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

1998 ◽  
Vol 79 (2) ◽  
pp. 595-604 ◽  
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.

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.

Analysis of Excitatory and Inhibitory Spontaneous Synaptic Activity in Mouse Retinal Ganglion Cells

1998 ◽  
Vol 80 (3) ◽  
pp. 1327-1340 ◽  
Author(s):  
Ning Tian ◽  
Thomas N. Hwang ◽  
David R. Copenhagen
Keyword(s):  
Retinal Ganglion Cells ◽  
Time Constant ◽  
Decay Time ◽  
Ganglion Cells ◽  
Glycine Receptor ◽  
Synaptic Activity ◽  
Decay Time Constant ◽  
Retinal Ganglion ◽  
Synaptic Inputs ◽  
Perforated Patch

Tian, Ning, Thomas N. Hwang, and David R. Copenhagen. Analysis of excitatory and inhibitory spontaneous synaptic activity in mouse retinal ganglion cells. J. Neurophysiol. 80: 1327–1340, 1998. Spontaneous inhibitory and excitatory postsynaptic currents (sIPSCs and sEPSCs) were identified and characterized with whole cell and perforated patch voltage-clamp recordings in adult mouse retinal ganglion cells. Pharmacological dissection revealed that all cells were driven by spontaneous synaptic inputs mediated by glutamate and γ-aminobutyric acid-A (GABAA) receptors. One-half (7/14) of the cells also received glycinergic spontaneous synaptic inputs. Both GABAA and glycine receptor–mediated sIPSCs had rise times (10–90%) of <1 ms. The decay times of the GABAA receptor–mediated sIPSCs were comparable with those of the glycine receptor–mediated sIPSCs. The average decay time constant for monoexponentially fitted sIPSCs was 63.2 ± 74.1 ms (mean ± SD, n = 3278). Glutamate receptor–mediated sEPSCs had an average rise time of 0.50 ± 0.20 ms ( n = 109) and an average monoexponential decay time constant of 5.9 ± 8.6 ms ( n = 2705). Slightly more than two-thirds of the spontaneous synaptic events were monoexponential (68% for sIPSCs and 76% for sEPSCs). The remainder of the events was biexponential. The amplitudes of the spontaneous synaptic events were not correlated with rise times, suggesting that the electrotonic filtering properties of the neurons and/or differences in the spatial location of synaptic inputs could not account for the difference between the decay time constants of the glutamate and GABAA/glycine receptor–mediated spontaneous synaptic events. The amplitudes of sEPSCs were similar to those recorded in tetrodotoxin (TTX), consistent with the events measured in control saline being the response to the release of a single quantum of transmitter. The range of the sIPSC amplitudes in control saline was wider than that recorded in TTX, consistent with some sIPSCs being evoked by presynaptic spikes having an average quantal size greater than one. The rates of sIPSCs and sEPSCs were determined under equivalent conditions by recording with perforated patch electrodes at potentials at which both types of event could be identified. Two groups of ganglion cell were observed; one group had an average sEPSCs/sIPSCs frequency ratio of 0.96 ± 0.77 ( n = 28) and another group had an average ratio of 6.63 ± 0.82 ( n = 7). These findings suggest that a subset of cells is driven much more strongly by excitatory synaptic inputs. We propose that this subset of cells could be off ganglion cells, consistent with the higher frequency of spontaneous action potentials found in off ganglion cells in other studies.

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.

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

2003 ◽  
Vol 89 (1) ◽  
pp. 199-211 ◽  
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.

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

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%).

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.

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.

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.

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