scholarly journals AMPA receptor-mediated rapid EPSCs in vestibular calyx afferents

2017 ◽  
Vol 117 (6) ◽  
pp. 2312-2323 ◽  
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.

Rapid Kinetics and Inward Rectification of Miniature EPSCs in Layer I Neurons of Rat Neocortex

1997 ◽  
Vol 77 (5) ◽  
pp. 2416-2426 ◽  
Author(s):  
Fu-Ming Zhou ◽  
John J. Hablitz
Keyword(s):  
Ampa Receptor ◽  
Time Constant ◽  
Decay Time ◽  
Ampa Receptors ◽  
Decay Time Constant ◽  
Inward Rectification ◽  
Decay Times ◽  
Rat Neocortex ◽  
Layer I ◽  
Rapid Kinetics

Zhou, Fu-Ming and John J. Hablitz. Rapid kinetics and inward rectification of miniature EPSCs in layer I neurons of rat neocortex. J. Neurophysiol. 77: 2416–2426, 1997. With the use of the whole cell patch-clamp technique combined with visualization of neurons in brain slices, we studied the properties of miniature excitatory postsynaptic currents (mEPSCs) in rat neocortical layer I neurons. At holding potentials (−50 to −70 mV) near the resting membrane potential (RMP), mEPSCs had amplitudes of 5–100 pA and were mediated mostly by α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate (AMPA) receptors. Amplitude histograms were skewed toward large events. An N-methyl-d-aspartate (NMDA) component was revealed by depolarization to −30 mV or by the use of a Mg2+-free bathing solution. At RMP, averaged AMPA mEPSCs had a 10–90% rise time of ∼0.3 ms (uncorrected for instrument filtering). The decay of averaged mEPSCs was best fit by double-exponential functions in most cases. The fast, dominating component had a decay time constant of ∼1.2 ms and comprised ∼80% of the total amplitude. A small slow component had a decay time constant of ∼4 ms. Positive correlations were found between rise and decay times of both individual and averaged mEPSCs, indicative of dendritic filtering. Some large-amplitude mEPSCs and spontaneous EPSCs (recorded in the absence of tetrodotoxin) had slower kinetics, suggesting a role of asynchronous transmitter release in shaping EPSCs. The amplitudes of mEPSCs were much smaller at +60 mV than at −60 mV, indicating that synaptic AMPA-receptor-mediated currents were inwardly rectifying. These results suggest that neocortical layer I neurons receive both NMDA- and AMPA-receptor-mediated synaptic inputs. The rapid decay of EPSCs appears to be largely determined by AMPA receptor deactivation. The observed rectification of synaptic responses suggests that synaptic AMPA receptors in layer I neurons may lack GluR-2 subunits and may be Ca2+ permeable.

Amplitude and time course of spontaneous and evoked excitatory postsynaptic currents in bushy cells of the anteroventral cochlear nucleus

1996 ◽  
Vol 76 (3) ◽  
pp. 1566-1571 ◽  
Author(s):  
J. S. Isaacson ◽  
B. Walmsley
Keyword(s):  
Ampa Receptor ◽  
Time Constant ◽  
Decay Time ◽  
Cochlear Nucleus ◽  
Receptor Desensitization ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Anteroventral Cochlear Nucleus ◽  
Wide Range ◽  
Bushy Cells

