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At least 235 records · Page 13Linked to original sources
PubMed1993

Imaging terminals of Aplysia sensory neurons demonstrates role of enhanced Ca2+ influx in presynaptic facilitation.

Modulation of transmitter release underlies several forms of learning-related synaptic plasticity, including presynaptic facilitation and long-term potentiation. Although the presynaptic terminals of most neurons are not accessible for direct study, it has often been possible to correlate changes in calcium influx in the cell body, owing to modulation of K+ or Ca2+ channels, with changes in release. Some forms of presynaptic plasticity, however, do not involve changes in Ca2+ influx. Moreover, the presence of multiple types of K+ and Ca2+ channels with different subcellular distributions makes the direct measurement of Ca2+ influx into presynaptic terminals essential. Using synapses reconstituted in culture between Aplysia sensory and motor neurons, we have imaged Ca2+ influx in presynaptic terminal regions in response to action potentials, and demonstrate that presynaptic facilitation produced by 5-hydroxytryptamine involves enhanced Ca2+ influx through dihydropyridine (DHP)-insensitive Ca2+ channels present near release sites. This increased influx is attributable to spike broadening and is significantly correlated with the magnitude of presynaptic facilitation. By contrast, DHP-sensitive channels appear to aid the recovery from depression due to high-frequency stimulation.

Action Potentials↗
PubMed1998

Active sleep-related depolarization of feline trigemino-thalamic afferent terminals.

Presynaptic depolarization of trigemino-thalamic (TGT) terminals may contribute to modulation of ascending oro-facial somatosensory information during active (or rapid eye movement) sleep. The relative excitability of TGT terminals was inferred from changes in the current required to maintain an antidromic firing probability of 50% (EC50) during quiet wakefulness as compared to active sleep. Depolarization or hyperpolarization of TGT terminals was defined as a decrease or increase, respectively, in the EC50. Overall, the EC50 of 8 TGT terminals was reduced by a mean 8.8+/-3.6 microA during active sleep relative to quiet wakefulness. This result suggests that depolarization of TGT terminals, which may act to suppress the transfer of sensory information from the trigeminal nucleus to the thalamus, occurs during active sleep.

Action Potentials↗
PubMed2001

Local synthesis of nuclear-encoded mitochondrial proteins in the presynaptic nerve terminal.

One of the central tenets in neuroscience has been that the protein constituents of distal compartments of the neuron (e.g., the axon and nerve terminal) are synthesized in the nerve cell body and are subsequently transported to their ultimate sites of function. In contrast to this postulate, we have established previously that a heterogeneous population of mRNAs and biologically active polyribosomes exist in the giant axon and presynaptic nerve terminals of the photoreceptor neurons in squid. We report that these mRNA populations contain mRNAs for nuclear-encoded mitochondrial proteins to include: cytochrome oxidase subunit 17, propionyl-CoA carboxylase (EC 6.4.1.3), dihydrolipoamide dehydrogenase (EC 1.8.1.4), and coenzyme Q subunit 7. The mRNA for heat shock protein 70, a chaperone protein known to be involved in the import of proteins into mitochondria, has also been identified. Electrophoretic gel analysis of newly synthesized proteins in the synaptosomal fraction isolated from the squid optic lobe revealed that the large presynaptic terminals of the photoreceptor neuron contain a cytoplasmic protein synthetic system. Importantly, a significant amount of the cycloheximide resistant proteins locally synthesized in the terminal becomes associated with mitochondria. PCR analysis of RNA from synaptosomal polysomes establishes that COX17 and CoQ7 mRNAs are being actively translated. Taken together, these findings indicate that proteins required for the maintenance of mitochondrial function are synthesized locally in the presynaptic nerve terminal, and call attention to the intimacy of the relationship between the terminal and its energy generating system. J. Neurosci. Res. 64:447-453, 2001. Published 2001 Wiley-Liss, Inc.

Animals↗
PubMed2000

A method for measuring colocalization of presynaptic markers with anatomically labeled axons using double label immunofluorescence and confocal microscopy.

Information concerning the location and distribution of presynaptic neurotransmitter release sites within anatomically labeled axons would be of value for a large number of studies in functional anatomy, development, and plasticity. Here we report a method for localizing presynaptic sites within identified arbors of interest using anterograde anatomical tracer injections to label axonal projections and synaptic vesicle protein (SVP) antibodies to label presumptive presynaptic terminals. The axons and presynaptic sites are independently visualized with double label immunofluorescence and confocal microscopy. Stacks of images representing adjacent focal planes are collected, and image processing techniques are applied to identify the location of each axonal branch segment and each cluster of SVP label in three-dimensional space. Segmentation of the SVP label into distinct pixel clusters in three-dimensional space, followed by colocalization of these clusters with the labeled axons (object-based analysis), yields much more reliable and sensitive measures of colocalization than a simple determination of the number (or summed intensities) of colocalized pixels in a single optical section (pixel-based analysis). The method has been extended to measure the colocalization of antigens that are not located at the presynaptic terminal with a labeled population of axons.

