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PubMed2005

Increased cholesterol in Abeta-positive nerve terminals from Alzheimer's disease cortex.

Synapse loss in Alzheimer's disease (AD) is poorly understood but evidence suggests it is a key pathological event. In order to precisely detect stable synaptic changes, we have developed methods for flow cytometry analysis of synaptosomes prepared from cryopreserved AD samples, and have previously shown that amyloid-beta (Abeta) accumulates in surviving presynaptic terminals in AD cortex. In the present experiments we have examined amyloid-containing terminals in more detail, first dual labeling synaptosomes from AD cortex for Abeta and a series of markers, and then using quadrant analysis to compare amyloid-positive and amyloid-negative terminals. Amyloid-positive synaptosomes were larger in size than amyloid-negatives (p<0.007), and significant increases were observed in mean fluorescence for the lipid raft markers cholesterol (27%; p<0.0005) and GM1 ganglioside (24%; p<0.005). SNAP-25 immunofluorescence was increased by 31% (p<0.0001) in amyloid-bearing terminals, consistent with a sprouting response to amyloid accumulation. These results suggest that Abeta accumulation in synaptic terminals may underly dysfunction prior to or independent of extracellular amyloid deposition.

Adaptation, Physiological↗
PubMed2005

Nogo-A, -B, and -C are found on the cell surface and interact together in many different cell types.

Nogo-A, -B, and -C are generated from the Nogo/RTN-4 gene and share a highly conserved C-terminal domain. They lack an N-terminal signal sequence and are predominantly localized to the endoplasmic reticulum (ER). We found the N terminus of endogenous Nogo-A exposed on the surface of fibroblasts, DRG neurons, and myoblasts. Surface-expressed Nogo-A was also present on presynaptic terminals of the neuromuscular junction and on DRG neurons in vivo. Surface biotinylations confirmed the presence of all Nogo isoforms on the surface. To search for proteins that interact with Nogo-A and suggest a function for the large intracellular pool of Nogo-A, immunoprecipitations were performed. Surprisingly, the most predominant proteins that interact with Nogo-A are Nogo-B and Nogo-C as seen with radiolabeled lysates and as confirmed by Western blotting in multiple cell lines. Nogo-A, -B, and -C share a 180-amino acid C-terminal domain with two highly conserved hydrophobic stretches that could form a channel or transporter in the ER and/or on the cell surface.

3T3 Cells↗
PubMed1991

GABA-Mediated Presynaptic Inhibition in Crayfish Primary Afferents by Non-A, Non-B GABA Receptors.

GABAergic presynaptic inhibition has been investigated in primary afferents using an in vitro preparation of the crayfish, Procambarus clarkii. Presynaptic terminals of a leg proprioceptor, the coxo-basal (CB) chordotonal organ, were impaled in the neuorpil of the 5th thoracic ganglion. Pressure ejection of small volumes of the GABAA or GABAB receptor agonists, muscimol and 3-aminopropylphosphinic acid (3-APA), both induce depolarizing responses in the impaled CB sensory terminal. These depolarizations are not blocked by the specific GABAA and GABAB receptor antagonists, SR-95531 and phaclofen, but they are abolished by picrotoxin. Both muscimol- and 3-APA-induced depolarizations are carried by an increase in conductance to Cl-. The presynaptic increase in conductance to Cl- by GABA receptor activation leads to a depression of sensory synaptic transmission through a shunting of the incoming spikes. Monosynaptic EPSPs elicited in motor neurons by CB sensory nerve stimulation are depressed by muscimol and 3-APA. GABA-mediated presynaptic modulation occurs in crayfish primary afferents which can adjust the gain of reflexes. These results show that GABA-activated Cl- channels can induce a modulation of synaptic transmission, but also that the distinction between GABAA and GABAB receptors, as in vertebrates, is not applicable to the crustacean primary afferents.

Journal Article↗
PubMed1972

Properties and distribution of peripherally evoked presynaptic hyperpolarization in cat lumbar spinal cord.