1. Spontaneous and evoked excitatory postsynaptic currents (EPSCs) were recorded in slices of the rat anteroventral cochlear nucleus (AVCN) at the endbulb-bushy cell synaptic connection. 2. The amplitudes of alpha-amino-3-hydroxy-5-methy-4-isoxa-zolepropionic acid (AMPA)-receptor-mediated spontaneous EPSCs were large (54 +/- 6 pA, mean +/- SD; membrane potential = -70 mV, 22-25 degrees C) and, in the same cell, exhibited a very wide range of peak amplitudes (CM = 0.42 +/- 0.01, n - 15 cells). There was no significant correlation between rise times or decay time constants and the peak amplitudes of spontaneous EPSCs recorded in the same cell, demonstrating that electrotonic attenuation is not responsible for the large amplitude variability of spontaneous EPSCs. 3. Cyclothiazide, a potent blocker of AMPA-receptor desensitization, did not affect the amplitude of spontaneous EPSCs in AVCN bushy cells, suggesting that background desensitization of AMPA receptors is not significant in these cells. However, the decay time constant of spontaneous EPSCs was prolonged significantly (2.6-fold increase). In addition, cyclothiazide produced a marked increase (approximately 40%, n = 6 cells) in the frequency of spontaneous EPSCs, indicating a likely presynaptic site of action of this drug. 4. Cyclothiazide produced a small increase (approximately 10%, n = 7 cells) in the peak amplitude of the evoked endbulb EPSC, but this effect could be explained by the action of cyclothiazide to increase the decay time constant of the underlying quantal EPSCs in conjunction with the asynchrony of quantal transmitter release at the endbulb synapse. 5. These results indicate that neither electrotonic attenuation nor receptor desensitization are responsible for the wide range of peak amplitudes of spontaneous EPSCs in bushy cells. The large quantal variability therefore is likely to be due entirely to intrinsic fluctuations at each release site and site-to-site variability in the numbers of available receptors.

Variations in amplitude and time course of inhibitory postsynaptic currents

1986 ◽  
Vol 56 (5) ◽  
pp. 1424-1438 ◽  
Author(s):  
D. Gardner
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Time Course ◽  
Decay Time Constant ◽  
Peak Amplitude ◽  
Short Term ◽  
Presynaptic Neuron ◽  
Inhibitory Postsynaptic Currents ◽  
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.

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

2000 ◽  
Vol 84 (2) ◽  
pp. 771-779 ◽  
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%).

scholarly journals The quantal component of synaptic transmission from sensory hair cells to the vestibular calyx

2015 ◽  
Vol 113 (10) ◽  
pp. 3827-3835 ◽  
Author(s):  
Stephen M. Highstein ◽  
Mary Anne Mann ◽  
Gay R. Holstein ◽  
Richard D. Rabbitt
Keyword(s):  
Hair Cell ◽  
Time Constant ◽  
Hair Cells ◽  
Decay Time ◽  
Event Rate ◽  
Decay Time Constant ◽  
Ribbon Synapses ◽  
Diverse Species ◽  
Sensory Hair Cells ◽  
Cell Depolarization

Spontaneous and stimulus-evoked excitatory postsynaptic currents (EPSCs) were recorded in calyx nerve terminals from the turtle vestibular lagena to quantify key attributes of quantal transmission at this synapse. On average, EPSC events had a magnitude of ∼42 pA, a rise time constant of τ0 ∼229 μs, decayed to baseline with a time constant of τR ∼690 μs, and carried ∼46 fC of charge. Individual EPSCs varied in magnitude and decay time constant. Variability in the EPSC decay time constant was hair cell dependent and due in part to a slow protraction of the EPSC in some cases. Variability in EPSC size was well described by an integer summation of unitary quanta, with each quanta of glutamate gating a unitary postsynaptic current of ∼23 pA. The unitary charge was ∼26 fC for EPSCs with a simple exponential decay and increased to ∼48 fC for EPSCs exhibiting a slow protraction. The EPSC magnitude and the number of simultaneous unitary quanta within each event increased with presynaptic stimulus intensity. During tonic hair cell depolarization, both the EPSC magnitude and event rate exhibited adaptive run down over time. Present data from a reptilian calyx are remarkably similar to noncalyceal vestibular synaptic terminals in diverse species, indicating that the skewed EPSC size distribution and multiquantal release might be an ancestral property of inner ear ribbon synapses.

