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PubMed1976

Physiological and morphological effects of post-ganglionic axotomy on presynaptic nerve terminals.

1. Electrophysiological and electron microscope studies were done on cells in the ciliary ganglion of chickens which had been axotomized on the day of hatching. 2. By the third day after post-ganglionic axotomy both electrical and chemical transmission through the ganglion were severely depressed; by the fifth day ganglionic transmission had disappeared. 3. Action potential initiation and conduction in axotomized cells and in their associated presynaptic nerve terminals were unimpaired 3-4 days after axotomy. 4. Depression of ganglionic transmission in 3-4 day axotomized preparations was due to a reduction in amplitude of both the excitatory post-synaptic potential (e.p.s.p.) and the electrical coupling potential in individual ganglion cells. 5. In addition to being reduced in amplitude, e.p.s.p.s in axotomized cells were more subject to fatigue during low frequency (1/sec) stimulation. 6. The reduction in e.p.s.p. amplitude was due to a reduction in both the mean quantal content of the e.p.s.p.s and the calculated depolarization produced by an individual quantum of transmitter. On the average the e.p.s.p. was reduced by a factor of about 4, the mean quantum content to about two thirds normal and the quantal size to about a third normal, compared with responses in unaxotomized cells of the same age. 7. Ultrastructural studies revealed a progressive maturation of pre-synaptic terminals in normal ganglia between 0 and 9 days after hatching. Over this period the content of synaptic vesicles and mitochondria in the terminals increased and the background matrix became more dense. 8. After axotomy these signs of maturation was abolished or reversed, particularly from the third day onward. In addition there was an increase in the number of cell sections in which no synaptic terminals were observed. 9. It was concluded that loss of synaptic transmission was due to at least three factors: a reduction in release of transmitter from presynaptic terminals, a reduction in quantal size, probably due to a loss of post-synaptic sensitivity, and a partial loss of presynaptic contact.

Action Potentials↗
PubMed1989

Quantification of the synapses in the hippocampus of aged rats.

The synapses in the stratum lacunosum-molecular (str. L-M) of CA1 hippocampal field in 3-month old and 24-month old rats were examined using quantitative ultrastructural methods. No significant difference in the density of synapses and postsynaptic dendritic spines was found between the two age groups. The area of presynaptic terminals and postsynaptic dendritic spines was decreased slightly but significantly in the group of aged as compared to that in the group of young-mature rats. The vesicle number per presynaptic terminal, per area of presynaptic terminals and per volume of neuropil was not changed while the vesicle number per area of synaptic contact zones (SCZ) was increased in the group of aged rats. The mean length, total length and total surface of SCZ were diminished in the group of aged as compared to those in the group of young-mature rats. The same width of the str.radiatum and str.L-M in the two age groups showed that there was no any shrinkage of the neuropil in aged rats. The quantitative alterations in the synapses were accompanied by an increased number of dense and lamellar bodies in presynaptic terminals as well as with a presence of hypertrophic astroglial processes.

Aging↗
PubMed1988

The regulation of cytosolic pH in isolated presynaptic nerve terminals from rat brain.

Cytosolic pH (pHi) was measured in presynaptic nerve terminals isolated from rat brain (synaptosomes) using a fluorescent pH indicator, 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The synaptosomes were loaded with BCECF by incubation with the membrane-permanent acetoxy-methyl ester derivative of BCECF, which is hydrolyzed by intracellular esterases to the parent compound. pHi was estimated by calibrating the fluorescence signal after permeabilizing the synaptosomal membrane by two different methods. Synaptosomes loaded with 15-90 microM BCECF were estimated to have a pHi of 6.94 +/- 0.02 (mean +/- standard error; n = 54) if the fluorescence signal was calibrated after permeabilizing with digitonin; a similar value was obtained using synaptosomes loaded with 10 times less BCECF (6.9 +/- 0.1; n = 5). When the fluorescence signal was calibrated by permeabilizing the synaptosomal membrane to H+ with gramicidin and nigericin, pHi was estimated to be 7.19 +/- 0.03 (n = 12). With the latter method, pHi = 6.95 +/- 0.09 (n = 14) when the synaptosomes were loaded with 10 times less BCECF. Thus, pHi in synaptosomes was approximately 7.0 and could be more precisely monitored using the digitonin calibration method at higher BCECF concentrations. When synaptosomes were incubated in medium containing 20 mM NH4Cl and then diluted into NH4Cl-free medium, pHi immediately acidified to a level of approximately 6.6. After the acidification, pHi recovered over a period of a few minutes. The buffering capacity of the synaptosomes was estimated to be approximately 50 mM/pH unit. Recovery was substantially slowed by incubation in an Na-free medium, by the addition of amiloride (KI = 3 microM), and by abolition of the Nao/Nai gradient. pHi and its recovery after acidification were not affected by incubation in an HCO3-containing medium; disulfonic stilbene anion transport inhibitors (SITS and DIDS, 1 mM) and replacement of Cl with methylsulfonate did not affect the rate of recovery of pHi. It appears that an Na+/H+ antiporter is the primary regulator of pHi in mammalian brain nerve terminals.

