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Results for “Presynaptic Terminals”

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At least 19 recordsLinked to original sources

PubMed1996

Noradrenaline modulates transmitter release by enhancing the Ca2+ sensitivity of exocytosis in the chick ciliary presynaptic terminal.

1. The giant presynaptic terminal of chick ciliary ganglion was used to examine how noradrenaline (NA) modulates neurotransmitter release. The cholinergic excitatory postsynaptic currents (EPSCs) were recorded under whole-cell voltage clamp of the postsynaptic neuron. 2. Although the EPSC was potentiated by NA, the current directly activated by acetylcholine (IACh) was unaffected. NA also increased the quantal contents without changing the quantal size. 3. The NA-dependent potentiation was antagonized by neither phentolamine nor propranolol. The EPSC was also potentiated by adrenaline and dopamine but not by normetanephrine, phenylephrine or isoprenaline. The EPSC was attenuated by clonidine. Therefore, NA potentiated the transmitter release through a receptor pharmacologically different from both alpha- and beta-adrenergic receptors. 4. The Ca2+ increment produced by an action potential (delta[Ca2+]pre) was reduced by NA through an alpha 2-adrenergic receptor. However, when alpha 2-adrenergic receptors were blocked, neither delta[Ca2+]pre nor resting Ca2+ were changed by NA. 5. The [Ca2+]o-EPSC relation was shifted by NA, decreasing the half-saturating [Ca2+]o, without changing the maximum. 6. It is concluded that NA-dependent potentiation of transmitter release was due to an increase in the Ca2+ sensitivity of the exocytotic process. The enhancement of the fusion probability is suggested.

Action Potentials↗

PubMed1993

The spatial distribution of calcium signals in squid presynaptic terminals.

1. The fluorescent Ca2+ indicator dye, fura-2, was used to examine the spatial distribution of intracellular Ca2+ signals in giant presynaptic terminals of squid. Brief trains of presynaptic action potentials were evoked to open Ca2+ channels within the giant presynaptic terminals and elevate presynaptic Ca2+ concentration. 2. Electrical stimulation produced pronounced rises in presynaptic Ca2+ concentration. These rises were much larger in the terminal region than in the adjacent axonal region of the presynaptic neuron, suggesting that Ca2+ channels are most abundant in the terminal. 3. Stimulation also produced gradients in Ca2+ concentration across the width of the presynaptic terminal. During stimulation, Ca2+ concentration was highest in the compartment of the presynaptic terminal closest to the postsynaptic neuron. This suggests that the Ca2+ channels are localized to this region of the presynaptic terminal. 4. Following the end of action potential trains, the rises in Ca2+ concentration became uniform across the width of the terminal. The redistribution of Ca2+ presumably is due to diffusion of Ca2+ throughout the presynaptic cytoplasm. Stimulus-evoked rises in Ca2+ declined slowly over several tens of seconds. 5. Histological examination of a giant presynaptic terminal used for imaging experiments revealed that the spatial compartments where stimulus-induced rises in Ca2+ concentration were highest were also enriched in active zones, the presynaptic sites of transmitter secretion. The co-localization of Ca2+ transients and active zones strongly suggests that neurons cluster Ca2+ channels selectively at active zones and that they do so to enhance the magnitude of Ca2+ signals in the vicinity of the active zone. 6. Longitudinal gradients in Ca2+ concentration also occur within presynaptic terminals and can be quantitatively accounted for by gradients in surface/volume ratio and density of active zones along the length of the presynaptic terminal.

Action Potentials↗

PubMed1995

Calcium transients in cerebellar granule cell presynaptic terminals.

Calcium ions act presynaptically to modulate synaptic strength and to trigger neurotransmitter release. Here we detect stimulus-evoked changes in residual free calcium ([Ca2+]i) in rat cerebellar granule cell presynaptic terminals. Granule cell axons, known as parallel fibers, and their associated boutons, were labeled with several calcium indicators. When parallel fibers were extracellularly activated with stimulus trains, calcium accumulated in the terminals, producing changes in the fluorescence of the indicators. During the stimulus train, the fluorescence change per pulse became progressively smaller with the high affinity indicators Fura-2 and calcium green-2 but remained constant with the low affinity dyes BTC and furaptra. In addition, fluorescence transients of high affinity dyes were slower than those of low affinity indicators, which appear to accurately report the time course of calcium transients. Simulations show that differences in the observed transients can be explained by the different affinities and off rates of the fluorophores. The return of [Ca2+]i to resting levels can be approximated by an exponential decay with a time constant of 150 ms. On the basis of the degree of saturation in the response of high affinity dyes observed during trains, we estimate that each action potential increases [Ca2+]i in the terminal by several hundred nanomolar. These findings indicate that in these terminals [Ca2+]i transients are much larger and faster than those observed in larger boutons, such as those at the neuromuscular junction. Such rapid [Ca2+]i dynamics may be found in many of the terminals in the mammalian brain that are similar in size to parallel fiber boutons.

