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.

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.

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%).

Reduction of Zolpidem Sensitivity in a Freeze Lesion Model of Neocortical Dysgenesis

1999 ◽  
Vol 81 (1) ◽  
pp. 404-407 ◽  
Author(s):  
R. Anthony Defazio ◽  
John J. Hablitz
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Brain Slices ◽  
Pyramidal Cells ◽  
Benzodiazepine Receptor ◽  
Decay Time Constant ◽  
Α Subunit ◽  
Rat Neocortex

DeFazio, R. Anthony and John J. Hablitz. Reduction of zolpidem sensitivity in a freeze lesion model of neocortical dysgenesis. J. Neurophysiol. 81: 404–407, 1999. Early postnatal freeze lesions in rat neocortex produce anatomic abnormalities resembling those observed in human patients with seizure disorders. Although in vitro brain slices containing the lesion are hyperexcitable, the mechanisms of this alteration have yet to be elucidated. To test the hypothesis that changes in postsynaptic inhibitory receptors may underlie this hyperexcitability, we examined properties of γ-aminobutyric acid type A receptor (GABAAR)–mediated miniature inhibitory postsynaptic currents (mIPSCs). Recordings were obtained in layer II/III pyramidal cells located 1–2 mm lateral to the lesion. mIPSC peak amplitude and rate of rise were increased relative to nonlesioned animals, whereas decay time constant and interevent interval were unaltered. Bath application of zolpidem at a concentration (20 nM) specific for activation of the type 1 benzodiazepine receptor had no significant effect on decay time constant in six of nine cells. Exposure to higher concentrations (100 nM) enhanced the decay time constant of all cells tested ( n = 7). Because mIPSCs from unlesioned animals were sensitive to both concentrations of zolpidem, these results suggest that freeze lesions may decrease the affinity of pyramidal cell GABAARs for zolpidem. This could be mediated via a change in α-subunit composition of the GABAAR, which eliminates the type 1 benzodiazepine receptor.

Dynamics of the Firing Probability of Noisy Integrate-and-Fire Neurons

2002 ◽  
Vol 14 (9) ◽  
pp. 2057-2110 ◽  
Author(s):  
Nicolas Fourcaud ◽  
Nicolas Brunel
Keyword(s):  
Firing Rate ◽  
Time Constant ◽  
Decay Time ◽  
High Frequency ◽  
Decay Time Constant ◽  
Phase Lag ◽  
Frequency Limit ◽  
Integrate And Fire ◽  
High Frequency Limit ◽  
Decay Times

Cortical neurons in vivo undergo a continuous bombardment due to synaptic activity, which acts as a major source of noise. Here, we investigate the effects of the noise filtering by synapses with various levels of realism on integrate-and-fire neuron dynamics. The noise input is modeled by white (for instantaneous synapses) or colored (for synapses with a finite relaxation time) noise. Analytical results for the modulation of firing probability in response to an oscillatory input current are obtained by expanding a Fokker-Planck equation for small parameters of the problem—when both the amplitude of the modulation is small compared to the background firing rate and the synaptic time constant is small compared to the membrane time constant. We report here the detailed calculations showing that if a synaptic decay time constant is included in the synaptic current model, the firing-rate modulation of the neuron due to an oscillatory input remains finite in the high-frequency limit with no phase lag. In addition, we characterize the low-frequency behavior and the behavior of the high-frequency limit for intermediate decay times. We also characterize the effects of introducing a rise time to the synaptic currents and the presence of several synaptic receptors with different kinetics. In both cases, we determine, using numerical simulations, an effective decay time constant that describes the neuronal response completely.

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.

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

1992 ◽  
Vol 67 (6) ◽  
pp. 1698-1701 ◽  
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.

Inwardly Rectifying and Ca2+-Permeable AMPA-Type Glutamate Receptor Channels in Rat Neocortical Neurons

1997 ◽  
Vol 78 (5) ◽  
pp. 2592-2601 ◽  
Author(s):  
Shun-Ichi Itazawa ◽  
Tadashi Isa ◽  
Seiji Ozawa
Keyword(s):  
Glutamate Receptor ◽  
Ampa Receptor ◽  
Inward Rectification ◽  
Type I ◽  
Type Ii ◽  
Neocortical Neurons ◽  
Rat Neocortex ◽  
Type I Neuron ◽  
Inwardly Rectifying ◽  
Ampa Receptor Channels