Amiloride↗
PubMed1985

Calcium-activated potassium channels in isolated presynaptic nerve terminals from rat brain.

86Rb efflux was examined in isolated presynaptic nerve terminals (synaptosomes) from rat brain in a study designed to assess K permeability (PK) changes sensitive to alterations in internal Ca activity. Rb efflux from 86Rb-loaded synaptosomes into nominally Ca-free physiological saline (PSS) containing 5 mM-K was about 0.3-0.4%/s. Raising extracellular K concentration [( K]o), to depolarize the synaptosomes, stimulated the 86Rb efflux. Addition of Ca to the 5 mM-K PSS had no effect, but Ca did further stimulate 86Rb efflux into K-rich solutions. The effect of Ca was graded, with apparent half-maximal activation, KA approximately equal to 0.5 mM-Ca. These data fit the view that, during depolarization, Ca enters the terminals through voltage-regulated Ca channels, and that the rise in intracellular Ca concentration opens certain (Ca-activated) K channels. The Ca-dependent stimulation of 86Rb efflux was greatest during the initial seconds of incubation (component CT), and then declined to a much lower rate (component CS). Much of this change in rate could be attributed to inactivation of voltage-regulated Ca channels and reduced entry of Ca. The Ca-dependent increase in 86Rb efflux was completely inhibited by 100 microM-La. In the presence of Ca, but not in its absence, the Ca ionophore A23187 stimulated 86Rb efflux both in 5 and 100 mM-K PSS. The effect in 100 mM-K was quantitatively greater, perhaps because of the increased outward driving force on Rb in depolarized synaptosomes. When synaptosomes were suspended in media containing the voltage-sensitive fluorescent dye, DiS-C3-(5) (1,1'-dipentyl-2,2'-thiocarbocyanine), the addition of Ca+ A23187 decreased the fluorescence intensity (= synaptosome hyperpolarization) when the media contained 5 mM-K but not 100 mM-K. This implies that in the presence of Ca + A23187, PK was increased, and the membrane potential moved closer to the K equilibrium potential, EK. Quinine sulphate, a blocker of Ca-activated K channels, reduced the Ca-stimulated 86Rb efflux with high affinity (apparent half-maximal inhibition, KI approximately equal to 1 microM). Tetraethylammonium chloride, another agent known to block Ca-activated K channels, was also a relatively potent inhibitor of Ca-stimulated 86Rb efflux (KI approximately equal to 0.2 mM). The K-channel blocker, 4-aminopyridine, partially inhibited Ca-stimulated 86Rb efflux at concentrations below 0.5 mM, but stimulated this efflux at concentrations greater than or equal to 1 mM.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed2003

Presence and functional significance of presynaptic ryanodine receptors.

