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PubMed1975

Discrete and discontinuous action of brown widow spider venom on the presynaptic nerve terminals of frog muscle.

1. A study was made of the effects of the venom of the brown widow spider (Latrodectus geometricus) on end-plates of the frog sartorius muscle. 2. The increase in the frequency of the minature end-plate potentials (m.e.p.p.s), elicited by the venom in normal-"Ca2+" Ringer solution, occurs in discrete volleys having a sharp onset and end. The frequency of the m.e.p.p.s is high (up to 300 sec-1) and relatively constant during the volley. 3. The volleys recur at intervals during a period from 5 to 10 min after addition of the venom until the onset of electrical silence, up to 4 hr later. The activity occurs in groups containing volleys of loing and short duration. 4. Simultaneous intracellular and extracellular recording from single end-plates indicates that the volleys originate at highly localized areas of the nerve terminals. The high-frequency release of m.e.p.p.s in hypertonic sol solutions, which was studied for comparison purposes, occurs randomly over the entire end-plate. Volleys originating simultaneously at different sites are often superimposed in the intracellular recordings. 5. In high-"Ca2+" Ringer solution, the initial frequency of the m.e.p.p.s in a volley is comparatively higher. However, the frequency drops to one half its value in a few seconds. The volley then terminates or else the frequency of m.e.p.p.s remains high for some time and the volley has no sharp end. Activity occurs in groups containing both long and short volleys. Many more short (less than 5 sec) and long (greater than 30 sec) volleys occur in high-"Ca2+" solution than in normal-"Ca2+" solutions. 6. In low-"Ca2+", high-"Mg2+" Ringer solution, the volleys of m.e.p.p.s are fewer in number and much longer in duration. Intra- and extra-cellular recording of uninterruped activity during long periods suggests that in this solution the m.e.p.p.s originate diffusely rather than at discrete areas of the nerve terminals. 7. Implications of the above data on possible modes of action of the venom are discussed.

Animals↗
PubMed1985

The early time course of potassium-stimulated calcium uptake in presynaptic nerve terminals isolated from rat brain.

K-stimulated (voltage-dependent) 45Ca uptake in rat brain synaptosomes was measured at times ranging from 0.1 to 10 s, in experiments that employed a rapid-mixing device to initiate and terminate radiotracer uptake. The rapid mixing did not disrupt the functional integrity of the synaptosomes, as judged by their ability to take up Ca. In solutions containing a low (0.02 mM) concentration of Ca, the rate of K-stimulated Ca uptake measured after 0-0.12 s depolarization was 8 times greater than that measured after 5-10 s of depolarization. The decline in rate of K-stimulated Ca uptake was not due to tracer backflux from the synaptosomes, nor to Ca loading of the nerve terminals, since it also occurred after synaptosomes were depolarized in solutions without Ca. It is suggested that this decline in rate of Ca uptake after depolarization was due to inactivation of voltage-dependent Ca channels in the nerve terminals. This inactivation appeared to be voltage rather than Ca dependent. The extent to which K-stimulated Ca uptake declined after depolarization in high-K solution depended on the K concentration that was used to depolarize the synaptosomes. Whereas pre-incubation in solution with one-half of the Na replaced by K significantly reduced subsequent K-stimulated Ca uptake, pre-incubation in non-depolarizing solution, with one-half of the Na replaced by choline, had no significant effect on subsequent K-stimulated Ca uptake. In solutions containing a high (0.5-2 mM) concentration of Ca, the rate of K-stimulated Ca uptake measured after 0-0.12 s was 40 times greater than that measured after 5-10 s. High Ca accelerated the rate at which K-stimulated Ca uptake declined with prolonged depolarization. The effect was mimicked by high (10 mM) concentrations of Sr, but not of Ba. The accelerated rate of decline observed with high Ca could be either a direct effect of Ca on the Ca channels or, more probably, an indirect effect of Ca loading on the nerve terminals. The apparent efficacy of several Ca-channel blockers (Ni, La and verapamil) in reducing K-stimulated Ca uptake was enhanced when the synaptosomes were depolarized in the presence of inhibitory agents for brief (less than 1 s) intervals before K-stimulated Ca uptake was measured.

Animals↗
PubMed1996

Hikaru genki protein is secreted into synaptic clefts from an early stage of synapse formation in Drosophila.