1. The action of peripheral nerve volleys on the polarization of presynaptic terminals of inactive sensory fibres in cat lumbar spinal cord has been investigated by recording (a) the dorsal root potential (DRP), (b) intracellular changes in polarization of single preterminal axons (PAD or PAH), and (c) changes in excitability of populations of preterminal axons.2. Presynaptic hyperpolarization (positive DRP-PAH) can be evoked by stimulation of muscle group III afferents as well as by volleys in cutaneous Abeta, Adelta and C afferents. These volleys can also produce presynaptic depolarization (negative DRP-PAD).3. The positive DRP is observed in the decerebrate state and increases in amplitude following spinalization.4. Picrotoxin blocks the positive DRP at the same dosages required to block the negative DRP. Test negative DRPs are depressed during a conditioning positive DRP. These results are used to support earlier suggestions that the positive DRP results from inhibition of interneurones mediating the negative DRP.5. Trains of group III stimuli at 20/sec evoke a steady positive DRP. Trains of the same intensity at 200/sec evoke a phasic negative DRP. This frequency dependence is observed for PAD and PAH in single sensory axons.6. The DRPs recorded from different dorsal root filaments in response to a given stimulus vary widely in the ratio of negative to positive DRP.7. Intracellular recording from single axons reveals that the same stimuli evoke widely varying ratios of PAD and PAH.8. Stimulation of FRA evokes PAH > PAD in PBST group I afferents, PAD > PAH in sural A fibres and intermediate effects in G-S group I units.9. It is suggested that activation of flexor reflex afferents may selectively potentiate the synaptic efficacy of large muscle afferents mediating the flexor reflex rather than large skin afferents or large afferents from extensor muscles.

Animals↗
PubMed1994

Presynaptic actions of GABA and baclofen in CA1 region of the guinea-pig hippocampus in vitro.

The presynaptic actions of GABA and (+/-) baclofen on the stratum radiatum in the CA1 region of guinea-pig hippocampal slices were investigated using a modified grease-gap recording technique. D.c. potential shifts were recorded in response to varying concentrations of GABA and (+/-) baclofen. In Ca(2+)-free media containing tetrodotoxin, bath applications of GABA (2.5 microM to 20 mM) produced depolarizations which were concentration-dependent. Maximum depolarization was attained with 10 mM GABA. Superfusion of (+/-) baclofen (0.125-500 microM) produced a concentration-dependent hyperpolarization which peaked at a concentration of 250 microM. The GABA-induced depolarization but not the (+/-) baclofen-induced hyperpolarization was depressed by the GABAA antagonists bicuculline and picrotoxinin. The (+/-) baclofen-induced hyperpolarization but not the GABA-induced depolarization was suppressed by CGP 35,348, a GABAB antagonist. In the presence of bicuculline, GABA (0.5-5.0 mM) occasionally caused a hyperpolarization which could be blocked by CGP 35,348. These results indicate that the primary presynaptic action of GABA on the d.c. potential in the CA1 region of the hippocampus is to produce a GABAA receptor-mediated depolarization, while (+/-) baclofen induces a GABAB receptor-mediated hyperpolarization. The grease-gap d.c. potential recording technique, described in this paper, is expected to be useful in examining changes in the membrane potentials of presynaptic terminals.

Animals↗
PubMed1974

Crayfish neuromuscular facilitation activated by constant presynaptic action potentials and depolarizing pulses.

1. Experiments were conducted to test the hypothesis that facilitation of transmitter release in response to repetitive stimulation of the exciter motor axon to the crayfish claw opener muscle is due to an increase in the amplitude or duration of the action potential in presynaptic terminals. No consistent changes were found in the nerve terminal potential (n.t.p.) recorded extracellularly at synaptic sites on the surface of muscle fibres.2. Apparent changes in n.t.p. are attributed to three causes.(i) Some recordings are shown to be contaminated by non-specific muscle responses which grow during facilitation.(ii) Some averaged n.t.p.s exhibit opposite changes in amplitude and duration which suggest a change in the synchrony of presynaptic nerve impulses at different frequencies.(iii) Some changes in n.t.p. are blocked by gamma-methyl glutamate, an antagonist of the post-synaptic receptor, which suggests that these changes are caused by small muscle movements.3. The only change in n.t.p. believed to represent an actual change in the intracellular signal is a reduction in n.t.p. amplitude to the second of two stimuli separated by a brief interval.4. Tetra-ethyl ammonium ions increase synaptic transmission about 20% and prolong the n.t.p. about 15%. This result suggests that an increase in n.t.p. large enough to increase transmission by the several hundred per cent occurring during facilitation would be detected.5. The nerve terminals are electrically excitable, and most synaptic sites have a diphasic or triphasic n.t.p., which suggests that the motor neurone terminals are actively invaded by nerve impulses.6. When nerve impulses are blocked in tetrodotoxin, depolarization of nerve terminals increases the frequency of miniature excitatory junctional potentials (e.j.p.s), and a phasic e.j.p. can be evoked by large, brief depolarizing pulses. Responses to repetitive or paired depolarizations of constant amplitude and duration exhibit a facilitation similar to that of e.j.p.s evoked by nerve impulses.7. It is concluded that facilitation in the crayfish claw opener is not due to a change in the presynaptic action potential, but is due to some change at a later step in the depolarization-secretion process.