Animals↗

PubMed1985

Calcium entry into voltage-clamped presynaptic terminals of squid.

Voltage-clamp measurements of Ca current and Arsenazo III measurements of intracellular Ca concentration were used to assess Ca ion entry into voltage-clamped presynaptic terminals of squid 'giant' synapses. Depolarization of voltage-clamped terminals filled with Arsenazo III produced absorbance changes consistent with intracellular accumulation of Ca ions. These intracellular Ca transients had a bell-shaped dependence on presynaptic potential and were maximal at approximately -10 mV. Arsenazo III signals recorded from the proximal portion of voltage-clamped presynaptic terminals had a dependence on command potential which was shifted relative to signals recorded from other presynaptic regions. Micro-electrode measurements of presynaptic membrane potential showed that during voltage-clamp depolarizations the proximal region was less depolarized than the rest of the presynaptic terminal. This indicates that voltage-clamped presynaptic terminals may be poorly controlled at their proximal region due to current flow into the adjacent axon. This poor control can cause heterogeneous Ca entry into the presynaptic terminal and thus heterogeneous release of transmitter along the terminal. Application of Ca ions from an extracellular pipette positioned near the distal end of the presynaptic terminal was used to restrict Ca entry to this well-controlled region. Local Ca application decreased the contribution of release from the poorly controlled proximal region to synaptic transfer curves. Presynaptic Ca currents were derived by correcting membrane currents for leakage and capacitive currents and other currents measured in the absence of Ca application. Ca currents measured in this way activated along a sigmoidal time course and did not inactivate for depolarizations as long as 25 ms. Peak Ca currents occurred at approximately -10 mV and inward Ca currents had an apparent 'reversal potential' near +60 mV. Ca channel activation, assessed with tail current measurements, was half-maximal at -13 mV and maximal at +20 mV. Simultaneous measurements of presynaptic Ca currents and Arsenazo III transients revealed a quantitative correspondence between Ca current integrals and Arsenazo III signal amplitude. This suggests that both methods provide reliable measures of Ca ion entry into presynaptic terminals under these conditions.

Action Potentials↗

PubMed1996

The role of remaining presynaptic terminals in the hippocampal CA1 after selective neuronal death: ischemia-induced glutamate efflux.

Following selective neuronal death, numerous presynaptic terminals maintain their structural integrity in the brain region. The role that these remaining presynaptic terminals play in the brain region showing selective neuronal death is not known. In the present study, we investigated the possibility that brief transient ischemia induces an excessive release of glutamate from the remaining presynaptic terminals, which then spreads by diffusion. The glutamate could act as an excitotoxin and be a pathogenic factor in the local injured brain region. Transient ischemia of 3.5 min duration was used in the gerbil as a pretreatment to obtain hippocampal CA1 in which most of postsynaptic neurons were eliminated but numerous presynaptic terminals remained normal. At 10-14 days after the pretreatment, brain microdialysis experiments were performed in vivo in the CA1 to measure the levels of extracellular glutamate induced by 5 min ischemia. Prior to 5 min ischemia the basal concentration of glutamate in the CA1 was the same as that observed in gerbils that had been subjected to sham pretreatment. During 5 min ischemia, no significant increase in glutamate was induced in the CA1 which showed selective neuronal death. However, a massive increase in glutamate was induced in the CA1 of the sham-pretreated gerbils. These results suggest that the remaining presynaptic terminals are unlikely to play a pathogenic role in the CA1 after selective neuronal death has occurred.

Animals↗

PubMed1997

Delayed localization of synelfin (synuclein, NACP) to presynaptic terminals in cultured rat hippocampal neurons.