Animals↗
PubMed1989

Calcium currents in a vertebrate presynaptic nerve terminal: the chick ciliary ganglion calyx.

Ca currents (ICa) were recorded from presynaptic nerve terminals in the chick ciliary ganglion. Ciliary neurons are innervated by a single nerve terminal that extends over a wide area of the neuron surface to form a 'calyx'. The neurons were dissociated enzymatically with the calyx intact and the patch clamp technique was used in the whole cell mode to record ion currents. A small inward ICa (peak current 20-80 pA) was recorded that was blocked by external Cd. Only one component of ICa was detected. This was recruited at positive membrane potentials, exhibited no evidence of inactivation during a 25-ms depolarizing pulse, and deactivated rapidly. Thus, the ICa recorded in this vertebrate presynaptic nerve terminal was similar to the high-voltage activated, fast deactivating, current reported in other neurons.

Animals↗
PubMed2004

The architecture of the active zone in the presynaptic nerve terminal.

Active zones are highly specialized sites for release of neurotransmitter from presynaptic nerve terminals. The architecture of the active zone is exquisitely designed to facilitate the regulated tethering, docking, and fusing of the synaptic vesicles with the plasma membrane. Here we present our view of the structural and molecular organization of active zones across species and propose that all active zones are organized according to a common principle in which the structural differences correlate with the kinetics of transmitter release.

Animals↗
PubMed1999

Regulation of transmitter release from retinal bipolar cells.

Mb1 bipolar cells (ON-type cells) of the goldfish retina have exceptionally large (approximately 10 microns in diameter) presynaptic terminals, and thus, are suitable for investigating presynaptic mechanisms for transmitter release. Using enzymatically dissociated Mb1 bipolar cells under whole-cell voltage clamp, we measured the Ca2+ current (ICa), the intracellular free Ca2+ concentration ([Ca2+]i), and membrane capacitance changes associated with exocytosis and endocytosis. Release of transmitter (glutamate) was monitored electrophysiologically by a glutamate receptor-rich neuron as a probe. L-type Ca2+ channels were localized at the presynaptic terminals. The presynaptic [Ca2+]i was strongly regulated by cytoplasmic Ca2+ buffers, the Na(+)-Ca2+ exchanger and the Ca2+ pump in the plasma membrane. Once ICa was activated, a steep Ca2+ gradient was created around Ca2+ channels; [Ca2+]i increased to approximately 100 microM at the fusion sites of synaptic vesicles whereas up to approximately 1 microM at the cytoplasm. The short delay (approximately 1 ms) of exocytosis and the lack of prominent asynchronous release after the termination of ICa suggested a low-affinity Ca2+ fusion sensor for exocytosis. Depending on the rate of Ca2+ influx, glutamate was released in a rapid phasic mode as well as a tonic mode. Multiple pools of synaptic vesicles as well as vesicle cycling seemed to support continuous glutamate release. Activation of protein kinase C increased the size of synaptic vesicle pool, resulting in the potentiation of glutamate release. Goldfish Mb1 bipolar cells may still be an important model system for understanding the molecular mechanisms of transmitter release.

Animals↗
PubMed1996

Presynaptic calcium current modulation by a metabotropic glutamate receptor.

Metabotropic glutamate receptors (mGluRs) regulate transmitter release at mammalian central synapses. However, because of the difficulty of recording from mammalian presynaptic terminals, the mechanism underlying mGluR-mediated presynaptic inhibition is not known. Here, simultaneous recordings from a giant presynaptic terminal, the calyx of Held, and its postsynaptic target in the medial nucleus of the trapezoid body were obtained in rat brainstem slices. Agonists of mGluRs suppressed a high voltage-activated P/Q-type calcium conductance in the presynaptic terminal, thereby inhibiting transmitter release at this glutamatergic synapse. Because several forms of presynaptic modulation and plasticity are mediated by mGluRs, this identification of a target ion channel is a first step toward elucidation of their molecular mechanism.

Aminobutyrates↗
PubMed1994

Origin of ischemia-induced glutamate efflux in the CA1 field of the gerbil hippocampus: an in vivo brain microdialysis study.