The development of neural circuits is regulated by a large number of factors that are localized at distinct neural sites. We report here the localization of one of these factors, hikaru genki (hig) protein, at synaptic clefts in the pupal and adult nervous systems of Drosophila. In hig mutants, unusually frequent bursting activity of the muscles and abnormal motor behavior during the adult stage suggest the misfunction of neuromuscular circuitry. Our immunohistochemical analyses revealed that hig protein, produced by neurons, is secreted from the presynaptic terminals into the spaces between the presynaptic and postsynaptic terminals. In addition, we have found that the localization of this protein in the synaptic spaces temporally correlates with its functional requirement during a critical period that occurs in the middle stage of pupal formation, a period when a number of dendrite and axon growth cones meet to form synapses. These findings indicate that hig protein functions in the formation of functional neural circuits from the early stages of synapse formation.

Aging↗
PubMed1988

Synuclein: a neuron-specific protein localized to the nucleus and presynaptic nerve terminal.

We used an antiserum against purified cholinergic synaptic vesicles from Torpedo and expression screening to isolate a cDNA clone encoding synuclein, a 143 amino acid neuron-specific protein. A cDNA clone was also isolated from a rat brain cDNA library that encodes a highly homologous 140 amino acid protein. The amino terminal 100 amino acids of both proteins are comprised of an 11 amino acid repeating unit that contains a conserved core of 6 residues. The synuclein gene is expressed only in nervous system tissue, not in electric organ, muscle, liver, spleen, heart, or kidney. In the electric organ synapse Torpedo synuclein-immunoreactive proteins are found in 3 major molecular-weight classes of 17.5, 18.5, and 20.0 kDa. In the neuronal cell soma the 17.5 kDa species is predominant and immunoreactivity is localized to a portion of the nuclear envelope.

Amino Acid Sequence↗
PubMed1983

Quantitative features of synapse formation in the fly's visual system. I. The presynaptic photoreceptor terminal.

Photoreceptors of the adult fly's compound eye each form a population of stereotyped output synapses distributed over the surface of their terminal. The formation of this class of afferent synapses during development has been followed from serial electron microscopy of the same eye region in four pupal and several adult stages, all of female Musca domestica. These synapses, or tetrads, have an invariant postsynaptic composition of four members and so may provide a model for multiple-contact synapses in general. In the adult fly the four postsynaptic elements of each synapse are contributed by two interneurons, L1 and L2, and, usually, two alpha processes of an amacrine cell. These postsynaptic elements assemble at individual developing synapses by selective sequential addition. Assembly starts with L1 or L2, subsequent elements of the final tetrad adding in all conceivable permutations, at least as fast as one per 7 hr. They rarely (only once) incorporate incorrect or supernumerary elements, however. The synaptic population as a whole was also sampled during development to analyze the possible factors determining the normal precision of the size of the adult population. The number of synapses per terminal increases gradually until 74% pupal development. Thereafter it decreases so that the final number of synapses in each receptor's population is the consequence of a net loss. Synapses enlarge with age, chiefly by incorporating new elements, but the loss of synaptic sites is only partially offset by the increase in size of those that remain. Throughout all stages examined in pupal and adult life, total synaptic area is linearly proportional to the surface area of the axon terminal. Thus, from the 74% pupal development stage onward, a population of many small synapses closely spaced, on average, over the terminal's surface transforms into one characteristic of the adult with progressively fewer, larger, more widely spaced synapses.

Animals↗
PubMed1980

Experimental degeneration of motor and sensory cortical terminals in the cuneate nucleus of the monkey (Macaca fascicularis).

A total of nine monkeys (Macaca fascicularis) of both sexes was used for the present study. Eight monkeys were used for either motor or sensory cortical lesions, and were allowed to survive for 1--7 days post-operatively. No degenerating nerve terminals were observed 1 day following either motor or sensory cortical lesions. After a motor cortical lesion, most degenerating terminals were seen on the third and only a few on the fifth day. Following a sensory cortical lesion, most degenerating terminals were seen on the fifth and fewer on the third and seventh days. Two types of degenerative changes were observed: granular and electron-dense. Granular change was more evident after the shorter survival periods, while the electron-dense type of degeneration was more commonly seen in animals which were allowed to survive longer after operation. The cortical axon terminals were small and contained either round or flattened synaptic vesicles. Most of those axons containing flattened vesicles originated from the sensory cortex, but a few came from the motor cortex. Vice versa, most of those axons containing round vesicles appeared to arise from the motor cortex and only a few from the sensory cortex. Cortical axon terminals containing round synaptic vesicles formed asymmetrical synapses with small to medium-sized dendrites poor in organelles. In a few instances such cortical terminals were observed to be postsynaptic to other axon terminals containing flattened vesicles. No cortical axon terminal was observed to terminate presynaptically on another axon terminal. Cortical terminals containing flattened vesicles formed symmetrical synapses with dendritic profiles of varying diameters, some of which were the proximal dendrites of Group II neurons. No cortical axon terminals containing flattened vesicles have been observed to form axo-axonal synapses in the cuneate neuropil.