Itazawa, Shun-Ichi, Tadashi Isa, and Seiji Ozawa. Inwardly rectifying and Ca2+-permeable AMPA-type glutamate receptor channels in rat neocortical neurons. J. Neurophysiol. 78: 2592–2605, 1997. Current-voltage ( I-V) relations and Ca2+ permeability of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)type glutamate receptor channels were investigated in neurons of rat neocortex by using the whole cell patch-clamp technique in brain slices. To activate AMPA receptor channels, kainate was used as a nondesensitizing agonist. A patch pipette was filled with solution containing 100 μM spermine to maintain the inward rectification of Ca2+-permeable AMPA receptor channels. Three types of responses to kainate were observed: type I response with outwardly rectifying I-V relation, type II response with I-V relation of marked inward rectification, and intermediate response with I-V relation of weaker inward rectification. Neurons with type I, type II and intermediate I-V relations were referred to as type I, type II, and intermediate neurons, respectively. Of a total of 223 recorded cells, 90 (40.4%) were type I, 129 (57.8%) intermediate, and 4 (1.8%) type II neurons. Properties of AMPA receptor channels were examined in the former two types of neurons. The value of PCa:PCs, the ratio of the permeability coefficients of Ca2+ and Cs+, was estimated from the reversal potentials of kainate responses in the outside-out patches bathed in Na+-free solution containing 100 mM Ca2+ according to the constant-field equation. They ranged from 0.05 to 0.10 (0.08 ± 0.02, mean ± SD, n = 8) for type I neurons and from 0.14 to 1.29 (0.60 ± 0.37, n = 11) for the intermediate neurons. There was a close correlation between the inward rectification and the Ca2+ permeability in AMPA receptor channels in these neurons. Intermediate neurons stained with biocytin were nonpyramidal cells with ellipsoidal-shaped somata. Type I neurons had either triangular- or ellipsoidal-shaped somata. Excitatory postsynaptic currents (EPSCs) recorded in both type I and intermediate neurons had 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive fast and d−2-amino-5-phosphonovalerate-sensitiveslow components. The I-V relation of the fast component exhibited inward rectification in the intermediate neuron, whereas that in the type I neuron showed slight outward rectification. The fast component of EPSCs in the intermediate neuron was suppressed more prominently (to 56 ± 15% of the control, n = 12) than that in the type I neuron (to 78 ± 6% of the control, n = 6) by bath application of 1 mM spermine. These results indicate that inwardly rectifying and Ca2+-permeable AMPA receptor channels are expressed in a population of neurons of rat neocortex and are involved in excitatory synaptic transmission.

scholarly journals Enhanced Temporal Stability of Cholinergic Hippocampal Gamma Oscillations Following Respiratory Alkalosis In Vitro

2001 ◽  
Vol 85 (5) ◽  
pp. 2063-2069 ◽  
Author(s):  
Kerstin Stenkamp ◽  
J. Matias Palva ◽  
Marylka Uusisaari ◽  
Sebastian Schuchmann ◽  
Dietmar Schmitz ◽  
...  
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Oscillation Frequency ◽  
Hippocampal Slices ◽  
Temporal Stability ◽  
Field Potential ◽  
Gamma Oscillations ◽  
Decay Time Constant ◽  
The Mean

The decrease in brain CO2 partial pressure (pCO2) that takes place both during voluntary and during pathological hyperventilation is known to induce gross alterations in cortical functions that lead to subjective sensations and altered states of consciousness. The mechanisms that mediate the effects of the decrease in pCO2 at the neuronal network level are largely unexplored. In the present work, the modulation of gamma oscillations by hypocapnia was studied in rat hippocampal slices. Field potential oscillations were induced by the cholinergic agonist carbachol under an N-methyl-D-aspartate (NMDA)-receptor blockade and were recorded in the dendritic layer of the CA3 region with parallel measurements of changes in interstitial and intraneuronal pH (pHo and pHi, respectively). Hypocapnia from 5 to 1% CO2 led to a stable monophasic increase of 0.5 and 0.2 units in pHo and pHi, respectively. The mean oscillation frequency increased slightly but significantly from 32 to 34 Hz and the mean gamma-band amplitude (20 to 80 Hz) decreased by 20%. Hypocapnia induced a dramatic enhancement of the temporal stability of the oscillations, as was indicated by a two-fold increase in the exponential decay time constant fitted to the autocorrelogram. A rise in pHi evoked by the weak base trimethylamine (TriMA) was associated with a slight increase in oscillation frequency (37 to 39 Hz) and a decrease in amplitude (30%). Temporal stability, on the other hand, was decreased by TriMA, which suggests that its enhancement in 1% CO2 was related to the rise in pHo. In 1% CO2, the decay-time constant of the evoked monosynaptic pyramidal inhibitory postsynaptic current (IPSC) was unaltered but its amplitude was enhanced. This increase in IPSC amplitude seems to significantly contribute to the enhancement of temporal stability because the enhancement was almost fully reversed by a low concentration of bicuculline. These results suggest that changes in brain pCO2 can have a strong influence on the temporal modulation of gamma rhythms.

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