Synelfin is a presynaptic protein of unknown function that is differentially regulated in the avian song control circuit during the critical period for song learning; in humans, it gives rise to an amyloidogenic peptide found in senile plaques of Alzheimer's disease. To gain insight into the potential involvement of synelfin in synapse development, we investigated its expression in neurons cultured from the embryonic rat hippocampus. These neurons express a variety of defined synaptic proteins, and form numerous synaptic connections after several days in culture. Synapsin I, a synaptic vesicle-associated protein, was detected within one day after the neurons were put in culture, but significant immunoreactivity for synelfin was not detected until approximately 5 days in vitro (DIV). By 3 DIV, synapsin-positive puncta (previously shown to correspond to presynaptic specializations) were detected surrounding the soma and proximal dendritic processes, whereas comparable aggregations of synelfin did not appear until several days later. By 14 DIV the punctate concentrations of synelfin and synapsin overlapped completely. Thus synelfin is expressed in these cultured neurons and eventually becomes localized to presynaptic terminals, but it is absent from these specializations when they first form. We conclude that presynaptic terminals can change in molecular composition, and that synelfin is associated with later stages in synaptic development or modulation.

Amyloid↗

PubMed1991

Transitional elements with characteristics of both growth cones and presynaptic terminals observed in cell cultures of cerebellar neurons.

As growth cones interact with targets, they become presynaptic terminals by losing growth cone characteristics and acquiring presynaptic characteristics. Results presented here show that transitional elements can be identified in cell cultures of rat cerebellum, which have some characteristics of both growth cones and presynaptic terminals. During the first week in culture, slender growth cones have fine filopodia. Subsequently, many growth cones in contact with the polylysine substrate spontaneously enlarge and become non-motile. In transitional elements, the synaptic vesicle protein p65 extends into the peripheral domain and in some cases, extends into filopodia. Many of these transitional elements have active filopodia but show no movement over the substrate for periods of up to nine days. These transitional elements have lost the actin-rich peripheral domain of the growth cone but retain actin labelling in the filopodia. With electron microscopy, transitional elements were seen to contain accumulations of synaptic vesicles at the site of contact with the substrate. Electron microscopic immunocytochemistry showed these synaptic vesicles labelled for p65 with silver-developed gold particles. Thus, transitional elements have characteristics of both growth cones and presynaptic terminals, suggesting that they may also have functional attributes of both growth cones and presynaptic elements.

Actins↗

PubMed1987

Biogenesis of presynaptic terminal proteins.

The delivery of proteins to the presynaptic terminals of guinea pig retinal ganglion cells by two of the major components of axonal transport, and the subsequent persistence and turnover of those proteins were examined in this study. Ganglion cell proteins were radiolabeled by intravitreal injection of radiolabeled amino acids and radioactive axonally transported proteins were analyzed in synaptosomes prepared from the superior colliculi. This procedure allowed examination of presynaptic components of ganglion cell synapses without having to compensate for postsynaptic or other unidentified contaminants. Each of the two major axonal transport components supplies a large number of proteins to the presynaptic terminal, in relative quantities similar although not identical to those seen in the axon. Proteins conveyed by the fast component of axonal transport reached the terminals by 3 h after intraocular injection, peaked by 24 h, and were largely undetectable by 15 days. Slow component b proteins reached the terminals by 12 days, peaked around 21 days, and persisted up to 63 days in the terminals. Proteins in both components demonstrated differential turnover relative to cotransported proteins once they reached the terminals. Differential turnover may account for change in relative concentration of a particular protein required to meet new functional demands on that protein once it enters the terminal.

Animals↗

PubMed1991

Calcium-activated potassium conductance in presynaptic terminals at the crayfish neuromuscular junction.

Membrane potential changes that typically evoke transmitter release were studied by recording intracellularly from the excitor axon near presynaptic terminals of the crayfish opener neuromuscular junction. Depolarization of the presynaptic terminal with intracellular current pulses activated a conductance that caused a decrease in depolarization during the constant current pulse. This conductance was identified as a calcium-activated potassium conductance, gK(Ca), by its disappearance in a zero-calcium/EGTA medium and its block by cadmium, barium, tetraethylammonium ions, and charybdotoxin. In addition to gK(Ca), a delayed rectifier potassium conductance (gK) is present in or near the presynaptic terminal. Both these potassium conductances are involved in the repolarization of the membrane during a presynaptic action potential.

Action Potentials↗

PubMed1991

Selective fura-2 loading of presynaptic terminals and nerve cell processes by local perfusion in mammalian brain slice.