Action Potentials↗
PubMed2003

Mitochondria and release at hippocampal synapses.

Mitochondria are present in some, but not all presynaptic terminals in the hippocampus. Mitochondria are capable of sequestering and storing large amounts of calcium, but it is unclear whether they influence release probability at these synapses. Using FM dye imaging techniques and confocal microscopy, we have examined the relationship between mitochondrial presence/absence and presynaptic vesicle release from rat hippocampal neurones in primary dissociated culture at room temperature. Following staining with the mitochondrial dye mitotracker green, we were able to resolve putative individual mitochondria associated with neuronal processes. The majority of mitochondria were positionally stable, although some exhibited periods of rapid motility (up to 0.4 microm/s) interspersed with periods of immobility. Co-staining with mitotracker green and the synaptic vesicle dye FM 4-64 indicated that 180 of 506 (36%) synapses were devoid of mitochondria. A comparison of vesicular release in response to stimulation at 1 Hz and at 10 Hz revealed no differences in release properties between synapses with and without mitochondria.

Animals↗
PubMedDate not supplied

Calcium signaling and synaptic modulation: regulation of endocannabinoid-mediated synaptic modulation by calcium.

Postsynaptic Ca2+ signal influences synaptic transmission through multiple mechanisms. Some of them involve retrograde messengers that are released from postsynaptic neurons in a Ca2+-dependent manner and modulate transmitter release through activation of presynaptic receptors. Recent studies have revealed essential roles of endocannabinoids in retrograde modulation of synaptic transmission. Endocannabinoid release is induced by either postsynaptic Ca2+ elevation alone or activation of postsynaptic Gq/11-coupled receptors with or without Ca2+ elevation. The former pathway is independent of phospholipase Cbeta (PLCbeta) and requires a large Ca2+ elevation to a micromolar range. The latter pathway requires PLCbeta and is facilitated by a moderate Ca2+ elevation to a submicromolar range. This facilitation is caused by Ca2+-dependency of receptor-driven PLCbeta activation. The released endocannabinoids then activate presynaptic cannabinoid receptor type 1 (CB1), and suppress transmitter release from presynaptic terminals. Both CB1 receptors and Gq/11-coupled receptors are widely distributed in the brain. Thus, the endocannabinoid-mediated retrograde modulation may be an important and widespread mechanism in the brain, by which postsynaptic events including Gq/11-coupled receptor activation and Ca2+ elevation can retrogradely influence presynaptic function.

Animals↗
PubMed2001

Synapse-glia interactions at the mammalian neuromuscular junction.