Excitatory postsynaptic currents and glutamate receptors in neonatal rat sympathetic preganglionic neurons in vitro

1995 ◽  
Vol 73 (4) ◽  
pp. 1503-1512 ◽  
Author(s):  
J. Krupp ◽  
P. Feltz
Keyword(s):  
Nmda Receptor ◽  
Dorsal Horn ◽  
Time Constant ◽  
Decay Time ◽  
Rise Time ◽  
Total Charge ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Lateral Funiculus ◽  
Relationship Of

1. We obtained whole cell patch-clamp recordings from visually identified sympathetic preganglionic neurons (SPNs) in thin (200-300 microns) transverse spinal cord slices of neonatal rats (1-14 days postnatal). Exogenous application of glutamate (100 microM), N-methyl-D-aspartate (NMDA; 100 microM), kainate (100 microM), quisqualate (1 microM), and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA; 50 microM) induced inward currents at a holding potential of -30 mV. 2. Excitatory postsynaptic currents (EPSCs) were evoked by electrical stimulation either in the dorsal horn or the lateral funiculus. They reversed at 1.2 +/- 4.6 (SD) mV and could in most cases (49 of 51) be separated into two components. 3. In the presence of DL-2-amino-5-phosphonovalerate (10-40 microM) the current-voltage (I-V) relationship of the remaining EPSC was linear. When stimulated in the lateral funiculus, its rise time (10-90%) and the time constant of the monoexponential decay were 1.6 +/- 1.0 and 5.5 +/- 2.7 ms, respectively. By contrast, when stimulated in the dorsal horn, this component had a rise time (10-90%) of 3.0 +/- 0.8 ms and a decay time constant of 13.7 +/- 7.6 ms. 4. We studied the NMDA receptor-mediated component of the EPSCs after superfusion of 6-cyano-7-nitroquinoxaline-2,3-dione (5 microM). The I-V relationship of this component had a region of negative slope conductance between -30 and -80 mV, which was abolished in Mg(2+)-free saline. The rise time (10-90%) ranged from 3.3 to 9.5 ms and the decay was biexponential. Both decay time constants increased with depolarization. Mg(2+)-free saline reduced this voltage sensitivity. 5. At a membrane potential of -80 mV and in 1 mM extracellular Mg2+, the NMDA receptor-mediated component represented 74.8 +/- 11.2% of the total charge carried by the EPSCs evoked by stimulation in the dorsal horn. In contrast, when stimulated from the lateral funiculus, 28.9 +/- 18.9% of the total charge carried during the EPSC was mediated by the NMDA receptor-mediated component. The contribution of the NMDA receptor-mediated component increased in both cases with depolarization. In addition, in 2 of 18 SPNs the EPSC evoked in the dorsal horn was exclusively carried by NMDA receptors. 6. We conclude that L-glutamate or a related substance mediates the fast excitatory input onto SPNs. Viscerosomatic and supraspinal inputs form synapses with different topographical locations on the SPN.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Measurement of Decay Time Constant of Shielding Current in ITER-TF Joint Samples

2021 ◽  
Vol 1857 (1) ◽  
pp. 012013
Author(s):  
S Imagawa ◽  
H Kajitani ◽  
T Obana ◽  
S Takada ◽  
S Hamaguchi ◽  
...  
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Decay Time Constant

Rapidly Deactivating AMPA Receptors Determine Excitatory Synaptic Transmission to Interneurons in the Nucleus Tractus Solitarius From Rat

1997 ◽  
Vol 78 (1) ◽  
pp. 82-91 ◽  
Author(s):  
Stefan Titz ◽  
Bernhard U. Keller
Keyword(s):  
Synaptic Transmission ◽  
Ampa Receptor ◽  
Decay Time ◽  
Ampa Receptors ◽  
Time Course ◽  
Nucleus Tractus Solitarius ◽  
Synaptic Cleft ◽  
Excitatory Synaptic Transmission ◽  
Membrane Properties ◽  
Time Constants

