferent pathways, although forms consistent with retrograde infection were encountered. We conclude that the PRV strains we have used produce a local infection that progresses primarily in the retrograde direction in the central visual pathways. The infection is transneuronal and viral replication maintains the intensity of the label throughout the chain of connected neurons, providing a means of examining detailed circuitry within the visual pathway.

Animals↗
PubMed1987

Autoradiographic localization of high affinity uptake sites for 3H-D-aspartate in the rat olfactory bulb.

In order to reveal excitatory amino acid-ergic neuronal connections in the rat olfactory bulb, uptake sites for the tritiated D-aspartic acid were analyzed by high resolution autoradiography. Light microscopy revealed both cellular and terminal-like uptake. Based on electron microscopy, overwhelming majority of the cellular uptake was assigned to glial cells. A fairly high number of labelled terminals appeared in the surroundings of the mitral cell somata, within the deepest portion of the external plexiform layer, in the internal plexiform layer and in the outer half of the granule cell layer. Labelled terminals synapsed onto likely granule cell dendrites or spines, at asymmetric membrane thickenings. These results suggest that, although the output neurons may not utilize glutamic or aspartic acid as their transmitters, these amino acids may, however, contribute to the bulbar neurotransmission, as mediator substances of a subgroup of centrifugal fibers to the olfactory bulb.

Animals↗
PubMed2005

Laminar circuit formation in the vertebrate retina.

Neuronal function depends on the accurate wiring between pre- and postsynaptic cells. Determining the mechanisms underlying precision in neuronal connectivity is challenging because of the complexity of the nervous system. In diverse parts of the nervous system, regions of synaptic contact are organized into distinct parallel layers, or laminae, that are correlated with distinct functions. Such an arrangement enables the development of synapse specificity to be more readily investigated. Here, we present an overview of the developmental mechanisms that are thought to underlie the formation of synaptic layers in the vertebrate retina, a highly laminated CNS structure. We will contrast the roles of activity-dependent and activity-independent mechanisms in establishing functionally discrete sublaminae in the inner retina, where circuits involving many subtypes of retinal neurons are assembled precisely. In addition, we will discuss new optical imaging approaches for elucidating how retinal synaptic lamination occurs in vivo.

Animals↗
PubMed2004

Persistent, noncytolytic infection of neurons by Borna disease virus interferes with ERK 1/2 signaling and abrogates BDNF-induced synaptogenesis.

Infection of the central nervous system by Borna disease virus (BDV) provides a unique model to study the mechanisms whereby a persistent viral infection can impair neuronal function and cause behavioral diseases reminiscent of mood disorders, schizophrenia, or autism in humans. In the present work, we studied the effect of BDV infection on the response of hippocampal neurons, the main target for this virus, to the neurotrophin BDNF. We showed that persistent infection did not affect neuronal survival or morphology. However, it blocked BDNF-induced ERK 1/2 phosphorylation, despite normal expression of the TrkB BDNF receptor. In addition, BDNF-induced expression of synaptic vesicle proteins was abrogated, which resulted in severely impaired synaptogenesis and defects in synaptic organization. Thus, we provide the first evidence that a virus can interfere specifically with neurotrophin-regulated neuroplasticity, thereby hampering proper neuronal connectivity. These results may help to understand the behavioral disorders associated with BDV infection.

Animals↗
PubMed2005

The appearance of long-latency responses to a conditioned signal in the cortex is explained by strengthening of collateral connections between pyramidal neurons.

Experimental analysis and computer simulation of the neurophysiological processes underlying the "stable and local electrophysiological expression of conditioned reflexes" in the cerebral cortex, a phenomenon discovered in Asratyan's laboratory in the 1960s, showed that the long-latency components of cortical evoked potentials to a conditioned signal correspond to the late phases of the responses of motor cortex neurons, which are analogous to and probably generated by the same mechanism as long-latency epileptiform reactions of neurons in the epileptogenic cortex. Late long-latency components are generated via activation of NMDA receptors in the collateral connections between pyramidal neurons. The delay in the generation of responses depends on the initial activation of GABA(A) receptors and the slow kinetics of the current through NMDA channels. The appearance of late components as a result of training is explained by increases in the efficiency of collateral excitatory connections between pyramidal neurons.

Animals↗