Ca(2+)-induced Ca(2+) release (CICR) mediated by sarcoplasmic reticulum resident ryanodine receptors (RyRs) has been well described in cardiac, skeletal and smooth muscle. In brain, RyRs are localised primarily to endoplasmic reticulum (ER) and have been demonstrated in postsynaptic entities, astrocytes and oligodendrocytes where they regulate intracellular Ca(2+) concentration ([Ca(2+)](i)), membrane potential and the activity of a variety of second messenger systems. Recently, the contribution of presynaptic RyRs and CICR to functions of central and peripheral presynaptic terminals, including neurotransmitter release, has received increased attention. However, there is no general agreement that RyRs are localised to presynaptic terminals, nor is it clear that RyRs regulate a large enough pool of intracellular Ca(2+) to be physiologically significant. Here, we review direct and indirect evidence that on balance favours the notion that ER and RyRs are found in presynaptic terminals and are physiologically significant. In so doing, it became obvious that some of the controversy originates from issues related to (i) the ability to demonstrate conclusively the physical presence of ER and RyRs, (ii) whether the biophysical properties of RyRs are such that they can contribute physiologically to regulation of presynaptic [Ca(2+)](i), (iii) how ER Ca(2+) load and feedback gain of CICR contributes to the ability to detect functionally relevant RyRs, (iv) the distance that Ca(2+) diffuses from plasma membranes to RyRs to trigger CICR and from RyRs to the Active Zone to enhance vesicle release, and (v) the experimental conditions used. The recognition that ER Ca(2+) stores are able to modulate local Ca(2+) levels and neurotransmitter release in presynaptic terminals will aid in the understanding of the cellular mechanisms controlling neuronal function.

Animals↗
PubMed1992

Suppression of presynaptic calcium currents by hypoxia in hippocampal tissue slices.

We tested the hypothesis that suppression of inward calcium current in presynaptic terminals is the cause of failure of synaptic transmission early during cerebral hypoxia. Postsynaptic responses in CA1 zone of hippocampal tissue slices were blocked either by the combined administration of 6,7-dinitroquinoxaline-2,3-dione (DNQX) and 3-((+-)-2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid (CPP) or by lowering extracellular calcium concentration ([Ca2+]o). Repetitive orthodromic activation of central neurons caused transient decrease of [Ca2+]o (measured by ion selective microelectrodes) in neuropil, attributable to influx of Ca2+ in presynaptic terminals. Presynaptic [Ca2+]o responses were rapidly and reversibly suppressed when oxygen was withdrawn from hippocampal tissue slices. The 'resting' baseline level of [Ca2+]o declined at first gradually, then precipitously as in spreading depression (SD). Presynaptic volleys during high frequency train stimulation were also depressed somewhat before SD began. We conclude that (1) presynaptic Ca2+ currents fail during hypoxia, perhaps because 'resting' intracellular free Ca2+ activity is increased and, in part, also because of partial failure of presynaptic impulse conduction; (2) the influx of Ca2+ into brain cells in hypoxic spreading depression is not mediated by glutamate/aspartate dependent channels.

Action Potentials↗
PubMed2002

Allopregnanolone enhancement of GABAergic transmission in rat medial preoptic area neurons.

Gamma-aminobutyric acid (GABA)-mediated transmission in the medial preoptic area (MPOA) of the hypothalamus plays an important role in functions such as sex steroid hormone dynamics and control of body temperature. The action of allopregnanolone, the primary metabolite of progesterone, on GABAergic transmission was investigated by employing patch clamp whole cell recording on acutely dissociated rat MPOA neurons with the functional connection of presynaptic terminals. Allopregnanolone enhanced spontaneous GABA release on the MPOA neurons and induced prolonged decay of miniature GABAergic-inhibitory postsynaptic currents (mIPSCs). The facilitation of GABA release from the presynaptic terminals by allopregnanolone disappeared in Ca2+-free extracellular solution. The presynaptic action of this neurosteroid was also blocked by bumetanide, a blocker of cation-Cl- cotransporters, and by removal of extracellular Na+. The results suggest that allopregnanolone enhances GABAergic transmission at the MPOA neurons by pre- and postsynaptic mechanisms. The enhancement of GABA release by allopregnanolone might require a high Cl- concentration in the presynaptic terminal maintained by Na+-dependent, bumetanide-sensitive mechanisms (e.g., Na+-K+-Cl- cotransporter) and might be mediated by Ca2+ influx into presynaptic terminal.

Animals↗
PubMed1984

Electron microscopic analysis of the mesencephalic ventromedial tegmentum in the cat.