Animals↗
PubMed2000

How do presynaptic PLA2 neurotoxins block nerve terminals?

Snake presynaptic neurotoxins with phospholipase A2 activity block nerve terminals in an unknown way. Here, we propose that they enter the lumen of synaptic vesicles following endocytosis and hydrolyse phospholipids of the inner leaflet of the membrane. The transmembrane pH gradient drives the translocation of fatty acids to the cytosolic monolayer, leaving lysophospholipids on the lumenal layer. Such vesicles are highly fusogenic and release neurotransmitter upon fusion with the presynaptic membrane, but cannot be retrieved because of the high local concentration of fatty acids and lysophospholipids, which prevents vesicle neck closure.

Elapid Venoms↗
PubMedDate not supplied

Ultrastructural study of neurotensin immunoreactivity in the superficial laminae of the dorsal horn of the rat.

Neurotensin immunoreactivity was identified in cell bodies, dendrites, spines, axons, terminals and varicosities in superficial laminae of rat spinal cord with the electron microscope. Unlabeled terminals synapsed with neurotensin-immunoreactive cell bodies, dendrites and spines. Presynaptic terminals contained round or pleomorphic vesicles and generally made symmetrical contacts with medium-sized neurotensin-containing dendrites in outer lamina II, and asymmetrical or symmetrical contacts with large and small dendrites and spines in inner lamina II. Neurotensin immunoreactive axons were unmyelinated, and their terminals were presynaptic to unlabeled dendrites and spines in laminae I and II. Terminals contained small, round, clear vesicles (31 nm) and occasional large granular vesicles (78 nm). Contacts in outer lamina II were evenly distributed among dendrites of various sizes and spines, whereas the majority of labeled terminals in inner lamina II made contacts onto small dendrites and spines. These findings indicate that neurotensin effects in rat spinal cord are mediated by axodendritic synapses, and that neurotensin cells at the inner and outer borders of lamina II contact dendrites of efferent neurons or other interneurons in the dorsal horn.

Animals↗
PubMed2000

The role of brain-derived neurotrophic factor receptors in the mature hippocampus: modulation of long-term potentiation through a presynaptic mechanism involving TrkB.

The neurotrophin BDNF has been shown to modulate long-term potentiation (LTP) at Schaffer collateral-CA1 hippocampal synapses. Mutants in the BDNF receptor gene trkB and antibodies to its second receptor p75NTR have been used to determine the receptors and cells involved in this response. Inhibition of p75NTR does not detectably reduce LTP or affect presynaptic function, but analyses of newly generated trkB mutants implicate TrkB. One mutant has reduced expression in a normal pattern of TrkB throughout the brain. The second mutant was created by cre-loxP-mediated removal of TrkB in CA1 pyramidal neurons of this mouse. Neither mutant detectably impacts survival or morphology of hippocampal neurons. TrkB reduction, however, affects presynaptic function and reduces the ability of tetanic stimulation to induce LTP. Postsynaptic glutamate receptors are not affected by TrkB reduction, indicating that BDNF does not modulate plasticity through postsynaptic TrkB. Consistent with this, elimination of TrkB in postsynaptic neurons does not affect LTP. Moreover, normal LTP is generated in the mutant with reduced TrkB by a depolarization-low-frequency stimulation pairing protocol that puts minimal demands on presynaptic terminal function. Thus, BDNF appears to act through TrkB presynaptically, but not postsynaptically, to modulate LTP.

Animals↗
PubMed1995

Synaptogenesis and distribution of presynaptic axonal varicosities in low density primary cultures of neocortex: an immunocytochemical study utilizing synaptic vesicle-specific antibodies, and an electrophysiological examination utilizing whole cell recording.