In vivo brain microdialysis experiments were performed in the gerbil to evaluate the origin of accumulation of extracellular glutamate under transient ischemia. Microdialysis probes were positioned in the CA1 field of the hippocampus in which proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals had been induced by 5-min ischemia 10-14 days before the microdialysis experiment; in the white matter of the cerebral cortex, which contained few neurons, few presynaptic terminals, and many astrocytes; or in the histologically normal CA1 field of the hippocampus, and then 5- or 20-min ischemia was induced. When 5-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter of the cerebral cortex, whereas a significant increase in glutamate (15-fold) was observed in the histologically normal CA1 field. When 20-min ischemia was induced, no significant increase in glutamate content was observed in the CA1 field that showed proliferation of astrocytes, death of CA1 pyramidal neurons, and damage of presynaptic terminals and in the white matter during the first 10 min after the onset of 20-min ischemia, but remarkable ischemia-induced increases in glutamate were observed during the last 10 min of 20-min ischemia in both areas. An excessive increase in glutamate (100-fold) was observed during 20-min ischemia in the normal CA1 field of the hippocampus. When a probe was positioned in the CA1 field of the hippocampus in which presynaptic terminals of Schaffer collaterals and commissural fibers had been eliminated by bilateral kainate injections into the lateral ventricles 4-7 days before the microdialysis experiment and then 5-min ischemia was induced, a significant increase in glutamate was observed during the last half of 5-min ischemia. These results suggest that the efflux of glutamate from astrocytes does not contribute to the large ischemia-induced glutamate accumulation in the CA1 field of the hippocampus during 5-min ischemia but contributes to the ischemia-induced increase in glutamate level during ischemia with a longer duration and that ischemia-induced efflux of glutamate in the CA1 field during 5-min ischemia originates mainly from neuronal elements: presynaptic terminals and post-synaptic neurons.

Animals↗
PubMed2005

Transgenic mouse lines expressing synaptopHluorin in hippocampus and cerebellar cortex.

We generated six transgenic mouse lines in which synaptopHluorin (SpH), one of green fluorescent protein-based sensors of vesicular exocytosis, was expressed under the control of neuron-specific Thy-1.2 promoter. In situ hybridization study revealed that SpH mRNA was expressed in a broad spectrum of brain regions in four of them, whereas in others it was expressed in the specific regions of the hippocampus. In one particular line, SpH immunoreactivity was specifically observed in the mossy fiber presynaptic terminals of both hippocampus and cerebellar cortex. The fluorescence intensity of these presynaptic terminals was somewhat decreased by acidic buffer superfusion and greatly increased by vesicular neutralization of pH, indicating that the SpH molecules are mainly distributed in the synaptic vesicles. The exocytosis-dependent fluorescence increment was measured upon activation of a single presynaptic terminal. These transgenic lines are expected to facilitate morphological and physiological studies of presynaptic terminals in a variety of regions of the brain.

Animals↗
PubMed2001

Developmental changes in P2X purinoceptors on glycinergic presynaptic nerve terminals projecting to rat substantia gelatinosa neurones.

1. In mechanically dissociated rat spinal cord substantia gelatinosa (SG) neurones attached with native presynaptic nerve endings, glycinergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded using nystatin perforated patch recording mode under voltage-clamp conditions. Under these conditions, it was tested whether the changes in P2X receptor subtype on the glycinergic presynaptic nerve terminals occur during postnatal development. 2. ATP facilitated glycinergic mIPSC frequency in a concentration-dependent manner through all developmental stages tested, whereas alphabeta-methylene-ATP (alphabeta-me-ATP) was only effective at later developmental stages. 3. alphabeta-me-ATP-elicited mIPSC frequency facilitation was completely occluded in the Ca2+-free external solution, but it was not affected by adding 10(-4) M Cd2+. 4. alphabeta-me-ATP still facilitated mIPSC frequency even in the presence of 10(-6) M thapsigargin, a Ca2+ pump blocker. 5. In later developmental stages, ATP-elicited presynaptic or postsynaptic responses were reversibly blocked by 10(-5) M pyridoxal-5-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS), but only partially blocked by 10(-7) M 2',3'-O-(2,4,6-trinitrophenyl)-ATP (TNP-ATP). However, alphabeta-me-ATP-elicited presynaptic or postsynaptic responses were completely and reversibly blocked by either 10(-5) M PPADS or 10(-7) M TNP-ATP. 6. alphabeta-me-ATP significantly reduced the evoked glycinergic IPSC amplitude in postnatal 28-30 day neurones, whereas it had no effect in 10-12 day neurones. 7. It was concluded that alphabeta-me-ATP-sensitive P2X receptors were functionally expressed on the glycinergic presynaptic nerve terminals projecting to SG neurones in later developmental stages. Such developmental changes of presynaptic P2X receptor subtypes might contribute to synaptic plasticity such as the regulation of neuronal excitability and the fine controlling of the pain signal in spinal dorsal horn neurones.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Spontaneous miniature hyperpolarizations of presynaptic nerve terminals in the chick ciliary ganglion.