Perisynaptic Schwann cells (PSCs) play critical roles in regulating and stabilizing nerve terminals at the mammalian neuromuscular junction (NMJ). However, although these functions are likely regulated by the synaptic properties, the interactions of PSCs with the synaptic elements are not known. Therefore, our goal was to study the interactions between mammalian PSCs in situ and the presynaptic terminals using changes in intracellular Ca(2+) as an indicator of cell activity. Motor nerve stimulation induced an increase in intracellular Ca(2+) in PSCs, and this increase was greatly reduced when transmitter release was blocked. Furthermore, local application of acetylcholine induced Ca(2+) responses that were blocked by the muscarinic antagonist atropine and mimicked by the muscarinic agonist muscarine. The nicotinic antagonist alpha-bungarotoxin had no effect on Ca(2+) responses induced by acetylcholine. Local application of the cotransmitter ATP induced Ca(2+) responses that were unaffected by the P2 antagonist suramin, whereas local application of adenosine induced Ca(2+) responses that were greatly reduced by the A1 receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT). However, the presence of the A1 antagonist in the perfusate did not block responses induced by ATP. Ca(2+) responses evoked by stimulation of the motor nerve were reduced in the presence of CPT, whereas atropine almost completely abolished them. Ca(2+) responses were further reduced when both antagonists were present simultaneously. Hence, PSCs at the mammalian NMJ respond to the release of neurotransmitter induced by stimulation of the motor nerve through the activation of muscarinic and adenosine A1 receptors.

Acetylcholine↗
PubMed1988

[Ultrastructural organization of the synapses in ganglia of the hen intestinal nerve under various conditions of its activity].

The interneuronal connections in ganglia of the caudal part of the hen intestinal nerve of Remak are presented as axodendritic and axosomatic synapses and symmetric axo-axonal, dendro-dendritic and axodendritic contacts, often forming complicated complexes. Under conditions of preliminary decentralization or under certain disturbances of nervous connections with the intestine, a part of synapses remains, and a part of them degenerates, this demonstrates participation of peripheral afferent neurons in formation of the synaptic apparatus of the ganglia mentioned. The axonal terminals differentiate by composition of the synaptic vesicles: some contain mainly light agranular vesicles, others--a large amount of granular ones. The characteristic peculiarities of the hen intestinal nerve ganglia, in contrast to analogous mammalian ganglia, are abundant axosomatic synapses in some neurons, and presynaptic terminals, containing a large number of granular vesicles.

Animals↗
PubMed1995

Functional impact of syntaxin on gating of N-type and Q-type calcium channels.

Rapid and reliable synaptic transmission depends upon the close proximity of voltage-gated calcium channels and neurotransmitter-containing vesicles in the presynaptic terminal. Although it is clear that a local Ca2+ rise conveys the crucial signal from Ca2+ channels to the exocytotic mechanism, little is known about whether communication ever proceeds in the opposite direction, from the release machinery to Ca2+ channels. To look for such signalling, we examined the interaction of various types of voltage-gated Ca2+ channels with syntaxin, a presynaptic membrane protein of relative molecular mass 35,000 which may play a key part in synaptic vesicle docking and fusion and which interacts strongly with N-type Ca2+ channels. Here we report that co-expression of syntaxin 1A with N-type channels in Xenopus oocytes sharply decreases the availability of these channels. This is due to the stabilization of channel inactivation rather than to a simple block or lack of channel expression, because it is overcome by strong hyperpolarization. Deletion of syntaxin's carboxy-terminal transmembrane domain abolishes its functional effect on Ca2+ channels. Syntaxin produced a similar effect on Q-type Ca2+ channels encoded by alpha 1A but not on L-type Ca2+ channels. Thus, the syntaxin effect is specific for Ca2+ channel types that participate in fast transmitter release in the mammalian central nervous system. We hypothesize that, in addition to acting as a vesicle-docking site, syntaxin may influence presynaptic Ca2+ channels, opposing Ca2+ entry where it is not advantageous, but allowing it at release sites where synaptic vesicles have become docked and/or ready for fusion.

Animals↗
PubMed1977

Morphology and responses to light of the somata, axons, and terminal regions of individual photoreceptors of the giant barnacle.

