摘要:

AbstractFollowing reconstruction with high spatial resolution of the 3‐D geometry of the dendritic arborizations of two abducens motoneurons, we simulated the distribution of electrotonic voltage over the whole dendritic tree. Here, we demonstrate that the complex stochastic electrotonic structure of both motoneurons can be reduced to a statistically significant small set of well discriminated clusters. These clusters are formed by dendritic branches belonging to different dendrites of the neuron but with similar electrotonic properties. A cluster analysis was performed to estimate quantitatively the partition of the branches between the dendritic clusters. The contents of the clusters were analysed in relation to their stability under different values of specific membrane resistivity (Rm), to their remoteness from the soma and their location in 3‐D space. The cluster analysis was executed in a 2‐D parameter space in which each dendritic branch was described by the mean electrotonic voltage and gradient. The number of clusters was found to be four for each motoneuron when computations were made withRm=3 kΩ.cm2. An analysis of the cluster composition under differentRmrevealed that each cluster contained invariant and variant branches. Mapping the clusters upon the dendritic geometry of the arborizations allowed us to describe the cluster distribution in terms of the 3‐D space domain, the 2‐D path distance domain and the total surface area of the tree. As the cluster behaviour reflects both the geometry and the changes in the neuronal electrotonic structure, we conclude that cluster analysis provides a tool to handle the functional complexity of the arborizations without losing relevant information. In terms of synaptic activities, the stable dendritic branches in each cluster may process the synaptic inputs in a similar manner. The high percentage of stable branches indicates that geometry is a major factor of stability for the electrotonic clusters. Conversely, the variant branches introduce the conditions for mechanisms of functional postsynaptic

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00542.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe ability of exogenous nitric oxide (NO) to modify synaptic transmission was investigated in area CA1 of the rat hippocampal slice. The NO donorsS‐nitroso‐N‐acetylpenicillamine (SNAP) andS‐nitrosoglutathione (SNOG) depressed field excitatory postsynaptic potentials evoked by low frequency stimulation of the Schaffer collateral ‐ commissural pathway. Upon washout of the NO donors, synaptic transmission rapidly returned to control levels. A similar reversible synaptic depression was produced by SNAP when tetanic stimulation (100 Hz; 1 s) was delivered in its presence. The effect of SNAP was not mimicked by its precursor or breakdown product and was blocked by haemoglobin, indicating that the effect involved NO. Roussin's black salt, a photolabile NO donor, also depressed transiently field excitatory postsynaptic potentials following photolysis. The depression was induced rapidly following a flash of UV light (20 s duration) focused onto the slice using a confocal microscope. The depressant effect of the NO donors on synaptic transmission was mimicked by zaprinast, a specific cGMP ‐ phosphodiesterase inhibitor. Zaprinast depressed to a similar extent both the α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionate andN‐methyl‐d‐aspartate receptor‐mediated components of excitatory postsynaptic currents without affecting passive membrane properties, indicating a presynaptic locus of action. SNAP, SNOG and zaprinast all elevated cGMP levels in rat hippocampal slices. Immunocytochemical staining revealed that the cGMP accumulation was mainly in a network of varicose fibres running throughout the CA1 region, consistent with a presynaptic site of action of NO. We conclude that NO, possibly through activation of guanylate cyclase, may be involved in transient presynaptic depression in

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00543.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractA period of hypersensitivity toN‐methyl‐d‐aspartate (NMDA) has been described during the early development of different types of neuron. Since activation of NMDA receptors can also induce rapid neuron death, the hypersensitivity to NMDA may be tightly controlled. In the present study we show that mouse cerebellar granule neurons become transiently hypersensitive to NMDA between days 10 and 14 after plating in a culture medium containing 30 mM K+. The NMDA sensitivity is higher when cells are cultured in the presence of an NMDA receptor antagonist [30 mM K+plus 100 μM 3‐((±)‐2‐carboxypiperazine‐4‐yl)‐propyl‐1‐phosphonic acid (CPP)], and no hypersensitivity is observed when cells are cultured in the continuous presence of NMDA (12.5 mM K+plus 100 μM NMDA). The high NMDA sensitivity in control cells is associated with a higher density of NMDA receptors than that measured in NMDA‐treated cells, suggesting that the sensitivity to NMDA may be partly controlled by activity‐dependent NMDA receptor down‐regulation. We also examined the level of NMDA‐ζ1 mRNA and found no correlation between this parameter and the transient pattern of NMDA sensitivity. Such NMDA receptor plasticity may be of importance in the central nervous system, protecting developing cells from excitotoxicity