We describe a method for filling presynaptic terminals and cell dendrites in adult brain slices with the fluorescent calcium indicator fura-2 by localized perfusion of the acetoxymethyl (AM) ester derivative. The method provides labeling selectivity, similar to that produced by intracellular microinjection of fura-2, with the simplicity of bath application of membrane-permeant AM esters. Application of the method to mossy fiber tracts in hippocampal region CA3 and parallel fiber tracts in cerebellum resulted in distant presynaptic terminals well labelled with fura-2 without concomitant postsynaptic labelling, allowing optical measurements of calcium concentration in individual presynaptic terminals. Application of the method to CA1 pyramidal cells produced intracellular loading of apical dendrites with fura-2. Dendritic calcium changes produced by afferent fiber stimulation were similar to those determined from cells filled with fura-2 by intracellular microinjection. The method appears to be general, and should provide a means to fill projecting axons and dendritic processes in many areas of the brain with fluorescent indicators, allowing optical measurements of ion concentration dynamics to be performed in brain slice that were previously impractical.

Animals↗

PubMed1994

Omega-conotoxin-sensitive and -resistant transmitter release from the chick ciliary presynaptic terminal.

1. Synaptically evoked responses to stimulation of the oculomotor nerve were recorded from the ciliary nerve in chick embryos. The postsynaptic currents in response to presynaptic stimulation (EPSCs) were also recorded under whole-cell voltage clamp of the ciliary cell. 2. The ciliary nerve response was dependent on the extracellular Ca2+ concentration ([Ca2+]o). omega-Conotoxin GVIA (omega-CgTX, 100 nM) increased the [Ca2+]o necessary to evoke the half-maximal response by a factor of 1.7 without changing the slope of [Ca2+]o dependence. Dihydropyridine (DHP) derivatives, nifedipine or Bay K 8644, did not affect the [Ca2+]o sensitivity of ciliary nerve response. 3. The EPSC was usually preceded by the capacitive coupling response of the presynaptic action potential. In some records, the EPSCs were also preceded by the electrical coupling responses which were the mirror images of the presynaptic action potentials. The current-voltage relation of the EPSCs showed inward rectification. 4. The EPSC was potentiated by 4-aminopyridine (4-AP) as a result of prolongation of the falling phase of presynaptic action potential. In the presence of high [Ca2+]o and 4-AP, a small fraction of EPSC was resistant to omega-CgTX. 5. The resting potential of the presynaptic terminal was changed from -69 to -57 mV by increasing [K+]o from 1 to 10 mM. The same procedure decreased the omega-CgTX-resistant EPSC by 30%, whereas the omega-CgTX-untreated EPSC in low-Ca2+ saline was not affected by the change in [K+]o. 6. The nerve-evoked increase in intracellular Ca2+ was recorded from the presynaptic terminal (delta[Ca2+]pre). The delta[Ca2+]pre was larger in a solution containing 10 mM Ca2+ and 1 mM K+ after treating with omega-CgTX than in a solution containing 2 mM Ca2+ and 16 mM Mg2+ before treating with omega-CgTX. The EPSC was, in contrast, smaller in the 10 mM Ca(2+)-1 mM K+ solution after omega-CgTX treatment than in the 2 mM Ca(2+)-16 mM Mg2+ solution before omega-CgTX treatment. 7. Similarly, the EPSC was smaller in the 10 mM Ca(2+)-1 mM K+ solution containing 5 microM La3+ than in the 2 mM Ca(2+)-16 mM Mg2+ solution, whereas the delta [Ca2+]pre was larger in the 10 mM Ca(2+)-1 mM K+ solution containing 5 micrograms La3+ than in the 2 mM Ca(2+)-16 mM Mg2+ solution. 8. It is concluded that the omega-CgTX-sensitive Ca2+ conductance of the presynaptic terminal is the principal source of Ca2+ involved in transmitter release.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

High-resolution measurement of the time course of calcium-concentration microdomains at squid presynaptic terminals.