We have studied the normal ultrastructure of the ventral mesencephalic tegmentum (VMT) in the cat, particularly the morphology and distribution of presynaptic terminals and the types of synaptic junctions. The following subnuclei of the region were examined: n. linearis rostralis (LR), n. paranigralis (PN), and n. interfascicularis (IF). The qualitative and quantitative data revealed significant ultrastructural differences between these subnuclei. Each subnucleus had a characteristic dendritic structure. In LR the dendrites were nonspinous and cylindrical and had presynaptic terminals randomly distributed over their surface. In PN we observed varicose dendrites with spines; the presynaptic terminals formed clusters on the narrow segments of the dendrites and around the spines. Dendrodendritic synapses were also observed in this nucleus. In IF, there was an internal division regarding dendritic structure: in the rostral part of the nucleus there were cylindrical dendrites while in the caudal part irregularly shaped dendrites bearing long spines were found. In IF and LR some of the cylindrical dendrites were seen to be in direct contact with the basal lamina of blood vessels. Four types of presynaptic terminals were distinguished by the morphology of their vesicles, and the proportion of each type in the total terminal population was determined. On this basis the compositions of the presynaptic terminal population in the three subnuclei were found to be very similar. Most terminals contained clear, round vesicles (62.6%), or both clear and dense-cored vesicles (35.1%). Few terminals were seen with dense-cored vesicles only (1.4%) or with pleomorphic vesicles (0.9%). The majority of synapses in the VMT were found to have symmetrical densities. LR had twice as many asymmetrical synapses as the other two subnuclei. Eighty percent of the terminals formed synapses with dendrites, although axosomatic and axoaxonic synapses were also seen. The density of the terminals was significantly different for each subnucleus: 191/1,000 micrometers 2 in IF, 120/1,000 micrometers 2 in PN, and 81/1,000 micrometers 2 in LR. These data indicate that while the subnuclei of the VMT receive morphologically similar afferents, each has a unique way of processing the information provided by them, through a different internal circuitry.

Animals↗
PubMed2005

A null mutation for the alpha3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.

In vertebrates, synaptic activity exerts an important influence on the formation of neural circuits, yet our understanding of its role in directing presynaptic and postsynaptic differentiation during synaptogenesis is incomplete. This study investigates how activity influences synaptic differentiation as synapses mature during early postnatal life. Specifically, we ask what happens to presynaptic terminals when synapses develop without functional postsynaptic receptors and without fast synaptic transmission. To address this issue, we investigated cholinergic nicotinic synapses in sympathetic ganglia of mice with a null mutation for the alpha3 nicotinic ACh receptor gene. Disrupting the alpha3 gene completely eliminates fast excitatory synaptic potentials on postganglionic sympathetic neurons, establishing a crucial role for alpha3-containing postsynaptic receptors in synaptic transmission. Interestingly, the preganglionic nerve terminals form morphologically normal synapses with sympathetic neurons, and these synapses persist without activity in postnatal animals. Surprisingly, when stimulating the preganglionic nerve at physiological rates, we discovered a significant decrease in ACh output from the presynaptic terminals in these alpha3(-/-) sympathetic ganglia. We show that this decrease in ACh output from the presynaptic terminals results, in part, from a lack of functional high-affinity choline transporters. We conclude the following: (1) fast synaptic transmission in mammalian SCG requires alpha3 expression; (2) in the absence of activity, the preganglionic nerve forms synapses that appear morphologically normal and persist for several weeks; and (3) to sustain transmitter release, developing presynaptic terminals require an activity-dependent retrograde signal.

Animals↗
PubMed2003

Age-related changes in the release and uptake activity of presynaptic axon terminals of rat locus coeruleus neurons.

Age-related changes in the release and uptake activity of presynaptic axon terminals of rat locus coeruleus (LC) noradrenergic neurons were studied in the frontal cortex using an extracellular single unit recording technique in vivo. Clonidine, a selective alpha(2) adrenergic agonist, and nisoxetine, a selective noradrenaline uptake inhibitor, were infused locally into the frontal cortex to examine the effects of these drugs on release and uptake activities of the axon terminals of LC neurons. Although the infusion of clonidine produced a marked suppression of release, the effect did not change with age. Infusion of nisoxetine caused an inhibition of uptake, but the effect was attenuated in aged rats. These results suggest that the release activity mediated by the presynaptic autoreceptor did not change with age, but the uptake activity mediated by the NA transporter declined with age in the axon terminals of LC neurons.