Titz, Stefan and Bernhard U. Keller. Rapidly deactivating AMPA receptors determine excitatory synaptic transmission to interneurons in the nucleus tractus solitarius from rat. J. Neurophysiol. 78: 82–91, 1997. Excitatory synaptic transmission was investigated in interneurons of the parvocellular nucleus tractus solitarius (pNTS) by performing patch-clamp experiments in thin slice preparations from rat brain stem. Stimulation of single afferent fibers evoked excitatory postsynaptic currents (EPSCs) mediated by glutamate receptors of the dl-α-amino-3-hydroxy-5-methylisoxazole-propionic acid (AMPA) and N-methyl-d-aspartate types. AMPA-receptor-mediated EPSCs displayed decay time constants of 3.5 ± 1.2 (SD) ms (13 cells), which were slow compared with EPSC decay time constants in neurons of the cerebellum or hippocampus. Slow EPSC decay was not explained by dendritic filtering, because the passive membrane properties of pNTS interneurons provided favorable voltage-clamp conditions. Also, the slowness of EPSC decay did not result from slow deactivation of AMPA receptors (0.7 ± 0.2 ms, 5 cells), which was investigated during rapid application of agonist to outside-out patches. Comparison of AMPA receptor kinetics with EPSC decay time constants suggested that the slow time course of EPSCs resulted from the prolonged presence of glutamate in the synaptic cleft.

scholarly journals Fast, Slow, and Steady-State Effects of Contralateral Acoustic Activation of the Medial Olivocochlear Efferent System in Awake Guinea Pigs: Action of Gentamicin

1997 ◽  
Vol 78 (4) ◽  
pp. 1826-1836 ◽  
Author(s):  
Deise Lima da Costa ◽  
Anne Chibois ◽  
Jean-Paul Erre ◽  
Christophe Blanchet ◽  
RENAUD CHARLET de Sauvage ◽  
...  
Keyword(s):  
Steady State ◽  
Time Constant ◽  
Decay Time ◽  
Guinea Pigs ◽  
Round Window ◽  
Broadband Noise ◽  
Decay Time Constant ◽  
Efferent System ◽  
Medial Olivocochlear ◽  
Medial Olivocochlear Efferent System

Lima da Costa, Deise, Anne Chibois, Jean-Paul Erre, Christophe Blanchet, Renaud Charlet de Sauvage, and Jean-Marie Aran. Fast, slow, and steady-state effects of contralateral acoustic activation of the medial olivocochlear efferent system in awake guinea pigs: action of gentamicin. J. Neurophysiol. 78: 1826–1836, 1997. The function of the medial olivocochlear efferent system was observed in awake guinea pigs by recording, in the absence of ipsilateral external acoustic stimulation, the ensemble background activity (EBA) of the VIIIth nerve from an electrode chronically implanted on the round window of one ear. The EBA was measured by calculating the power value of the round window signal in the 0.5- to 2.5-kHz band after digital or analog (active) filtering. This EBA was compared with and without the addition of a low-level broadband noise to the opposite ear. The contralateral broadband noise (CLBN, 55 dB SPL) induced, via the efferent system, a decrease (suppression) of this EBA. With the use of noise bursts of different durations, two components in this suppression could be observed. After the onset of a 1-s CLBN, the power value of the EBA decreased rapidly by 38.0 ± 4.2% (mean ± SD, n = 3), with a latency of <10 ms and a decay time constant of 13.1 ± 1.0 ms (fast effect). At the offset of the 1-s CLBN, EBA came back to prestimulation values with a similar latency and a time constant of 15.5 ± 2.9 ms. During longer CLBN stimulation (≥1 min), EBA presented, after the fast decrease, an additional, slower decrease of 15.6 ± 3.1%, with a delay of 9.8 ± 1.3 s and a decay time constant of 16.1 ± 5.0 s ( n = 12, slow effect), and then remained remarkably constant for as long as observed, i.e., >2 h (steady state). The average global suppression was thus up to 47.8 ± 5.8% of the basal, pre-CLBN-stimulation EBA value. At the offset of the CLBN, EBA returned to pre-CLBN level with fast and slow phases, with, for the slow phase, no delay and a time constant of 32.1 ± 8.1 s. Fast and slow changes in EBA power values were observed after a single injection of gentamicin (GM) at different doses (150, 200, and 250 mg/kg). At 150 and 200 mg/kg, GM progressively and reversibly blocked the rapid effect, but the slow component of the efferent medial suppression remained remarkably unchanged. However, at higher doses both the fast and slow suppressions were totally yet still reversibly blocked. These observations indicate that the medial olivocochlear efferent system exerts sustained influences on outer hair cells and that this effect develops in two different steps that may have different basic cellular mechanisms.