Intracellular recordings from presynaptic nerve terminals in the chick ciliary ganglion revealed the presence of spontaneous miniature hyperpolarizations in virtually all (approximately 86%) nerve terminals examined. These spontaneous events appeared as small, brief hyperpolarizations at resting potential and were observed to increase or decrease as the membrane potential was depolarized or hyperpolarized from rest, respectively. The hyperpolarizing potentials were sensitive to blockade by tetraethylammonium and Ba2+, while caffeine increased then abolished these events. The voltage fluctuations were unaffected by tetrodotoxin, low Ca2+ external solution or the synaptic blockers, picrotoxin and strychnine. These spontaneous, transient, miniature hyperpolarizations may be due to the brief and co-ordinated activation of between 15-60 Ca(2+)-dependent K+ channels following the release of Ca2+ from internal stores.

Animals↗
PubMed2005

Neural mechanisms controlling jaw-jerk reflex in the cat.

Signal substances of axon terminals presynaptic to jaw spindle Ia afferents and their ultrastructural features were examined using a combination of intra-axonal horseradish peroxidase injection and postembedding immunogold-labeling techniques in cats. A total of 35 axon terminals presynaptic to 22 horseradish peroxidase-labeled Ia boutons were examined. Of the 35 presynaptic axon terminals, 14 (40%) were immunoreactive for both gamma-aminobutyric acid and glycine, 9 (26%) for gamma-aminobutyric acid alone and 9 (26%) for glycine alone. The bouton volume, mitochondrial volume, active zone area, and apposed surface area were larger for Ia boutons than for presynaptic axon terminals, while each of the values is similar among the three types of presynaptic axon terminals. These results suggest that gamma-aminobutyric acid and glycine play an important role for modulating the jaw-jerk reflex presynaptically and that the smaller size of presynaptic axon terminals is important to prevent action potential generation from Ia afferents.

Analysis of Variance↗
PubMed1989

Ultrastructural immunocytochemical localization of B-50/GAP43, a protein kinase C substrate, in isolated presynaptic nerve terminals and neuronal growth cones.

Accumulating evidence indicates that the neuron-specific B-50/GAP43, a substrate for protein kinase C, plays a role in neuronal differentiation and neuritogenesis during nervous tissue development and axonal regeneration. An ultrastructural immunocytochemical study on the localization of B-50 in presynaptic terminals (synaptosomes) isolated from the frontal cortex of 6-week-old rats, and in neuronal growth cones, isolated from forebrains of 5-day-old rats, the majority of B-50 is detected at the surrounding neuronal plasma membrane. In both neuronal growth cones and synaptosomes, a relatively small fraction of B-50 in the cytoplasm was not evidently associated with internal membranes. Our results indicate that B-50 is mainly located at the cytoplasmic face of the synaptosomal and neuronal growth cone plasma membrane. The similar B-50 localization in neuronal growth cones and synaptosomes suggests that, both in extending axons and mature synaptic terminals, B-50 may exert identical functions as a protein kinase C substrate at the plasma membrane.

Animals↗
PubMed2005

The Niemann-Pick C1 protein in recycling endosomes of presynaptic nerve terminals.

Niemann-Pick type C (NPC) disease is a fatal, neurodegenerative disorder caused in 95% of cases by loss of function of NPC1, a ubiquitous endosomal transmembrane protein. A biochemical hallmark of NPC deficiency is cholesterol accumulation in the endocytic pathway. Although cholesterol trafficking defects are observed in all cell types, neurons are the most vulnerable to NPC1 deficiency, suggesting a specialized function for NPC1 in neurons. We investigated the subcellular localization of NPC1 in neurons to gain insight into the mechanism of action of NPC1 in neuronal metabolism. We show that NPC1 is abundant in axons of sympathetic neurons and is present in recycling endosomes in presynaptic nerve terminals. NPC1 deficiency causes morphological and biochemical changes in the presynaptic nerve terminal. Synaptic vesicles from Npc1(-/-) mice have normal cholesterol content but altered protein composition. We propose that NPC1 plays a previously unrecognized role in the presynaptic nerve terminal and that NPC1 deficiency at this site might contribute to the progressive neurological impairment in NPC disease.

