Role of Ca2+ in the Synchronization of Transmitter Release at Calyceal Synapses in the Auditory System of Rat

2002 ◽  
Vol 87 (1) ◽  
pp. 222-228 ◽  
Author(s):  
Nao Chuhma ◽  
Harunori Ohmori
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Presynaptic Terminal ◽  
Eosin Y ◽  
Early Postnatal Development ◽  
Medial Nucleus ◽  
Combined Application ◽  
Asynchronous Release ◽  
Trapezoid Body

The synchronization of transmitter release in the synapse of the medial nucleus of the trapezoid body (MNTB) is achieved during early postnatal development as a consequence of elimination of delayed asynchronous releases and appears to reflect changes in the dynamics of Ca2+ entry and clearance. To examine the role of Ca2+ in regulating synchronization of transmitter release in the mature synapse (after postnatal day 9, P9), we perturbed Ca2+ dynamics systematically. Replacement of external Ca2+ (2 mM) with Sr2+ induced delayed asynchronous release following the major EPSC. We tried to reproduce asynchronous releases without using Sr2+ and instead by manipulating the time course and the size of Ca2+ transient in the presynaptic terminal, under the assumption that replacement of external Na+ with Li+ or application of eosin-Y would prolong the lifetime of Ca2+ transient by reducing the rate of Ca2+ extrusion from the terminal. With application of Li+, Ca2+ transient in the terminal was prolonged, the EPSC decay time course was prolonged, and the EPSC amplitude increased. However, these EPSCs were not followed by delayed asynchronous release. When Ca2+ influx was reduced, either by partial Ca2+ channel blockade with a low concentration of Cd2+ or ω-agatoxin IVA, a marked asynchronous release resulted. This was further enhanced by the combined application of Li+ or eosin-Y. These results suggest that cooperative increases of both Ca2+ influx and Ca2+ clearance capacities leading to a sharper Ca2+ spike in the presynaptic terminal underlie synchronized transmitter release in the presynaptic terminal of the MNTB.

scholarly journals Differences in Glycinergic mIPSCs in the Auditory Brain Stem of Normal and Congenitally Deaf Neonatal Mice

2004 ◽  
Vol 91 (2) ◽  
pp. 1006-1012 ◽  
Author(s):  
Richardson N. Leao ◽  
Sharon Oleskevich ◽  
Hong Sun ◽  
Melissa Bautista ◽  
Robert E.W. Fyffe ◽  
...  
Keyword(s):  
Time Course ◽  
Single Channel ◽  
Fluctuation Analysis ◽  
Electron Microscopic ◽  
Early Postnatal Development ◽  
Fundamental Properties ◽  
Medial Nucleus ◽  
Synaptic Structure ◽  
Auditory Brain Stem ◽  
Brain Slice Preparation

We have investigated the fundamental properties of central auditory glycinergic synapses in early postnatal development in normal and congenitally deaf ( dn/dn) mice. Glycinergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded using patch-clamp methods in neurons from a brain slice preparation of the medial nucleus of the trapezoid body (MNTB), at 12-14 days postnatal age. Our results show a number of significant differences between normal and deaf mice. The frequency of mIPSCs is greater (50%) in deaf versus normal mice. Mean mIPSC amplitude is smaller in deaf mice than in normal mice (mean mIPSC amplitude: deaf, 64 pA; normal, 106 pA). Peak-scaled fluctuation analysis of mIPSCs showed that mean single channel conductance is greater in the deaf mice (deaf, 64 pS; normal, 45 pS). The mean decay time course of mIPSCs is slower in MNTB neurons from deaf mice (mean half-width: deaf, 2.9 ms; normal, 2.3 ms). Light- and electron-microscopic immunolabeling results showed that MNTB neurons from deaf mice have more (30%) inhibitory synaptic sites (postsynaptic gephyrin clusters) than MNTB neurons in normal mice. Our results demonstrate substantial differences in glycinergic transmission in normal and congenitally deaf mice, supporting a role for activity during development in regulating both synaptic structure (connectivity) and the fundamental (quantal) properties of mIPSCs at central glycinergic synapses.

scholarly journals Effect of changes in action potential shape on calcium currents and transmitter release in a calyx–type synapse of the rat auditory brainstem

1999 ◽  
Vol 354 (1381) ◽  
pp. 347-355 ◽  
Author(s):  
J. G. G. Borst ◽  
B. Sakmann
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Time Course ◽  
Calcium Influx ◽  
Auditory Brainstem ◽  
Calcium Currents ◽  
Medial Nucleus ◽  
Potential Shape ◽  
Presynaptic Calcium ◽  
Rat Brainstem

We studied the relation between the size of presynaptic calcium influx and transmitter release by making simultaneous voltage clamp recordings from presynaptic terminals, the calyces of Held and postsynaptic cells, the principal cells of the medial nucleus of the trapezoid body, in slices of the rat brainstem. Calyces were voltage clamped with different action potential waveforms. The amplitude of the excitatory postsynaptic currents depended supralinearly on the size of the calcium influx, in the absence of changes in the time–course of the calcium influx. This result is in agreement with the view thact at this synapse most vesicles are released by the combined action of multiple calcium channels.

scholarly journals Intracellular Ca2+Stores and Ca2+Influx Are Both Required for BDNF to Rapidly Increase Quantal Vesicular Transmitter Release

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Michelle D. Amaral ◽  
Lucas Pozzo-Miller
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Receptor Activation ◽  
Trpc Channels ◽  
Styryl Dyes ◽  
Trkb Receptors ◽  
Mepsc Frequency ◽  
Intracellular Ca

Brain-derived neurotrophic factor (BDNF) is well known as a survival factor during brain development as well as a regulator of adult synaptic plasticity. One potential mechanism to initiate BDNF actions is through its modulation of quantal presynaptic transmitter release. In response to local BDNF application to CA1 pyramidal neurons, the frequency of miniature excitatory postsynaptic currents (mEPSC) increased significantly within 30 seconds; mEPSC amplitude and kinetics were unchanged. This effect was mediated via TrkB receptor activation and required both full intracellular Ca2+stores as well as extracellular Ca2+. Consistent with a role of Ca2+-permeable plasma membrane channels of the TRPC family, the inhibitor SKF96365 prevented the BDNF-induced increase in mEPSC frequency. Furthermore, labeling presynaptic terminals with amphipathic styryl dyes and then monitoring their post-BDNF destaining in slice cultures by multiphoton excitation microscopy revealed that the increase in frequency of mEPSCs reflects vesicular fusion events. Indeed, BDNF application to CA3-CA1 synapses in TTX rapidly enhanced FM1-43 or FM2-10 destaining with a time course that paralleled the phase of increased mEPSC frequency. We conclude that BDNF increases mEPSC frequency by boosting vesicular fusion through a presynaptic, Ca2+-dependent mechanism involving TrkB receptors, Ca2+stores, and TRPC channels.

Activation and Deactivation of Voltage-Dependent K+ Channels During Synaptically Driven Action Potentials in the MNTB

2006 ◽  
Vol 96 (3) ◽  
pp. 1547-1555 ◽  
Author(s):  
Achim Klug ◽  
Laurence O. Trussell
Keyword(s):  
Action Potentials ◽  
Time Course ◽  
Low Voltage ◽  
Multiple Roles ◽  
Synaptic Activity ◽  
Leak Current ◽  
Medial Nucleus ◽  
Voltage Dependent ◽  
Spike Waveforms ◽  
Trapezoid Body

K+ channels shape individual action potentials and determine their pattern of firing. In auditory relays, both high- and low-voltage–activated K+ channels (HVA and LVA) are critical for preservation of auditory timing cues. We examined how these channels participate in firing in the medial nucleus of the trapezoid body. Principal cells at physiological temperature were voltage clamped using spike waveforms previously recorded in response to calyceal firing. Current components were isolated by digital subtraction of traces recorded in the channel antagonists dendrotoxin-I or tetraethylammonium. During orthodromic spikes delivered at 300 and 600 Hz, both currents activated with a slight delay, peaking just after the crest of the spike. The decay of HVA was sufficiently fast to match the time course of the spike. By contrast, with 300-Hz stimuli, LVA continued to decay after the spikes reached a stable interspike potential. Although LVA currents partially inactivate during prolonged voltage steps, their peak amplitudes remained stable or increased during trains of spikelike stimuli. At 600 Hz, LVA did not fully deactivate between the spikes and therefore generated a leak current. To determine the effect of blocking LVA channels on spiking, prerecorded postsynaptic conductances were injected, with and without dendrotoxin-I. After block of LVA channels, strong synaptic conductances produced broader spikes, greater spike jitter, and prolonged depolarized states. HVA blockade with tetraethylammonium also broadened spikes but led to less error in timing. These results reveal multiple roles for LVA channels in spike repolarization and timing during synaptic activity.

Calcium transients recorded with arsenazo III in the presynaptic terminal of the squid giant synapse

1981 ◽  
Vol 212 (1187) ◽  
pp. 197-211 ◽  
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Sea Water ◽  
Light Signal ◽  
Presynaptic Terminal ◽  
Arsenazo Iii ◽  
Intracellular Ca ◽  
Squid Giant Synapse ◽  
Giant Synapse ◽  
Light Absorbance

Transient changes in free intracellular Ca 2+ concentration were monitored in the presynaptic terminal of the giant synapse of the squid, by means of the Ca 2+ -sensitive dye arsenazo III. Calibration experiments showed a linear relation between the amount of Ca 2+ injected by iontophoresis into the terminal, and the peak size of the arsenazo light absorbance record. A light signal could be detected on tetanic stimulation of the presynaptic axon bathed in sea water containing 45 mm Ca 2+ . During a 1 s tetanus the light signal rose approximately linearly, even though transmitter release declined rapidly and the light signal subsequently declined with a half-time of 2-6 s. The Ca 2+ transient elicited by single nerve impulses was recorded by signal averaging, and showed a time course very much slower than the duration of transmitter release.

scholarly journals Multiple Sources of Cholinergic Input to the Superior Olivary Complex

2021 ◽  
Vol 15 ◽  
Author(s):  
Nichole L. Beebe ◽  
Chao Zhang ◽  
R. Michael Burger ◽  
Brett R. Schofield
Keyword(s):  
Auditory System ◽  
Cholinergic Neurons ◽  
Auditory Brainstem ◽  
Cholinergic Innervation ◽  
Superior Olivary Complex ◽  
Multiple Sources ◽  
Cholinergic Modulation ◽  
Medial Nucleus ◽  
Trapezoid Body

The superior olivary complex (SOC) is a major computation center in the brainstem auditory system. Despite previous reports of high expression levels of cholinergic receptors in the SOC, few studies have addressed the functional role of acetylcholine in the region. The source of the cholinergic innervation is unknown for all but one of the nuclei of the SOC, limiting our understanding of cholinergic modulation. The medial nucleus of the trapezoid body, a key inhibitory link in monaural and binaural circuits, receives cholinergic input from other SOC nuclei and also from the pontomesencephalic tegmentum. Here, we investigate whether these same regions are sources of cholinergic input to other SOC nuclei. We also investigate whether individual cholinergic cells can send collateral projections bilaterally (i.e., into both SOCs), as has been shown at other levels of the subcortical auditory system. We injected retrograde tract tracers into the SOC in gerbils, then identified retrogradely-labeled cells that were also immunolabeled for choline acetyltransferase, a marker for cholinergic cells. We found that both the SOC and the pontomesencephalic tegmentum (PMT) send cholinergic projections into the SOC, and these projections appear to innervate all major SOC nuclei. We also observed a small cholinergic projection into the SOC from the lateral paragigantocellular nucleus of the reticular formation. These various sources likely serve different functions; e.g., the PMT has been associated with things such as arousal and sensory gating whereas the SOC may provide feedback more closely tuned to specific auditory stimuli. Further, individual cholinergic neurons in each of these regions can send branching projections into both SOCs. Such projections present an opportunity for cholinergic modulation to be coordinated across the auditory brainstem.

The Superior Paraolivary Nucleus

2018 ◽  
pp. 394-420
Author(s):  
Anna K. Magnusson ◽  
Marcelo Gómez-Álvarez
Keyword(s):  
Auditory Brainstem ◽  
Superior Olivary Complex ◽  
High Survival ◽  
Complex Sounds ◽  
Robust Detection ◽  
Medial Nucleus ◽  
Superior Paraolivary Nucleus ◽  
The Brain ◽  
Trapezoid Body

This chapter summarizes the current concepts of the superior paraolivary nucleus (SPON)—a structure embedded in the superior olivary complex in the mammalian auditory brainstem. SPON is driven by input pathways from two of the most temporally secure neurons in the brain: the octopus cells in the cochlear nucleus and the neurons of the medial nucleus of the trapezoid body. These inputs activate spiking activity that marks the onset and offset of sound, the latter based on a rebound depolarization mechanism. This makes the SPON an excellent detector of transient sound energy. Robust detection of the coarse sound pattern over time further gives SPON the capacity to track the temporal envelope of complex sounds with supreme precision. Since the SPON circuitry is constant in mammals and resilient to sensory perturbation, it indicates its high survival value. A possible neuroevolutionary role of SPON in the processing of vocalizations is discussed.

scholarly journals Presynaptic calcium currents and facilitation of serotonin release at synapses between cultured leech neurones

1989 ◽  
Vol 144 (1) ◽  
pp. 1-12
Author(s):  
R. R. Stewart ◽  
W. B. Adams ◽  
J. G. Nicholls
Keyword(s):  
Transmitter Release ◽  
Time Course ◽  
Divalent Cations ◽  
Serotonin Release ◽  
Calcium Currents ◽  
Postsynaptic Potentials ◽  
The Central Nervous System ◽  
Presynaptic Calcium ◽  
Retzius Cells

1. The role of presynaptic Ca2+ entry in facilitation of transmitter release has been analysed by voltage-clamp measurements at synapses formed in culture by Retzius and P neurones isolated from the central nervous system (CNS) of the leech. The transmitter released by Retzius cells is serotonin. 2. Synaptic transmission persisted in solutions containing raised concentrations of divalent cations, reduced concentrations of Na+, and tetraethylammonium (TEA+) and 4-AP (to block K+ currents). Ca2+ and Sr2+ were more effective in promoting transmitter release than Ba2+, as assessed by the postsynaptic potentials in P cells. The degree and time course of facilitation in Ca2+- and Sr2+-containing solutions were similar to those observed for synapses bathed in normal L-15 medium. 3. Transmitter release depended upon the amplitude and the duration of presynaptic depolarization and inward Ca2+ current. Peak Ca2+ currents and postsynaptic potentials occurred with depolarizing steps to +15 mV. Frequent or prolonged pulses depressed the postsynaptic potentials. 4. Pairs of depolarizing pulses that caused facilitation were accompanied by identical inward Ca2+ currents. These results indicate that the mechanism responsible for facilitated serotonin release must occur following Ca2+ entry and that residual Ca2+ plays a role.

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