Transmitter release is considered to be a secretory event triggered by localized calcium influx which, by binding to a low-affinity Ca2+ site at the presynaptic active zone, initiates vesicular exocytosis (1-7). In previous experiments with aequorin-loaded presynaptic terminals we visualized, upon tetanic presynaptic stimulation, small points of light produced by calcium concentration microdomains of about 300 microM (5). These microdomains had a diameter of about 0.5 microns (5) and covered 5-10% of the total presynaptic membrane with an average density of 8.4 microns2 per 100 microns2, corresponding closely to the size and distribution of the active zones in that junction (6, 7). To understand in more detail the nature of these concentration microdomains, we obtained rapid video images (400/s) after injecting the photoprotein n-aequorin-J into the presynaptic terminals of squid giant synapses. Using that experimental approach, we determined that microdomains evoked by presynaptic spike activation had a duration of about 800 microseconds. Spontaneous quantum emission domains (QEDs) observed at about the same locations as the microdomains were smaller in amplitude, shorter in duration, and less frequent. These results illustrate the time course of the calcium concentration profiles responsible for transmitter release. Their extremely short duration compares closely with that of calcium current flow during a presynaptic action potential and indicates that, as theorized in the past (6-8), intracellular calcium concentration at the active zone remains high only for the duration of transmembrane calcium flow.

Action Potentials↗

PubMed1994

Direct patch recording from identified presynaptic terminals mediating glutamatergic EPSCs in the rat CNS, in vitro.

1. An in vitro brainstem slice preparation of the superior olivary complex has been developed permitting patch recording from a presynaptic terminal (calyx of Held) and from its postsynaptic target--the principal neurone of the medial nucleus of the trapezoid body (MNTB). 2. The fluorescent stain DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate) was used in fixed tissue and Lucifer Yellow in living slices, to identify calices enclosing single MNTB neuronal somata. 3. Whole-cell recording from the MNTB neurone shows evoked EPSCs preceded by a prespike, corresponding to the presynaptic action potential (AP). In some cases one patch pipette recorded from both pre- and postsynaptic elements, but confirmation of exclusively presynaptic recording was obtained using pipettes containing Lucifer Yellow in a further eleven cases. 4. Under current clamp, the pre- and postsynaptic sites could be distinguished by their response to step depolarizations; presynaptic terminals generated a train of APs at frequencies up to 200 Hz, while MNTB neurones gave a single AP. Each presynaptic AP had an after-hyperpolarization lasting less than 2 ms. 5. Under voltage clamp, step depolarizations of presynaptic terminals generated a tetrodotoxin-sensitive inward current followed by rapidly activating outward potassium currents at potentials more positive than -60 mV. The outward current exhibited little inactivation over the 150 ms steps and 4-aminopyridine (200 microM) blocked 63.0 +/- 14.5% (mean +/- S.D., n = 3) of the sustained current at 0 mV. Like the squid giant synapse, mammalian terminals express rapidly activating 'delayed rectifier'-type potassium currents.

Action Potentials↗

PubMed1996

Remodeling of the peripheral processes and presynaptic terminals of leg motoneurons during metamorphosis of the hawkmoth, Manduca sexta.

During metamorphosis of the hawkmoth, Manduca sexta, the muscles, cuticular structures, and most sensory neurons of the larval thoracic legs are replaced by new elements in the adult legs. The thoracic leg motoneurons, however, survive the loss of the larval muscles and persist to innervate new targets in the imaginal legs. Here we have used biocytin staining, immunocytochemistry, and confocal microscopy to follow the fates of the peripheral processes and presynaptic terminals of the leg motoneurons. Although the most distal processes of the motor nerves retract following the degeneration of larval leg muscles, the axon terminals always retain close association with the muscle remnants and the anlagen of the new adult muscles. As the imaginal muscles differentiate and enlarge, the motor terminals expand to form adult presynaptic terminals. An antibody to the presynaptic protein, synaptotagmin, revealed its localization to the terminal varicosities in both larval and adult stages but distribution within pre-terminal branches during adult development. Electrophysiological methods revealed that functional neuromuscular transmission first occurs quite early during metamorphosis, before the differentiation of contractile elements in the muscle fibers.

Animals↗

PubMed1985

Protein kinase C activation leading to protein F1 phosphorylation may regulate synaptic plasticity by presynaptic terminal growth.