Animals↗
PubMed1994

Age-related and region-specific increase in number of concentric lamellar bodies in axon terminals and presynaptic axons in central nervous system of groggy mutant rat.

In some regions of the central nervous system (CNS) of the groggy rat, a mutant with a movement disorder, concentric lamellar bodies (CLBs) were formed in numerous axon terminals and presynaptic axons. These bodies were counted electron microscopically in the lateral cerebellar nuclei of Slc:Wistar and groggy mutant rats at 20 to 180 days of age. In the Slc:Wistar rat groups, the mean numbers of axonal CLBs were mostly under 1.0 per 100 microns2, except for the 30-day-old rat group which showed a value of 1.7. In the groggy rat groups, the numbers of axonal CLBs greatly increased from 40 days of age onward, reaching the maximum mean number of 23.7 per 100 microns2 in the 90-day-old rat group and subsequently decreasing; however, significant numbers were still present in the 180-day-old rat group. Since these bodies have been reported to contain an acid phosphatase (ACPase), the regional specificity of their appearance in the CNS was examined by light and electron microscopic ACPase histochemistry. In the 90- and 180-day-old groggy rats, numerous particulate deposits of ACPase reaction products were found in the neuropil of the lateral, interposed and medial cerebellar nuclei, the superior, lateral and spinal vestibular nuclei, and the spinal gracile nuclei. By electron microscopy, the particulate deposits in the cerebellar and vestibular nuclei were confirmed as the CLBs in axon terminals, while those in the gracile nuclei were revealed to be the dystrophic axons. Thus, it was suggested that the axon terminals and presynaptic axons, having a high capacity to form the CLBs in the groggy rats from 40 days of age onward, belong to the Purkinje cells.

Acid Phosphatase↗
PubMed2000

Identification of signal substances in synapses made between primary afferents and their associated axon terminals in the rat trigeminal sensory nuclei.

The relationships between primary afferent terminals (PATs) and their associated presynaptic terminals in the rat trigeminal sensory nuclear complex (TSNC) were examined with special reference to amino acid transmitters glutamate (Glu) and gamma-aminobutyric acid (GABA). Primary afferent terminals anterogradely labeled from the trigeminal ganglion with the B subunit of cholera toxin conjugated to horseradish peroxidase (CTB-HRP) were sectioned for electron microscopy. Serial sections from the principal nucleus (Vp), dorsomedial parts of the oral and interpolar nuclei (Vdm), and lamina III/IV of caudal nucleus (Vc) were immunostained for Glu and GABA by using a postembedding immunogold technique. The tracer, CTB-HRP to the trigeminal ganglion, preferentially labeled myelinated primary afferents. Sections immunostained with Glu antiserum showed that most labeled PATs were enriched with immunoreactivity (IR) for Glu. The Glu-IR PATs contained clear, round, synaptic vesicles and formed asymmetric synaptic contacts with somata or dendrites. They were frequently postsynaptic to, unlabeled axon terminals filled with a mixture of clear, round, oval, and flattened vesicles (p-endings), with symmetric synaptic junctions. The frequency of synapses onto somata or primary dendrites per Glu-IR PAT was higher in the Vdm than in either the Vp or Vc lamina III/IV. The frequency of contacts of the p-endings per Glu-IR PAT was higher in the Vp than in the Vdm and Vc lamina III/IV. Sections immunostained with GABA antiserum showed that most axon terminals presynaptic to PATs were enriched with GABA in the three nuclei. The GABA-IR axon terminals and their postsynaptic PATs had a similar ultrastructural character to p-endings and their postsynaptic Glu-IR PATs, respectively. The present study suggests that primary afferent neurons with large-caliber fibers use glutamate as a neurotransmitter and are subject to presynaptic modulation by GABAergic fibers.

Animals↗
PubMed1987

Light microscopic visualisation of the presynaptic nerve terminal calyx in dissociated chick ciliary ganglion neurons.

The pre- and postsynaptic elements of the calyx-type synapse in the chick ciliary ganglion were stained with Lucifer yellow in situ, and the structure of this synapse was examined after enzymatic dissociation of the ganglion. Back-staining of the ciliary nerve resulted in darkly stained neuronal cell bodies. Foreward-staining of the presynaptic oculomotor nerve did not stain the neurons, but instead resulted in a 'halo' of fluorescence around the cell bodies, corresponding to the large presynaptic calyxes. This study demonstrates the feasability of staining the presynaptic terminals in dissociated ciliary neurons and demonstrates the range of calyx structure at this physiologically interesting synapse.

Animals↗