Low-density primary cultures of neocortical neurons were utilized to examine: (i) early interactions of growing neurites with morphological characteristics of axons with other neuronal elements, and (ii) the distribution of presynaptic axonal varicosities closely apposed to MAP-2 immunoreactive, putatively postsynaptic, dendrites. At the light microscopical level axonal varicosities, presumably presynaptic terminals, were identified using immunocytochemistry incorporating antibodies specific for the synaptic vesicle antigens synaptophysin and synapsin. The presence of synaptophysin- and synapsin-immunoreactive swellings along axonal processes was first detected at 5 days post-plating and was also apparent in axons growing in isolation. At 5-7 days in vitro, immunolabelled axonal varicosities in close apposition to putative postsynaptic dendrites (MAP-2 immunoreactive) dendrites were detected. Electrophysiologically active synaptic contacts can also readily be detected at this stage. After 3 weeks in vitro presynaptic contacts do appear to be distributed heterogeneously along postsynaptic dendrites of many neurons in culture. As the culture matures a higher number of presynaptic profiles can be seen along dendrites, with a centrifugal distribution, e.g. a higher density of presynaptic axonal terminals in close apposition to more distal regions of larger dendrites, putatively considered to be apical dendrites of pyramidal-like neurons. In our cultures, the overall increase in the density and the pattern of distribution of presynaptic axon terminals immunoreactive for synaptic vesicle antigens closely apposed to putative post-synaptic structures mimics the general postnatal increase of synaptic density in the neocortex in vivo. Thus, low density primary cultures of neocortical neurons offer a valuable system to explore and manipulate (i) the molecular and cellular basis of neocortical synaptogenesis, and (ii) the pharmacology of neocortical synaptic transmission.

Animals↗
PubMed2000

Expression of presynaptic proteins is closely correlated with the chronotopic pattern of axons in the retinotectal system of the chick.

Newly synthesized presynaptic integral membrane proteins in neurons are transported in precursor vesicles from the site of protein biosynthesis in the cell body by fast axonal flow to the presynaptic terminal. We followed the path that presynaptic proteins travel on the way to their central targets of the highly ordered primary visual pathway of the chick and analyzed the developmental changes in the expression of synaptic vesicle protein 2 (SV2), synaptotagmin, and syntaxin. Immunofluorescences revealed that: (1) the onset of protein expression in the retinal ganglion cells occurs in a central to peripheral developmental pattern from embryonic day 4 (E4) onward; (2) the proteins were found first in the inner and later in the outer plexiform layer of the retina; and (3) they were redistributed from the photoreceptor inner segments and cell bodies to the terminals in the outer plexiform layer. From E4 onward, immunopositive axons for SV2, synaptotagmin, and syntaxin were found in the optic nerve, disappearing after E9 for SV2 and synaptotagmin. The optic tract was stained for SV2 and synaptotagmin between E7 and E12, for syntaxin until the posthatching period. Finally, immunoreactivities for the investigated proteins were present at the surface of the tectum from E8 onward, when first retinal axons arrived there. The present study revealed that SV2 and synaptotagmin, but not syntaxin, are, expressed in a transient wave that follows the advancement of optic axons and the proteins towards the optic tectum.

Animals↗
PubMed2002

The requirement of presynaptic metabotropic glutamate receptors for the maintenance of locomotion.

Spinal circuits known as central pattern generators maintain vertebrate locomotion. In the lamprey, the contralaterally alternating ventral root activity that defines this behavior is driven by ipsilateral glutamatergic excitation (Buchanan and Grillner, 1987) coupled with crossed glycinergic inhibition (Buchanan, 1982; Alford and Williams, 1989). These mechanisms are distributed throughout the spinal cord. Glutamatergic excitatory synapses activate AMPA and NMDA receptors known to be necessary for the maintenance of the locomotor rhythm. Less is known of the role and location of metabotropic glutamate receptors (mGluRs), although group I mGluRs enhance transmitter release at giant synapses in the lamprey spinal cord, whereas group II/III receptors may inhibit release. In this study we show that group I mGluR antagonists block fictive locomotion, a neural correlate of locomotion, by acting at the presynaptic terminal. Under physiological conditions, synaptically released glutamate activates presynaptic group I mGluRs (autoreceptors) during the repetitive activation of glutamatergic terminals. The resulting rise in [Ca2+]i caused by the release from presynaptic intracellular stores is coincident with an enhancement of synaptic transmission. Thus, blocking mGluRs reduces glutamate release during the repetitive activity that is characteristic of locomotion, leading to the arrest of locomotor activity. We found the effects of group I mGluRs on locomotion to be inconsistent with a postsynaptic effect on the central pattern generator. Consequently, the activation of metabotropic glutamate autoreceptors is necessary to maintain rhythmic motor output. Our results demonstrate the role of presynaptic mGluRs in the physiological control of movement for the first time.

Animals↗