It has recently been proposed by the author that protein kinase C regulates the expression of synaptic plasticity. In the present review it is suggested that this regulation involves a growth of presynaptic terminals. This proposal was based on the discovery that one of the substrates of protein kinase C, protein F1 (molecular mass = 47 kDa, pI = 4.5) is increased in its phosphorylation 5 min, 1 hr, and 3 days following long-term potentiation (LTP) in the intact hippocampal formation. No other phosphoprotein studied was altered by LTP. The amplitude or persistence of synaptic plasticity was directly related to the extent of protein F1 phosphorylation. As a critical control, it was shown that protein F1 was unaltered following synaptic activation that did not alter synaptic strength. Protein F1 in the hippocampus was also altered in its phosphorylation after an experience involving memory of a spatial environment. Phosphorylation F1 may thus participate in both neurophysiological and behavioral events that evoke plasticity. The identification of the F1 substrate has recently been sought. The physical characteristics of protein F1 (mol wt., isoelectric point) indicate that it is the same as the B-50 protein and the growth protein, GAP-43. Protein F1 is then a brain-specific, synaptically enriched phosphoprotein. Recent evidence indicates that protein F1 is present in high concentration in growth cones of late embryonic rat brain in which postsynaptic specializations are not detected, suggesting a presynaptic locus. With respect to the identity of the F1 kinase, we have shown that protein F1, like B-50, is a substrate for protein kinase C, a Ca2+/phospholipid-dependent kinase. Activation of this enzyme by tumor-promoting phorbol esters can trigger cell growth and neurite extension. Recent evidence indicates a presynaptic localization of the enzyme. On the basis of the colocalization of enzyme and substrate in the presynaptic terminal it is proposed that protein kinase C control of the phosphorylation state of protein F1 may regulate the expression of synaptic plasticity via presynaptic terminal growth.

Animals↗

PubMed1992

Microdomains of high calcium concentration in a presynaptic terminal.

Increases in intracellular calcium concentration are required for the release of neurotransmitter from presynaptic terminals in all neurons. However, the mechanism by which calcium exerts its effect is not known. A low-sensitivity calcium-dependent photoprotein (n-aequorin-J) was injected into the presynaptic terminal of the giant squid synapse to selectively detect high calcium concentration microdomains. During transmitter release, light emission occurred at specific points or quantum emission domains that remained in the same place during protracted stimulation. Intracellular calcium concentration microdomains on the order of 200 to 300 micromolar occur against the cytoplasmic surface of the plasmalemma during transmitter secretion, supporting the view that the synaptic vesicular fusion responsible for transmitter release is triggered by the activation of a low-affinity calcium-binding site at the active zone.

Aequorin↗

PubMed1990

Chronic maintenance of presynaptic terminals in gliotic hippocampus following ischemia.

Following brief cerebral ischemia, neurons are selectively damaged and die, whereas glial cells and blood vessels survive. This phenomenon of selective vulnerability is well illustrated in the hippocampal CA1 region. Five min of forebrain ischemia in the Mongolian gerbil produced selective neuronal necrosis in the hippocampal CA1 sector. After destruction and loss of CA1 neurons, a remarkable glial reaction (gliosis) was seen. The thickness of the CA1 subfield remained unchanged until 1 month after ischemia and then gradually shrank over several months. Ultrastructural observation of this region revealed persistent maintenance of presynaptic structures. Numerous presynaptic terminals containing synaptic vesicles were scattered throughout the gliotic scar tissue. These presynaptic terminals were apposed to degenerative structures which seemed most likely to be remnants of dendrites. In another group of animals, at one month following ischemic damage in the CA1 sector, the CA3 neurons were destroyed by kainic acid injection. In these animals, numerous degenerating presynaptic boutons were seen in the CA1 sector when fixed 4 days following kainate injection. These results indicate that even in gliotic tissue, presynaptic terminals can survive and maintain their structural characteristics although neuronal cell bodies are almost absent.

Animals↗

PubMed1990

Alzheimer patients and Down patients: abnormal presynaptic terminals are related to cerebral preamyloid deposits.

In Alzheimer's disease, in Down syndrome and in normal aging, scattered deposits of amyloid fibril precursors occur in both cerebral cortex and subcortical grey structures. Within such preamyloid deposits, no degenerating neurites with paired helical filaments have ever been observed. This study, carried out on brains from Alzheimer patients and Down patients, reports on the relationship between preamyloid deposits and neuritic changes. These changes were represented by presynaptic terminal swellings immunolabeled by antisynaptophysin and antiubiquitin antibodies, not by Alz50. These findings support the view that the deposition of amyloid fibril precursors in the neuropil is closely related to presynaptic terminals, although whether the former precedes or follows the development of presynaptic terminal changes is still undetermined.

Adult↗