Adrenergic Uptake Inhibitors↗
PubMed1968

Further study of the relationship between pre- and postsynaptic potentials in the squid giant synapse.

The minimal presynaptic depolarization (MPD) for producing a detectable postsynaptic potential (PSP) was lower than 25 mv in normal or tetrodotoxin (TTX)-containing seawater. The MPD was about 10 mv when a small amount of tetraethylammonium ions (TEA) was injected into the presynaptic terminal. Application of linearly increasing depolarizing current to the normal presynaptic terminal at times produced a PSP before a presynaptic spike was evoked; the rate of rise of the resulting PSP was much slower than that of a PSP triggered by the normal presynaptic spike. A brief depolarizing pulse that preceded the presynaptic spike in normal seawater or the initial transient presynaptic depolarization in TTX decreased the PSP. It increased the PSP when it was applied during the spike or initial transient depolarization. Hyperpolarizing pulses had the reverse effect. The Off-PSP was also modified by inserting pulses at an initial part of the recovery phase of the strong presynaptic depolarization. These results indicate further that increases in Na(+) and K(+) conductance during presynaptic spike activity are not a requirement for transmitter release; the rate of release of transmitter can be controlled by electrical manipulation of the presynaptic terminal; there is a superficial correspondence between the time courses of presynaptic depolarization and the resulting PSP. Thus presynaptic depolarization appears to be only the first step in the series of events constituting excitation-transmitter release coupling. It may not be a necessary step for the release mechanism.

Animals↗
PubMed1994

A comparison of synapses onto the somata of intrinsically bursting and regular spiking neurons in layer V of rat SmI cortex.

Regular spiking (RS) and intrinsically bursting (IB) neurons show distinct differences in their inhibitory responses. Under various conditions, the synaptic responses of RS cells display marked inhibitory postsynaptic potentials (IPSPs), whereas the responses of most IB cells do not (Silva et al: Soc Neurosci Abstr 14:883, 1988; Chagnac-Amitai and Connors: J Neurophysiol 61:747, 62:1149, 1989; Connors and Gutnick: TINS 13:99, 1990). This investigation is designed to determine if differences in the inhibitory responses of RS versus IB cells are reflected in differences in the concentration of inhibitory synapses onto their somata. RS and IB neurons in rat somatosensory cortex were identified by using intracellular recording and labeling, examined with the light microscope, and then serial thin-sectioned prior to examination with the electron microscope. Axonal terminals presynaptic to their somata and proximal dendrites were identified and classified according to criteria described by Peters and coworkers (Peters et al: J Neurocytol 19:584, 1990; Peters and Harriman: J Neurocytol 19:154, 1990; 21:679, 1992). The locations of these boutons were displayed on the surfaces of 3-D reconstructions of the somata and proximal dendrites. The reconstructions were produced directly from the serial thin sections by using a novel, electron microscopic, image-processing computer resource. Our analysis showed no significant difference in the types and concentration of boutons presynaptic to the cell bodies and proximal dendrites of intrinsically bursting versus regular spiking neurons. We conclude that the differences observed in the inhibitory responses of intrinsically bursting versus regular spiking neurons cannot be explained by differences in the concentrations of synapses onto their somata.

Action Potentials↗
PubMed2001

Quantitative ultrastructure of synapses on functionally identified primary afferent neurons in the cat trigeminal mesencephalic nucleus.