1. The median eye of the giant barnacle, B. nubilus, comprises four large photoreceptor neurones which are visible under the dissecting microscope for almost their entire length. We have studied the structure of, and the responses to light recorded in, the somata, axons, and terminal regions of these neurones.2. The photoreceptor somata, each 40-70 mum in diameter, extend numerous light-sensitive dendritic processes whose membranes form rhabdomeric microvilli. Recordings from the soma show that dim light evokes a steady, noisy depolarization; brighter light elicits a transient depolarization which decays to a maintained plateau, followed by a hyperpolarization when the light is turned off.3. Light-induced voltage changes spread decrementally along the photoreceptor axons, which average 10 mm in length and 25 mum in diameter. In distal parts of the axon, near the presynaptic terminals, depolarizations and hyperpolarizations can be as large as 50% or more of their values in the soma.4. There is no demonstrable electrical coupling between photoreceptor neurones as shown by simultaneous recordings from two receptor somata or axons.5. Each photoreceptor axon enters the mid line commissure of the supraoesophageal ganglion, bifurcates, and arborizes in a restricted zone of neuropil in each hemiganglion. The large size of the terminal processes of these neurones and their characteristic cytoplasmic inclusions enable one to trace them with the electron microscope as they branch in the neuropil.6. The terminal processes subdivide and end in 1-3 mum diameter branches which are the sites of apparently chemical synapses. Vesicle-containing, presynaptic loci on these processes of the receptor cell are invariably apposed to two post-synaptic processes from cells as yet unidentified.

Animals↗
PubMed1983

A comparison of the effects of acute and chronic cholinesterase inactivation on spontaneous transmitter release.

The irreversible inhibitor of acetylcholinesterase (AChE), paraoxon, when given in vivo to rats in a single injection (0.23 mg/kg s.c.) raised the miniature endplate potential (MEPP) frequency to values greater than 3 times control levels in 34% of the fibers in the rat phrenic nerve-hemidiaphragm preparation. The elevated MEPP frequencies were observed in areas of extensive muscle twitching and were associated with high frequencies of giant MEPPs. Following 3 daily injections of paraoxon; the overall MEPP frequency was reduced below control levels, the frequency of giant MEPPs returned to normal, and a greater percentage of fibers showed no spontaneous activity. This depressant effect of chronic AChE inhibition on the overall MEPP frequency diminished during 1-2 weeks of daily paraoxon treatment (0.12 mg/kg s.c. paraoxon/day). After one week of recovery from 14 daily paraoxon injections (0.12 mg/kg, 1 injection/day), the original response to a single injection (0.23 mg/kg) was restored. In an attempt to determine whether paraoxon exerts its effects on spontaneous release by depolarizing the presynaptic terminal, the effect of increases in the potassium concentration on the MEPP and giant potential frequency were examined in control (saline injection) preparations, and preparations treated with 1 or 3 daily injections of paraoxon. The results suggest that paraoxon does not act by reducing the presynaptic membrane potential, but may interact more directly with the mechanism(s) responsible for regulating the release of MEPPs and giant MEPPs.

Animals↗
PubMed1989

Putative receptor for inositol 1,4,5-trisphosphate similar to ryanodine receptor.

Inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) serves as an intracellular second messenger for several neurotransmitters, hormones and growth factors by initiating calcium release from intracellular stores. A cerebellar Ins(1,4,5)P3 receptor has been characterized biochemically and shown by immunocytochemistry to be present in intracellular membranes in Purkinje cells. We show that a previously described Purkinje-cell messenger RNA encodes a protein of relative molecular mass 260,000 (260 K) with the same properties as the cerebellar Ins(1,4,5)P3 receptor. Its sequence is partially homologous to the skeletal muscle ryanodine receptor. By immunocytochemistry and electron microscopy the protein is shown to be present in all parts of the endoplasmic reticulum, including those that extend into axon terminals and dendritic spines. Our results indicate that gated calcium release from intracellular stores in muscle and Purkinje cells uses similar calcium-channel proteins localized in analogous intracellular compartments. This implies that the intracellular calcium stores in the endoplasmic reticulum of neurons extend into presynaptic terminals and dendritic spines where they may play a direct role in regulating the efficacy of neurotransmission.

Amino Acid Sequence↗
PubMed1988

beta-Bungarotoxin-induced phospholipid hydrolysis in rat brain synaptosomes: effect of replacement of calcium by strontium.

We tested whether, upon substitution of Ca2+ by Sr2+ in a medium containing beta-bungarotoxin, sufficient Ca2+ remained bound to the tissue to support phospholipid hydrolysis in rat brain synaptosomes. The phrenic nerve--diaphragm preparation could not be used, since replacement of Ca2+ by Sr2+ prolonged time to block of indirectly evoked contractions; however, no phospholipid hydrolysis could be detected (either in the presence of Ca2+ or Sr2+), due to the small amounts of presynaptic terminals. Following initial exposure of synaptosomes to a Ca2+ containing medium and then removal of Ca2+, incubation with beta-bungarotoxin (1 or 10 micrograms/ml) caused significant phospholipid hydrolysis whether or not Sr2+ was present. Therefore, conclusions as to whether phospholipase A2 activity is required for presynaptic actions of beta-bungarotoxin cannot be derived from studies in which Sr2+ is used to inhibit enzymatic activity.