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00544.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractTo extend our study of the inhibitory synaptic network we have developed an isolated whole‐brain preparation of the 52‐h‐old zebrafish(Brachydanio redo)in which the structural and functional integrity of the brain is preserved. We report the characterization of quantal inhibitory events and the correlation of their properties with those of the underlying activated channels. During whole‐cell recordings of the Mauthner cells, applications of 10−6M tetrodotoxin greatly reduced the frequency and amplitude of the spontaneously occurring synaptic events, which were dominated by Cl−‐dependent inhibitory postsynaptic currents (IPSCs). Lowering Ca2+and adding Mg2+to tetrodotoxin‐containing solutions resulted in a further decrease in amplitude of the recorded synaptic currents, the remaining ones being considered as miniature IPSCs (mISCs). Applications of 0.5–1 μMM strychnine in the presence of tetrodotoxin eliminated>90% of the inhibitory currents in the preparation. The amplitude histograms of these mIPSCs exhibited two initial equally spaced peaks, followed by a skewed distribution for higher values. The first two components were well fitted by the sum of two Gaussian curves, giving a mean quantal amplitude of 35.7 pA (at a holding potential of‐50 mV) and a coefficient of variation of 0.25 for the first peak. Outside‐out recordings showed at least two classes of glycine receptor channels, one having multiple conductance levels with a main state of 81–86 pS and another displaying only one opening level of 41–43 pS. These two mean conductance states had similar mean open times, of 0.6–1 and 4.5–6 ms respectively. In addition, three mean closed times were observed for the 41–43 pS level. The shortest group (0.6–1 ms) was considered as representing gaps within bursts. Burst analysis revealed three mean burst durations, of 0.6, 4 and 35 ms. Comparisons of the amplitude of the first class of mIPSCs and of the open channel conductances indicated that one quantum opens 14–22 channels. Moreover, the correspondence between the mean decay time of mIPSCs and the mean open time or medium burst duration (4–5 ms) suggests that glycine‐activated channels open only once in response to a single exocytosis. The pre‐and postsynaptic origins of mIPSCs amplitude fluctuations are discussed in the context of multivesicular release versus the hypo

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00545.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractKainate, a potent excitatory and neurotoxic agent, has also proved useful in studies on other glutamate‐driven phenomena, such as neuronal plasticity. Long‐term effects of kainate are apparently dependent on its influence on the expression of various genes, including those encoding the AP‐1 transcription factor, consisting of proteins belonging to the Fos and Jun families. In our studies we analysed c‐fos, fos B, c‐jun, jun Bandjun DmRNA levels as well as a functional feature of AP‐1, its DNA‐binding activity, in the rat brain following systemic injection of kainate. Two phases of elevated AP‐1 DNA‐binding activity were observed in the hippocampus and entorhinal cortex, and were correlated with period of seizures (2 and 6 h after kainate injection) and neuron damage (48–72 h). At 72 h after kainate treatment DNA fragmentation, believed to be diagnostic of apoptotic processes typical of programmed cell death phenomena, was noted. Two and six hours after the treatment, AP‐1 consisted predominantly of Fos B, c‐Fos, Fra‐2 and Jun B, while at 72 h Jun D constituted the major AP‐1 component in place of Jun B, and no c‐Fos was detected. Only a slight AP‐1 increase was seen 24 h after kainate treatment. In the sensory cortex, only the late phase of AP‐1 elevation was detected. Contrary to AP‐1, no effect of kainate on levels of two other transcription factors, CREB/ATF (cAMP‐responsive element binding proteins) and OCT (octamer element DNA‐binding activity) was seen. However, the level of OCT DNA‐binding activity was higher in the sensory cortex than in other two structures examined. These data point to a selective effect of kainate on AP‐1 in brain structures known to be particularly vulnerable to kainate, and suggest a role of AP‐1 transcription factor, and more selectively Jun D protein

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00546.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThis study presents an ultrastructural analysis of layers 8 and 9 in the optic tectum ofXenopus laevis.Retinotectal axons were labelled with horseradish peroxidase and tectal cells were labelled with antibody to GABA. Four distinct axonal and dendritic structures were identified. GABA‐negative axon terminals formed asymmetric synapses and were categorized as type a‐1 (which included retinotectal axons), characterized by medium size synaptic vesicles and pale mitochondria, and type a‐2 (non‐retinotectal) with large vesicles and dense mitochondria. GABA‐negative dendrites (type d) contained dense mitochondria, microtubules in the dendritic shafts, and dendritic spines devoid of microtubules. GABA‐positive structures contained small synaptic vesicles and dense mitochondria. Some dendrites (type D) were not only postsynaptic but were also presynaptic elements, as defined by the presence of vesicles and distinct synaptic clefts with symmetric specializations. GABA‐positive presynaptic structures were mostly located in vesicle‐filled, bulbous extensions of dendritic shafts and usually terminated onto dendritic spines. Some type D dendrites were the middle element in serial synapses, with input from either GABA‐positive or GABA‐negative structures and output to GABA‐negative structures. Retinotectal terminals were identified as one of the synaptic inputs to GABA‐positive processes. Glia were characterized by granular cytoplasm and large mitochondria, often displaying a crystalline matrix structure. These results indicate that GABA‐positive neurons are a prominent component of circuitry in the superficial layers of the tectum ofXenopusand that, as in mammals, they participate in serial synaptic arrangements in which retinotectal axons are the first element. These arrangements are consistent with complex processing of visual input to the tectum and a central role for inhibitory processes in the sh

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00547.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe sense of form is poor in indirect view. Yet the cortical magnification theory asserts that the disadvantage can be made up by scaling the image size according to the spatial variation in the mapping of the retina onto the cortex. It is thus assumed that all visual information passes through a functionally homogeneous neural circuitry, with the spatial sampling of input signals varying across the visual field. We challenge this notion by showing that character recognition in the visual field cannot be accommodated by any concept of sole size scaling but requires increasing both size and contrast of the target being viewed. This finding is formalized into a hyperbolic law which states that target size multiplied by log contrast is constant across the visual field. We conclude that the scalar cortical magnification theory fails for character recognition since the latter depends on multidimensional pattern representations in higher, i.e. striate and prestriate, cortical areas.