Though a number of studies have reported the presence of synapses on neurons in the trigeminal mesencephalic nucleus (Vmes), there have been no quantitative studies of either the density of innervation, or the ultrastructure, of the synapses on single, physiologically identified neurons in this nucleus. In this study we recorded from single neurons in the Vmes, identified them as being either muscle spindle afferents (MS) or periodontal ligament mechanoreceptor afferents (PL), and then labeled the neurons by intra-axonal injection of horseradish peroxidase (HRP). The material was first processed to reveal the HRP activity, following which ultrathin sections through the labeled somata were cut and examined under the electron microscope. Complete serial reconstructions were made through the soma of one MS neuron and one PL neuron, and the contacts on the neurons reconstructed. Boutons were found on the soma, spines, appendages and the axon hillock and the initial segment of the axon. The numbers of boutons terminating on the two neurons were 198 (PL) and 424 (MS), giving a packing density of 4.4 and 10.7 boutons respectively (i.e., number of boutons/100 micron 2 of the postsynaptic membrane). Boutons could be separated into two types on the basis of their vesicles: those containing clear, round vesicles (i.e., S-type) and those containing a mixture of round, oval and flattened vesicles (P-type). Ninety-five (PL neuron) and 99% (MS neuron) of terminals on the two neurons were P-type. All the S-type boutons and 80% of the P-type boutons formed asymmetric synaptic contacts while 10% of the P-type boutons made symmetric contacts. Quantitative measurements of the P-type boutons on the labeled neurons, in which the data of MS and PL neurons were pooled, revealed that bouton volume was highly correlated with bouton surface area, active zone number, total active zone area, vesicle number, and mitochondrial volume. However, comparing the quantitative measurements of the P-type boutons with those of previously reported vibrissa afferent terminals and their associated axon terminals revealed that all the parameters were smaller for the P-type boutons (on Vmes neurons) than those of the vibrissa afferent terminals but similar to those of axon terminals presynaptic to the vibrissa afferents. Taken together, our results emphasize the wide scope for synaptic interactions in the Vmes and suggest that it may be more fruitful to view the Vmes as an integrating center.

Action Potentials↗
PubMed1994

Ultrastructural evidence for synaptic interactions between thalamocortical axons and subplate neurons.

Thalamic axons are known to accumulate in the subplate for a protracted period prior to invading the cortical plate and contacting their ultimate targets, the neurons of layer 4. We have examined the synaptic contacts made by visual and somatosensory thalamic axons during the transition period in which axons begin to leave the subplate and invade the cortical plate in the ferret. We first determined when geniculocortical axons leave the subplate and begin to grow into layer 4 of the visual cortex by injecting 1,1'-dioctadecyl-3,3,3',3'-tetramethyl indocarbocyanine (Dil) into the lateral geniculate nucleus (LGN). By birth most LGN axons are still confined to the subplate. Over the next 10 days LGN axons grow into layer 4, but many axons retain axonal branches within the subplate. To establish whether thalamic axons make synaptic contacts within the subplate, the anterograde tracer PHA-L was injected into thalamic nuclei of neonatal ferrets between postnatal day 3 and 12 to label thalamic axons at the electron microscope level. The analysis of the PHA-L injections confirmed the Dil data regarding the timing of ingrowth of thalamic axons into the cortical plate. At the electron microscope level, PHA-L-labelled axons were found to form synaptic contacts in the subplate. The thalamic axon terminals were presynaptic primarily to dendritic shafts and dendritic spines. Between postnatal days 12 and 20 labelled synapses were also observed within layer 4 of the cortex. The ultrastructural appearance of the synapses did not differ significantly in the subplate and cortical plate, with regard to type of postsynaptic profiles, length of postsynaptic density or presynaptic terminal size. These observations provide direct evidence that thalamocortical axons make synaptic contacts with subplate neurons, the only cell type within the subplate possessing mature dendrites and dendritic spines; they also suggest that functional interactions between thalamic axons and subplate neurons could play a role in the establishment of appropriate thalamocortical connections.

Animals↗
PubMed1986

Associative induction of posttetanic and long-term potentiation in CA1 neurons of rat hippocampus.

Electrical stimulation of fibers in the stratum radiatum causes an excitatory postsynaptic potential in CA1 neurons of the hippocampus. Other excitatory inputs to or direct depolarization of these CA1 neurons during stimulation of the stratum radiatum caused a subsequent increase in the excitatory postsynaptic potential. This enhancement was characterized as a brief potentiation (2 to 3 minutes, similar to posttetanic potentiation) and a long-term potentiation (presumed to be involved in learning and memory). These potentiations are probably induced by an interaction of the postsynaptic cell or other presynaptic terminals with the test presynaptic terminals.

Action Potentials↗
PubMed1977

The uptake of horseradish peroxidase by cortical synapses in rat brain. An in vivo study.