Properties of spontaneous inhibitory synaptic currents in cultured rat spinal cord and medullary neurons

1996 ◽  
Vol 76 (1) ◽  
pp. 448-460 ◽  
Author(s):  
C. A. Lewis ◽  
D. S. Faber
Keyword(s):  
Spinal Cord ◽  
Time Constant ◽  
Decay Time ◽  
Cultured Cells ◽  
Decay Time Constant ◽  
Inhibitory Synapses ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Receptor ◽  
Decay Times ◽  
Medullary Neurons

1. To identify the type(s) and properties of inhibitory postsynaptic receptor(s) involved in synaptic transmission in cultured rat embryonic spinal cord and medullary neurons, we have used whole cell patch-clamp techniques to record miniature inhibitory postsynaptic currents (mIPSCs) in the presence of tetrodotoxin, DL-2-amino-5-phosphonovaleric acid, and 6-cyano-7-nitroquinoxaline-2,3-dione. 2. The mIPSCs recorded from both spinal cord and medullary neurons had skewed amplitude distributions. 3. The glycinergic antagonist strychnine and the GABAergic antagonist bicuculline each decreased both the frequency and mean peak amplitudes of mIPSCs. We conclude that both glycine and gamma-aminobutyric acid (GABA) are neurotransmitters at inhibitory synapses in our cultured cells. 4. Most (approximately 96-97%) mIPSCs decay with single-exponential time constants, and decay time distributions were consistently best fitted by the sum of four Gaussians with decay constants as follows: D1 = 5.8 +/- 0.1 (SE) ms (n = 63), D2 = 12.2 +/- 0.2 ms (n = 61), D3 = 23.2 +/- 0.4 ms (n = 54), and D4 = 44.7 +/- 1.0 ms (n = 57). We conclude that the four classes of decay times represent kinetically different inhibitory postsynaptic receptor populations. 5. Strychnine and bicuculline usually had one of two different effects on the mIPSC decay time constant distributions; either selective decreases in the frequency of mIPSCs with decay times in certain classes (i.e., the D1 class was reduced by bicuculline, the D2 class by strychnine, and the D3 and D4 classes by both antagonists) or a nonselective depression in the frequency of mIPSCs with decay times in all four classes. The particular effect observed in a given neuron was correlated with the presence or absence of ATP and guanosine 5'-triphosphate (GTP) in the patch pipette. Namely, in 71% of the antagonist applications where the pipette contained ATP and GTP, the result was a nonselective decrease in mIPSCs in all decay time constant classes. Conversely, in 54% of the antagonist applications in their absence, the result was a selective decrease in the frequency of mIPSCs in specific decay time constant classes. 6. In some experiments, mIPSCs reappeared in antagonist solution after an essentially complete block. Recovery from block in the continued presence of antagonist was never observed in the absence of ATP and GTP (8 neurons), and, at the same time, 5 of 9 neurons patched with ATP and GTP in the pipette did show recovery (56%).

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