Animals↗
PubMed2005

Glutamate induces the rapid formation of spine head protrusions in hippocampal slice cultures.

Synaptic plasticity at neuronal connections has been well characterized functionally by using electrophysiological approaches, but the structural basis for this phenomenon remains controversial. We have studied the dynamic interactions between presynaptic and postsynaptic structures labeled with FM 4-64 and a membrane-targeted GFP, respectively, in hippocampal slices. Under conditions of reduced neuronal activity (1 muM tetrodotoxin), we observed extension of glutamate receptor-dependent processes from dendritic spines of CA1 pyramidal cells to presynaptic boutons. The formation of these spine head protrusions is blocked by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor antagonists and by agents that reduce the release of glutamate from presynaptic terminals. Moreover, spine head protrusions form in response to exogenously applied glutamate, with clear directionality toward the glutamate electrode. Our results suggest that spontaneously released glutamate is sufficient to activate nearby spines, which can then lead to the growth of new postsynaptic processes connecting to a presynaptic site. Spines thus can compare their recent history with that of neighboring synapses and modify local connectivity accordingly.

Animals↗
PubMed1995

Presynaptic inhibition by serotonin of glycinergic inhibitory synaptic currents in the rat brain stem.

1. With the use of a thin brain stem slice preparation, we recorded in visualized neonatal rat hypoglossal motoneurons unitary glycinergic inhibitory postsynaptic currents (IPSCs) that were evoked by extracellular stimulation of nearby interneurons. We found that 10 microM serotonin (5-HT) presynaptically inhibited this glycinergic synaptic transmission by 85.5%. 2. In the somata of presynaptic interneurons, 5-HT1A receptor activation potentiated inwardly rectifying K+ channels and inhibited voltage-activated calcium channels. 3. In contrast, the 5-HT1B receptor was primarily responsible for inhibition of evoked glycinergic IPSCs; a selective 5-HT1B receptor agonist, N-(3-trifluoromethylphenyl)piperazine (TFMPP, 10 microM), inhibited synaptic transmission by 97.3%. On the other hand, 5-HT1A receptor activation by (+)-8-OH-dipropylaminotetralin (8-OHDPAT, 1 microM) inhibited IPSCs by only 24.1%. A 5-HT1A antagonist, 1-(2-methyoxyphenyl)-4-[4-(2-phthalimido)-butyl]piperazine hydrobromide (NAN-190, 1 microM), had no effect on synaptic inhibition by 5-HT. 4. In the presence of tetrodotoxin (TTX) as well as TTX with cadmium (50 microM), we found that 5-HT1B receptor activation by TFMPP reduced the frequency of spontaneous miniature IPSCs (mIPSCs) without changing their mean amplitude. The results suggested that the 5-HT1B receptors activated at the presynaptic terminal inhibited synaptic transmission independent of inhibiting calcium influx through voltage-activated calcium channels. 5. These results indicate that activation of inwardly rectifying K+ channels and inhibition of voltage-activated calcium channels by 5-HT1A receptor activation do not constitute a main pathway for presynaptic inhibition by 5-HT of glycinergic synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Bursts of miniature end-plate potentials can be released from localized regions of the frog motor nerve terminal.

We examined spontaneous transmitter release by simultaneously recording from end-plates with both an intracellular electrode and a focal extracellular electrode. In normal Ringer's solution the focal releases appear to be a near random portion of the pooled output. But in elevated [Sr2+]out bursts of miniature end-plate potentials (m.e.p.p.s.) occur, and these can be localized at a portion of the presynaptic terminal. The bursts are not artifacts caused by the focal recording technique. In some conditions, sections of the nerve terminal can exhibit an enhanced probability of quantal release that persists for seconds. We occasionally observe extracellular events that must be generated by m.e.p.p.s. in adjacent fibers.

Animals↗