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00548.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractThe development of size and tonotopy in the inferior colliculus of the kitten was studied using the [14C]2‐deoxyglucose technique and tone stimulation with 2 and 15 kHz at a maximum 110 dB sound pressure level. At 2 days of age, frequency‐specific labelling cannot be detected. Two kilohertz labelling is distinctly visible in the rostral and central inferior colliculus at day 6; 15 kHz labelling occurs first at day 11. In the rostral and central inferior colliculus, 2 kHz labelling starts at a ventral and central position and shifts dorsalwards and to a more lateral location between postnatal days 6 and 21. Such a shift is not seen in the caudal inferior colliculus. There, the focus of 2 kHz labelling remains rather constant; only the extension of the labelling increases in the older animals. In all parts of the inferior colliculus, 15 kHz labelling starts at a ventromedial position and shifts to a more lateral location while extending also more dorsalwards as the age increases. These changes in 15 kHz labelling continue up to 3 months. In addition to the ventromedial‐to‐dorsolateral shift and expansion of labelling, there is also a rostral‐to‐caudal gradient of maturation, in that in older animals frequency‐specific labelling reaches farther caudalwards. The reported changes in frequency representation in the inferior colliculus can be explained on the basis of a shift in frequency input and input sensitivity to the laminae of the inferior colliculus, mainly due to maturational changes within the cochlea and/or as a consequence of the increasing size of the inferi

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00549.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractNeuronal nicotinic acetylcholine receptors consist of different subunits, α and β, with different subtype arrangement corresponding to distinct pharmacological and functional properties. The expression of α3, α7 and β2 mRNA in the human brain was studied byin situhybridization and compared to [3H]nicotine, [3H]cytisine and [125l]α‐bungarotoxin binding in contiguous sections. The β2 probe showed a strong hybridization signal in the granular layer of the dentate gyrus and in the CA2/CA3 region of the hippocampus and in the insular cortex, and a signal of lower intensity in the subicular complex and entorhinal cortex. The α3 probe showed strong hybridization in the dorsomedial, lateral posterior, ventroposteromedial and reticular nuclei of the thalamus, and a weak signal in the hippocampal region and in the entorhinal, insular and cingular cortex. The amount of α7 mRNA was high at the level of the dentate granular layer and the CA2/CA3 region of the hippocampus, in the caudate nucleus and in the pulvinar and ventroposterolateral nuclei of the thalamus. [3H]Nicotine and [3H]cytisine binding appeared to be identical in anatomical distribution and relative intensity. It was high in the thalamic nuclei, the putamen and in the hippocampal formation in the subicular complex and the stratum lacunosum moleculare. The level of [125l]α‐bungarotoxin binding was particularly high in the hippocampus and in the pyramidal cells of the CA1 region, but was relatively low in the subicular complex. Our data indicate that in the human brain nicotinic receptor subtypes have discrete distributions, which are in part different from those of

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00550.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

AbstractAxonal segments transected from their cell bodyin vivocommonly undergo degeneration within 3–4 days (Wallerian degeneration). In lower vertebrates and invertebrates, however, some transected axonal segments survive for long periods ranging between 30 and 200 days. To circumvent the technical complications of studying the mechanisms underlying long‐term survival of transected axonsin vivo, we developed anin vitrosystem. We found previously that isolated axonal segments of culturedAplysianeurons preserved their morphological integrity for an average duration of 7.6 days (range 2–14 days) and maintain their passive and excitable membrane properties. This survival occurred in the absence ofde novoprotein synthesis. In the present study we examined the influence of homologous neurons on the survival of transected axonal segments. We found that the average survival time of transected axons was doubled when co‐cultured in physical contact with intact homologous neurons (average 15.3 days, range 2–27 days). During this period, the transected axons extended neurites, maintained normal passive and excitable membrane properties, formed electrotonic junctions with the intact neurons and maintained normal free intracellular Ca2+levels. Consistent with these observations, electron micrographs of the transected axon revealed that the cytoskeletal elements of the axon appeared normal even 20 days after transection. In contrast, the mitochondria and smooth endoplasmic reticulum appeared damaged. As the prolonged survival was conditional on physical contact between the transected axon and the surrounding intact neurons, we suggest that the prolongation of survival time is promoted by the direct transfer of material from the intact neurons to the transected axon. However, co‐culture of transected axons with homologous neurons did not fully mimicin vivoconditions, in which transected axons can survive for sev

ISSN:0953-816X    

DOI:10.1111/j.1460-9568.1994.tb00551.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY