Variations in amplitude and time course of inhibitory postsynaptic currents

In order to examine the relative contributions of changes in amplitude and time course to synaptic plasticity, variations in peak amplitude and time constant of decay have been analyzed from inhibitory postsynaptic currents (PSC) recorded in voltage-clamped Aplysia buccal ganglia neurons. In these cells, synaptic currents with single time constant decay can be recorded with low noise under well-controlled space clamp. Over a population of 36 neurons, duration was more narrowly distributed than amplitude, but each varied. The coefficient of variation (CV) was 0.21 for decay time constant (tau) and 0.87 for peak conductance (g peak). Population variances are larger than can be accounted for by such variables as temperature and noise amplitude, suggesting that functional modifications alter each of these determinants of synaptic effectiveness over the long term. Recordings of up to several hundred PSC in each of 16 neurons show that both PSC amplitude and time course recorded in a single cell can vary independently over short time spans. Decay remained single exponential as time course changed. CV for tau averaged 0.11; CV for g peak was 0.19. Variability of tau was not an artifact of amplitude; CV was relatively uncorrelated with current amplitudes or sample size. Smoothing and adding excess noise to each individual PSC of a set produced only small changes to CV, showing that variability was not an artifact of noise. Several specific manipulations of the presynaptic neuron altered both PSC amplitude and time course. Tetanic stimulation of the presynaptic neuron produced short-term potentiation of both amplitude and time course of subsequent PSCs. Peak amplitude was increased by 80%; tau by 12%. Reducing interspike intervals from 10 to 1 s produced habituation of both amplitude and time course, with g peak decreasing by 35 to 40% and tau by 10%. Conditioning DC depolarization of the presynaptic neuron enhanced PSC amplitude with little effect on decay time constant. Although short-term plastic changes affect PSC amplitude more than duration, each is alterable. Parallel changes in both can synergistically alter synaptic charge transfer, and therefore efficacy. Similar mechanisms may produce larger long-term differences seen between neurons.

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Postsynaptic Receptor Occupancy During Evoked Transmission at Striatal GABAergic Synapses In Vitro

Journal of Neurophysiology ◽

10.1152/jn.2000.84.2.771 ◽

2000 ◽

Vol 84 (2) ◽

pp. 771-779 ◽

Cited By ~ 8

Author(s):

Eva Rumpel ◽

Jan C. Behrends

Keyword(s):

Time Constant ◽

Decay Time ◽

Rise Time ◽

Receptor Occupancy ◽

Decay Time Constant ◽

Peak Amplitude ◽

Postsynaptic Currents ◽

Quantal Size ◽

Convolution Model ◽

Quantal Responses

The effect of benzodiazepines (BZs) on GABAA-ergic synaptic responses depends on the control receptor occupancy: the BZ-induced enhancement of receptor affinity can lead to greater peak amplitudes of quantal responses only when, under normal conditions, receptors are not fully saturated at peak. Based on this fact, receptor occupancy at the peak of spontaneous miniature inhibitory postsynaptic currents (mIPSCs) has been assessed in various mammalian neuronal preparations. To use the same principle with compound (or multiquantal), action potential–evoked IPSCs, complications introduced by quantal asynchrony in conjunction with the BZ-induced increase in the decay time of the quantal responses have to be overcome. We used a simple analytic convolution model to calculate expected changes in the rise time and amplitude of postsynaptic currents when the decay time constant, but not the peak amplitude, of the underlying quantal responses is increased, this being the expected BZ effect at saturated synapses. Predictions obtained were compared with the effect of the BZ flunitrazepam on IPSCs recorded in paired pre- and postsynaptic whole cell voltage-clamp experiments on striatal neurons in cell culture. In 22 pairs, flunitrazepam (500 nM) reliably prolonged the decay of IPSCs (49 ± 19%, mean ± SE) and in 18 of 22 cases produced an enhancement in their peak amplitude that varied markedly between 3 and 77% of control (26.0 ± 5.3%). The corresponding change in rise time, however (+0.38 ± 0.11 ms, range −0.8 to +1.3 ms) was far smaller than calculated for the observed changes in peak amplitude assuming fixed quantal size. Because therefore an increase in quantal size is required to explain our findings, postsynaptic GABAA receptors were most likely not saturated during impulse-evoked transmission at these unitary connections. The peak amplitudes of miniature IPSCs in these neurons were also increased by flunitrazepam (500 nM, +26.8 ± 6.6%), and their decay time constant was increased by 26.3 ± 7.3%. Using these values in our model led to a slight overestimate of the change in compound IPSC amplitude (+28 to +30%).

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Effects of the GABA uptake inhibitor tiagabine on inhibitory synaptic potentials in rat hippocampal slice cultures

Journal of Neurophysiology ◽

10.1152/jn.1992.67.6.1698 ◽

1992 ◽

Vol 67 (6) ◽

pp. 1698-1701 ◽

Cited By ~ 144

Author(s):

S. M. Thompson ◽

B. H. Gahwiler

Keyword(s):

Time Constant ◽

Decay Time ◽

Time Course ◽

Hippocampal Slice ◽

Decay Time Constant ◽

Gabab Receptors ◽

Gaba Uptake ◽

Whole Cell ◽

Synaptic Potentials ◽

Hippocampal Slice Cultures

1. The effects of the gamma-aminobutyric acid (GABA) uptake blocker tiagabine on inhibitory synaptic potentials (IPSPs) were examined with microelectrode and whole-cell recording from CA3 pyramidal cells in rat hippocampal slice cultures. 2. Tiagabine (10-25 microM) greatly prolonged the duration of monosynaptic IPSPs elicited in the presence of excitatory amino acid antagonists but had no effect on their amplitude. Part of the prolonged time course resulted from a GABAB receptor-mediated component that was not detectable under control conditions. 3. The mean decay time constant of the underlying GABAA receptor-mediated synaptic current was increased from 16 to 250 ms. Spontaneous miniature IPSPs recorded with whole-cell clamp were unaffected by tiagabine. Pentobarbital sodium, in contrast, increased the decay time constant of both evoked and spontaneous GABAA-mediated currents. 4. Tiagabine (25 microM) inhibited spontaneous and evoked epileptiform bursting induced by increasing the extracellular potassium concentration to 8 mM. 5. We conclude that GABA uptake plays a significant role in determining the time course of evoked IPSPs and also limits the likelihood that GABAB receptors are activated.

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Paired individual and mean postsynaptic currents recorded in four-cell networks of Aplysia

Journal of Neurophysiology ◽

10.1152/jn.1990.63.5.1226 ◽

1990 ◽

Vol 63 (5) ◽

pp. 1226-1240 ◽

Cited By ~ 6

Author(s):

D. Gardner

Keyword(s):

Decay Time ◽

Time Course ◽

Current Amplitude ◽

Postsynaptic Neuron ◽

Synaptic Current ◽

Presynaptic Neuron ◽

Mean Values ◽

Postsynaptic Currents ◽

Cell Networks ◽

Presynaptic Neurons

1. Presynaptic neurons B4 and B5 of Aplysia buccal ganglia produce similar inhibitory postsynaptic currents (PSCs) in several postsynaptic follower cells. Two previous papers have characterized the variability of synaptic current amplitude and decay time both for individual PSCs and also for mean values characterizing synapses and have compared PSC amplitude and time course at different synapses sharing a common presynaptic or postsynaptic neuron. 2. To distinguish similarity in synaptic current amplitude or decay introduced by a common pre- or postsynaptic neuron from similarity because of factors common to the particular ganglion or animal, paired synapses were analyzed in four-cell networks in which each of two identified presynaptic neurons produces similar PSCs in each of two postsynaptic cells. Pairing the same synaptic data by common presynaptic or postsynaptic neuron tests if the presynaptic or postsynaptic element partially specifies a parameter; cross-pairing controls for more global factors. Paired values of peak conductance gpeak and decay time constant tau were compared for both individual sequential PSCs and for averages characterizing synapses. Analyses of individual PSCs examine processes affecting synaptic plasticity on a time scale of seconds to minutes, while average values compare more slowly varying factors. 3. Peak amplitudes were compared between individual PSCs in each of 24 paired sets. Correlations of gpeak fluctuations were significantly larger for PSCs produced by the same presynaptic neuron than for postsynaptic or cross pairings (P less than 0.05), consistent with partially correlated fluctuations in transmitter release at different presynaptic terminals. 4. Firing rates of individual presynaptic neurons were modulated to induce variability of test PSCs. These manipulations altered synaptic peak amplitudes in paired postsynaptic neurons, although not to the same degree. Manipulation of a single presynaptic neuron modulated input from that neuron alone to common postsynaptic cells without any effect on input from the paired presynaptic neuron. When fluctuations in the amplitude of gpeak were examined in runs incorporating presynaptic modulation, correlations were strong for sets of PSCs sharing a common presynaptic neuron (R = 0.87), significantly greater (P less than 0.001) than for other pairings. 5. In contrast to the partial presynaptic specification of fluctuations of individual PSCs, values of synaptic amplitude and time course averaged over 21-132 PSCs at a given synapse reflect postsynaptic determinants. Mean values of gpeak characterizing synapses paired by common postsynaptic cell are highly similar (P = 0.0001), in contrast to the lack of similarity seen when the same data are presynaptically (P = 0.11) or cross (P = 0.36) paired.(ABSTRACT TRUNCATED AT 400 WORDS)

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Choline acts as agonist and blocker for Aplysia cholinergic synapses

Journal of Neurophysiology ◽

10.1152/jn.1984.51.1.1 ◽

1984 ◽

Vol 51 (1) ◽

pp. 1-15 ◽

Cited By ~ 7

Author(s):

D. Gardner ◽

R. L. Ruff ◽

R. L. White

Keyword(s):

Time Constant ◽

Decay Time ◽

Time Course ◽

Voltage Dependence ◽

Partial Agonist ◽

Outward Current ◽

Decay Time Constant ◽

Inhibitory Synapses ◽

Cholinesterase Inhibition ◽

Current Component

Several identified neurons of the Aplysia buccal ganglia respond to choline. Iontophoretic applications of either choline or acetylcholine (ACh) to voltage-clamped inhibitory follower neurons produce similar currents. Peak amplitudes of choline responses were 10-100% of ACh responses on the same cell. Choline currents were curare blockable and reversed at -69 +/- 2 mV, within 1 mV of postsynaptic current (IPSC) reversal. Application of 1 mM choline to the bath produces more prolonged effects than an initial conductance change. Choline depressed IPSC amplitude by 42 +/- 5% and prolonged IPSC decay time constant by 25 +/- 7%. The slowing was reversible but the depression was not. Use of choline as a Na substitute may therefore involve unexpected partial agonist action; even where conductance changes are transient or inapparent, choline may alter synaptic responses. Bath choline had variable effects on cholinergic self-inhibitory synapses, blocking in six trials but not in three others. Voltage clamping cells BL and BR7, in which monosynaptic cholinergic PSPs are diphasic, reveals underlying early inward and late outward currents. Choline activates only the late outward current component. Correspondingly, bath choline blocks only the late outward component, as does eserine and ACh. This block is not seen with neostigmine, and so is unlikely to be related to cholinesterase inhibition. The early inward current component, revealed by block of the late component by choline or ACh, decays exponentially. Decay time constant is exponentially dependent on membrane potential over the range -20 to -100 mV, with 63-mV depolarization speeding decay e-fold. Eserine prolongs decay and steepens voltage dependence. The late outward component decays with voltage-independent time constant of 48 +/- 5 ms. Both the time integral of synaptic conductance and the ratio of synaptic charge transfer to peak synaptic current of the early inward component of the cell 7 response are reduced by depolarization. Voltage-dependent duration thus combines with reduced driving force in diminishing the excitatory effect of this component at depolarized levels, allowing the inhibitory component to predominate. In this diphasic synapse, voltage dependence of the time course of one component thus serves an easily identified function.

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Tetanic Stimulation Induces Short-Term Potentiation of Inhibitory Synaptic Activity in the Rostral Nucleus of the Solitary Tract

Journal of Neurophysiology ◽

10.1152/jn.1998.79.2.595 ◽

1998 ◽

Vol 79 (2) ◽

pp. 595-604 ◽

Cited By ~ 28

Author(s):

Gintautas Grabauskas ◽

Robert M. Bradley

Keyword(s):

Time Constant ◽

Decay Time ◽

High Frequency ◽

Synaptic Activity ◽

Decay Time Constant ◽

Tetanic Stimulation ◽

Solitary Tract ◽

Short Term ◽

Term Potentiation ◽

Rostral Nucleus

Grabauskas, Gintautas and Robert M. Bradley. Tetanic stimulation induces short-term potentiation of inhibitory synaptic activity in the rostral nucleus of the solitary tract. J. Neurophysiol. 79: 595–604, 1998. Whole cell recordings from neurons in the rostral nucleus of the solitary tract (rNST) were made to explore the effect of high-frequency tetanic stimulation on inhibitory postsynaptic potentials (IPSPs). IPSPs were elicited in the rNST by local electrical stimulation after pharmacological blockade of excitatory synaptic transmission. Tetanic stimulation at frequencies of 10–30 Hz resulted in sustained hyperpolarizing IPSPs that had a mean amplitude of −68 mV. The hyperpolarization resulted in a decrease in neuronal input resistance and was blocked by the γ-aminobutyric acid-A (GABAA) antagonist bicuculline. For most of the neurons ( n = 87/102), tetanic stimulation resulted in a maximum hyperpolarization immediately after initiation of the tetanic stimulation, but for some neurons the maximum was achieved after three or more consecutive shock stimuli in the tetanic train of stimuli. When the extracellular Ca2+ concentration was reduced, the maximum IPSP amplitude was reached after several consecutive shock stimuli in the tetanic train for all neurons. Tetanic stimulation at frequencies of 30 Hz and higher resulted in IPSPs that were not sustained but decayed to a more positive level of hyperpolarization. In some neurons the decay was sufficient to become depolarizing and resulted in a biphasic IPSP. It was possible to evoke this biphasic IPSP in all the neurons tested if the cells were hyperpolarized to −75 to −85 mV. The ionic mechanism of the depolarizing IPSPs was examined and was found to be due to an elevation of the extracellular K+ concentration and accumulation of intracellular Cl−. Tetanic stimulation increased the mean 80-ms decay time constant of a single shock–evoked IPSP up to 8 s. The length of the IPSP decay time constant was dependent on the duration and frequency of the tetanic stimulation as well as the extracellular Ca2+ concentration. Afferent sensory input to the rNST consists of trains of relatively high-frequency spike discharges similar to the tetanic stimulation frequencies used to elicit the IPSPs in the brain slices. Thus the short-term changes in inhibitory synaptic activity in the slice preparation probably occur in vivo and may play a key role in taste processing by facilitating synaptic integration.

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Different mechanisms regulate IPSC kinetics in early postnatal and juvenile hippocampal granule cells

Journal of Neurophysiology ◽

10.1152/jn.1996.76.6.3983 ◽

1996 ◽

Vol 76 (6) ◽

pp. 3983-3993 ◽

Cited By ~ 71

Author(s):

A. Draguhn ◽

U. Heinemann

Keyword(s):

Time Constant ◽

Decay Time ◽

Time Course ◽

Granule Cells ◽

Brain Slices ◽

Decay Time Constant ◽

Gaba Uptake ◽

Gamma Aminobutyric Acid ◽

Current Decay ◽

Mean Current

1. Monosynaptic inhibitory postsynaptic currents (IPSCs) were recorded from early postnatal and juvenile dentate granule cells in rat brain slices at room temperature. The focally evoked currents were mediated by gamma-aminobutyric acid-A (GABAA) receptors. 2. IPSCs were characterized by a steep rising phase and a slower, monoexponential decay time course. The decay time constant was potential dependent and average values ranged from 33 ms at a holding potential of -60 mV to 58 ms at a holding potential of +40 mV. 3. IPSCs were studied in tissue from animals between postnatal day (p) 3 and p25. All kinetic parameters as well as the mean current amplitude were unchanged during this ontogenetic period. 4. In juvenile granule cells from animals aged 13–16 days, addition of the GABA uptake blocker (R)-N-[4,4-bis (3-methyl-2-thienyl) but-3-en1-yl] nipecotic acid (tiagabine) (10 microM) prolonged the decaying phase of the IPSCs. The current decay remained monoexponential but the time constant increased to 250% of control values. Mean current amplitudes remained largely unchanged. 5. In contrast, tiagabine had no effect on IPSCs in early postnatal tissue. The decay time constant remained unchanged in cells recorded from animals aged p4-p6. Other uptake blockers were also ineffective during the first postnatal week, whereas beta-alanine, NNC-711, and L-2,3-diaminoproprionic acid enhanced the decay time constant in the older tissue (p13-p16). 6. Hypoosmolaric extracellular solution was applied to restrict the extracellular space. In juvenile tissue (p13-p16), IPSCs were not affected by this treatment, whereas early postnatal granule cells (p4-p6) displayed clearly prolonged IPSC decay time constants (165% of control). 7. We conclude that the mechanism governing the kinetics of evoked IPSCs in granule cells changes during ontogenesis. Whereas in early postnatal tissue the transmitter leaves the postsynaptic site by diffusion, GABA uptake becomes time limiting after 2 wk of postnatal development.

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Zinc and Zolpidem Modulate mIPSCs in Rat Neocortical Pyramidal Neurons

Journal of Neurophysiology ◽

10.1152/jn.1998.80.4.1670 ◽

1998 ◽

Vol 80 (4) ◽

pp. 1670-1677 ◽

Cited By ~ 30

Author(s):

Tony Defazio ◽

John J. Hablitz

Keyword(s):

Time Constant ◽

Decay Time ◽

Pyramidal Neurons ◽

Brain Slices ◽

Pyramidal Cells ◽

Decay Time Constant ◽

Peak Amplitude ◽

Dependent Manner ◽

Interevent Interval ◽

Neocortical Pyramidal Neurons

DeFazio, Tony and John J. Hablitz. Zinc and zolpidem modulate mIPSCs in rat neocortical pyramidal neurons. J. Neurophysiol. 80: 1670–1677, 1998. Pharmacological modulation of γ-aminobutyric acid-A (GABAA) receptors can provide important information on the types of subunits composing these receptors. In recombinant studies, zinc more potently inhibits αβ subunits compared with the αβγ combination, whereas modulation by nanomolar concentrations of the benzodiazepine type 1-selective agonist zolpidem is conferred by the α1βγ2 subunit combination. We examined four properties of miniature inhibitory postsynaptic currents (mIPSCs) from identified necortical pyramidal cells in rat brain slices: decay time constant, peak amplitude, rate of rise, and interevent interval. Exposure to 50 μM zinc reduced the decay time constant, peak amplitude, and rate of rise with no effect on interevent interval. Zolpidem enhanced mIPSCs in a concentration-dependent manner. Both 20 and 100 nM zolpidem increased the decay time constants of mIPSCs. In some cells, both peak amplitude and rate of rise were also enhanced. All cells treated with zinc were also responsive to zolpidem. These results show that neocortical pyramidal cells have a population of GABAA receptors sensitive to both zinc and zolpidem.

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Frequency-Dependent Properties of Inhibitory Synapses in the Rostral Nucleus of the Solitary Tract

Journal of Neurophysiology ◽

10.1152/jn.00963.2001 ◽

2003 ◽

Vol 89 (1) ◽

pp. 199-211 ◽

Cited By ~ 19

Author(s):

Gintautas Grabauskas ◽

Robert M. Bradley

Keyword(s):

Test Stimulus ◽

Time Constant ◽

Decay Time ◽

Time Course ◽

Synaptic Cleft ◽

Nerve Fibers ◽

Single Stimulus ◽

Decay Time Constant ◽

Solitary Tract ◽

Paired Pulse

To explore the parameters that define the characteristics of either inhibitory postsynaptic potentials (IPSP) or currents (IPSC) in the gustatory nucleus of the solitary tract (rNST), whole cell patch-clamp recordings were made in horizontal brain stem slices of newborn rats. Neurons were labeled with biocytin to confirm both their location and morphology. IPSPs or IPSCs were evoked by delivering either single, paired-pulse, or tetanic stimulus shocks (0.1-ms duration) via a bipolar stimulating electrode placed on the rNST. Pure IPSP/IPSCs were isolated by the use of glutamate receptor antagonists. For 83% of the single-stimulus-evoked IPSCs, the decay time course was fitted with two exponentials having average time constants of 38 and 181 ms, respectively, while the remainder could be fitted with one exponential of 59 ms. Paired-pulse stimulation resulted in summation of the amplitude of the conditioning and test-stimulus-evoked IPSCs. The decay time course of the test-stimulus-evoked IPSC was slower when compared to the decay time of the conditioning stimulus IPSC. Repeated stimulation resulted in an increase in the decay time of the IPSP/Cs where each consecutive stimulus contributed to prolongation of the decay time constant. Most of the IPSP/Cs resulting from a 1-s ≥ 30-Hz tetanic stimulus exhibited an S-shaped decay time course where the amplitude of the IPSP/Cs after termination of the stimulus was initially sustained before starting to decay back to the resting membrane potential. Elevation of extracellular Ca2+concentration 10 mM resulted in an increase in the amplitude and decay time of single-stimulus shock-evoked IPSP/Cs. The benzodiazepine GABAA receptor modulator diazepam increased the decay time of single-stimulus shock-evoked IPSCs. However, application of diazepam did not affect the decay time of tetanic-stimulation-evoked IPSP/Cs. These results suggest that the decay time of single-stimulus-evoked IPSCs is defined either by receptor kinetics or neurotransmitter clearance from the synaptic cleft or both, while the decay time course of the tetanic stimulus evoked IPSP/Cs is defined by neurotransmitter diffusion from the synaptic cleft. During repetitive stimulation, neurotransmitter accumulates in the synaptic cleft prolonging the decay time constant of the IPSCs. High-frequency stimulation elevates the GABA concentration in the synaptic cleft, which then oversaturates the postsynaptic receptors, and, as a consequence, after termination of the tetanic stimulus, the amplitude of IPSP/Cs is sustained resulting in an S shaped decay time course. This activity-dependent plasticity at GABAergic synapses in the rNST is potentially important in the encoding of taste responses because the dynamic range of stimulus frequencies that result in synaptic plasticity (0–70 Hz) corresponds to the breadth of frequencies that travels via afferent gustatory nerve fibers in response to taste stimuli.

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AMPA receptor-mediated rapid EPSCs in vestibular calyx afferents

Journal of Neurophysiology ◽

10.1152/jn.00394.2016 ◽

2017 ◽

Vol 117 (6) ◽

pp. 2312-2323 ◽

Cited By ~ 6

Author(s):

Matthew E. Kirk ◽

Frances L. Meredith ◽

Timothy A. Benke ◽

Katherine J. Rennie

Keyword(s):

Ampa Receptor ◽

Time Constant ◽

Hair Cells ◽

Decay Time ◽

Ampa Receptors ◽

Channel Blocker ◽

Decay Time Constant ◽

Type I ◽

Excitatory Postsynaptic Currents ◽

Postsynaptic Currents

In the vestibular periphery neurotransmission between hair cells and primary afferent nerves occurs via specialized ribbon synapses. Type I vestibular hair cells (HCIs) make synaptic contacts with calyx terminals, which enclose most of the HCI basolateral surface. To probe synaptic transmission, whole cell patch-clamp recordings were made from calyx afferent terminals isolated together with their mature HCIs from gerbil crista. Neurotransmitter release was measured as excitatory postsynaptic currents (EPSCs) in voltage clamp. Spontaneous EPSCs were classified as simple or complex. Simple events exhibited a rapid rise time and a fast monoexponential decay (time constant < 1 ms). The remaining events, constituting ~40% of EPSCs, showed more complex characteristics. Extracellular Sr2+ greatly increased EPSC frequency, and EPSCs were blocked by the AMPA receptor blocker NBQX. The role of presynaptic Ca2+ channels was assessed by application of the L-type Ca2+ channel blocker nifedipine (20 µM), which reduced EPSC frequency. In contrast, the L-type Ca2+ channel opener BAY K 8644 increased EPSC frequency. Cyclothiazide increased the decay time constant of averaged simple EPSCs by approximately twofold. The low-affinity AMPA receptor antagonist γ-d-glutamylglycine (2 mM) reduced the proportion of simple EPSCs relative to complex events, indicating glutamate accumulation in the restricted cleft between HCI and calyx. In crista slices EPSC frequency was greater in central compared with peripheral calyces, which may be due to greater numbers of presynaptic ribbons in central hair cells. Our data support a role for L-type Ca2+ channels in spontaneous release and demonstrate regional variations in AMPA-mediated quantal transmission at the calyx synapse. NEW & NOTEWORTHY In vestibular calyx terminals of mature cristae we find that the majority of excitatory postsynaptic currents (EPSCs) are rapid monophasic events mediated by AMPA receptors. Spontaneous EPSCs are reduced by an L-type Ca2+ channel blocker and notably enhanced in extracellular Sr2+. EPSC frequency is greater in central areas of the crista compared with peripheral areas and may be associated with more numerous presynaptic ribbons in central hair cells.

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