Horseradish peroxidase (HRP) was introduced directly into the cerebral cortex of adult rats, which were allowed to survive for 60 min before perfusion fixation. After the tissue had been incubated to demonstrate HRP at the LM and EM levels, blocks of cortical tissue were taken at varying distances from the injection site. These eight blocks of tissue constituted a time sequence for HRP diffusion. Qualitative examination of the presynaptic terminals showed that the most commonly encountered profiles are the plain synaptic vesicles, many of which accumulate tracer. In some terminals labelled vesicles are "lined-up" in tubular fashion. Other profiles commonly labelled are coated vesicles, tubular and vacuolar cisternae, and plain and coated pinocytotic vesicles. Quantitative analyses based on the number of terminals containing labelled profiles demonstrate an early rise in the rate of labelling of both plain synaptic vesicles and coated vesicles, after which synaptic vesicle labelling rises slowly towards a plateau. By contrast, there is a late parallel increase in the rate of labelling of coated vesicles and cisternae. A more detailed analysis, based on the actual numbers of labelled and total profiles within each presynaptic terminal, highlight early and late periods of rapid labelling for plain synaptic vesicles, coated vesicles and cisternae. A further aspect of HRP incorporation studied, concerns its uptake into four delineated regions of the presynaptic terminal. Our data indicate that membrane uptake into the presynaptic terminal is accomplished mainly via coated vesicles, although plain synaptic vesicles may also be involved. Coated vesicles, in turn, appear to give rise directly to plain synaptic vesicles, with some coalescing to produce vacuolar cisternae. The latter are involved in a two-way interchange of membrane with tubular cisternae, plain synaptic vesicles and coated vesicles. An additional source of plain synaptic vesicles are the tubular cisternae. Exocytosis of plain synaptic vesicles constitutes the mechanism by which transmitter is released from the presynaptic terminal.

Animals↗
PubMed1990

Monocular deprivation alters the development of synaptic structure in the ectostriatum of the zebra finch.

The effects of monocular deprivation, beginning at hatching, were examined in the neuropil of ectostriatum, a visual telencephalic projection area in birds. The volume of ectostriatum, the number of synapses and subsynaptic features like the presynaptic terminal size and the length of the postsynaptic contact zone were quantified in juvenile (20 d) and adult (100 d) zebra finches. Monocular deprivation affects almost all of the parameters mentioned above in juvenile birds, but only one (i.e., the size of presynaptic terminals) is permanently altered in adulthood. Both hemispheres are affected in juvenile birds with respect to the volume of ectostriatum, the length of synaptic contact zones and the presynaptic terminal size when compared to normal values. In normal birds the number of synaptic contacts is established at 20 days and remains fairly constant at 100 days. In experimental birds there is an increase in synapse number during this time period. However, no interhemispheric differences or differences compared to normal animals could be identified. The presynaptic terminals in experimental birds are smaller compared to normal values in young (25% for the deprived side; 19% for the non-deprived side) and adult (13% for the deprived side; 11% for the non-deprived side) animals. The only permanent effect caused by monocular deprivation in the ectostriatum is characterized by smaller presynaptic terminals. It is surprising that the tectofugal pathway that is believed to be mostly ipsilateral is not very vulnerable to monocular deprivation in adult animals. It is even more surprising that the deprivation effects are seen on both sides of the brain. The implications of this plasticity will be discussed in this paper.

Animals↗
PubMed1981

Antidromic inhibition of acetylcholine release from presynaptic nerve terminals in bullfrog's sympathetic ganglia.

In isolated bullfrog's sympathetic ganglia it was examined if the release of acetylcholine (ACh) from presynaptic nerve terminals was changed when postsynaptic ganglion cells were activated antidromically. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells was found to be depressed, whereas the nicotinic ACh potential of these cells was not depressed, immediately after these ganglion cells were activated by antidromic axonal or direct intracellular stimulations. This indicates that activation of ganglion cells results in inhibiton of the release of ACh from their presynaptic nerve terminals. Such an antidromic inhibition of ACh release could not be clearly observed when preparations were perfused with Ca2+-deficient solution or when adrenaline (10(-5) M) was added to the superfusion solution. Frequency of the spontaneous miniature EPSP was also found to be decreased after antidromic activation of ganglion cells. On the basis of these results it was concluded that some kind of transmitter was released from activated ganglion cells which inhibited ACh release by acting on preganglionic nerve terminals. This putative neurotransmitter was suggested to be adrenaline.

Acetylcholine↗