Three types of inhibitory postsynaptic potentials generated by interneurons in the anterior thalamic complex of cat

1991 ◽  
Vol 66 (4) ◽  
pp. 1190-1204 ◽  
Author(s):  
D. Pare ◽  
R. C. Dossi ◽  
M. Steriade
Keyword(s):  
Late Phase ◽  
Total Duration ◽  
Low Frequency ◽  
Reversal Potential ◽  
Equilibrium Potential ◽  
Gamma Aminobutyric Acid ◽  
Thalamic Nuclei ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Presynaptic Dendrites

1. These experiments were carried out to study how thalamic interneurons generate inhibitory postsynaptic potentials (IPSPs) in relay cells. Intracellular recordings were performed in the anterior thalamic (AT) nuclei, a nuclear group in which interneurons constitute the only intrathalamic source of gamma-aminobutyric acid (GABA). 2. In the AT complex, as in most dorsal thalamic nuclei, interneurons can influence relay cells through their presynaptic dendrites (PSDs) and their axons. This dual mode of action is paralleled by a different termination pattern of prethalamic fibers and cortical axons on interneurons. Prethalamic fibers, which in the AT nuclei arise in the mammillary bodies (MBs), end mostly on PSDs, whereas cortical terminals usually synapse on the parent dendrites of PSDs. We therefore took advantage of the differential mode of termination of cortical and MB afferents on interneurons to infer the respective roles of the axons and PSDs of interneurons in the genesis of the IPSPs recorded from relay cells. 3. In all responsive AT cells, cortical stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a biphasic IPSP, with an early and a late phase, having a total duration of 221.96 +/- 8.18 ms (mean +/- SE). The early part of the IPSP (termed A) had a reversal potential (ER) close to the equilibrium potential for Cl- ions: -79.25 +/- 2.14 mV. Furthermore, it reversed in polarity after impalement of the cells with KCl-filled pipettes. The late IPSP (termed B) always began before the end of the early IPSP, 45.93 +/- 2.50 ms after the onset of the A-IPSP. The B-IPSP had an ER of -109 +/- 2.4 mV and was not affected by Cl- injection. 4. By contrast, MB stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a triphasic IPSP having a total duration of 220.5 +/- 9.42 ms in most (61.2%) AT cells. The IPSP with the shortest latency (termed a) was evoked only by MB stimuli. Before the return of the membrane potential to the resting level, a second hyperpolarizing potential began (7.41 +/- 0.46 ms after the onset of the a-IPSP). This second inhibitory phase was biphasic and had electrophysiological characteristics similar to the biphasic A- and B-IPSP evoked by cortical stimulation. Both the MB-evoked a- and A-IPSPs had an ER close to the equilibrium potential for Cl- ions (-72.22 +/- 0.68 and -72 +/- 0.82 mV, respectively) and reversed in polarity after impalement of the cells with KCl-filled pipettes.(ABSTRACT TRUNCATED AT 400 WORDS)

The K+ channel opener diazoxide enhances glutamatergic currents and reduces GABAergic currents in hippocampal neurons

1993 ◽  
Vol 69 (2) ◽  
pp. 494-503 ◽  
Author(s):  
V. Crepel ◽  
C. Rovira ◽  
Y. Ben-Ari
Keyword(s):  
Intracellular Recording ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Input Resistance ◽  
Katp Channels ◽  
K Channel ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials

1. The effect of diazoxide, an opener of ATP-sensitive K+ channels (KATP channels) has been investigated in the rat hippocampal slices by the use of extracellular and intracellular recording techniques. 2. In control solution, diazoxide enhanced the CA1 and CA3 field excitatory postsynaptic potentials (EPSPs) and produced interictal activities in CA3. These effects were neither prevented by KATP blockers, including glibenclamide (3-30 microM) or tolbutamide (500 microM), nor mimicked by another KATP opener such as galanine (1 microM); thus these effects are probably not mediated by KATP channels. 3. Using intracellular recording, we then studied, in CA3 pyramidal neurons, the effect of diazoxide on the EPSPs and the fast and slow inhibitory postsynaptic potentials (IPSPs). 4. In presence of bicuculline (10 microM) and phaclofen (50 microM), to block, respectively, fast and slow IPSPs, diazoxide reversibly enhanced the EPSPs. 5. In presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM), to block EPSPs, diazoxide reversibly decreased both fast and slow IPSPs. 6. These effects of diazoxide on the EPSPs and fast and slow IPSPs were associated neither with a change of the reversal potential of the EPSPs or the fast and slow IPSPs nor with a change of the input resistance and membrane potential. 7. Using single electrode voltage-clamp technique, we then tested the effects of diazoxide on the currents generated by applications of glutamate or gamma-aminobutyric acid (GABA) -A and -B analogues. 8. In presence of tetrodotoxin (TTX; 1 microM), diazoxide reversibly enhanced the peak currents evoked by alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionate (AMPA; 3-5 microM), quisqualate (5-10 microM) and N-methyl-D-aspartate (NMDA; 10 microM), but not those evoked by kainate (1-3 microM). 9. In presence of TTX (1 microM), diazoxide reversibly decreased the GABA- (1-5 mM), isoguvacine- (30-60 microM), and baclofen- (10-30 microM) mediated peak currents. 10. It is concluded that, in the hippocampus, diazoxide enhances the excitatory glutamatergic currents and reduces the GABAergic inhibition, thus generating paroxystic activities. We suggest that these effects are mediated by second messenger cascades.

5-HT-mediated synaptic potentials in the dorsal raphe nucleus: interactions with excitatory amino acid and GABA neurotransmission

1989 ◽  
Vol 62 (2) ◽  
pp. 481-486 ◽  
Author(s):  
Z. Z. Pan ◽  
W. F. Colmers ◽  
J. T. Williams
Keyword(s):  
Amino Acid ◽  
Dorsal Raphe Nucleus ◽  
Excitatory Amino Acid ◽  
Total Duration ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Equilibrium Potential ◽  
Gamma Aminobutyric Acid ◽  
Synaptic Potentials ◽  
Dorsal Raphé

1. Intracellular recordings from neurons within dorsal raphe nucleus in slices from rat brain were used to study an inhibitory postsynaptic potential (IPSP) evoked by electrical stimulation. 2. The IPSP was observed in approximately 70% of neurons, had a latency to onset of 40-65 ms, reached a peak in 350-400 ms, had a total duration of 1-2 s, and reversed polarity at the potassium equilibrium potential. 3. This IPSP was blocked by spiperone (1 microM) and prolonged by fluoxetine (300 nM-30 microM) suggesting that it was mediated by 5-hydroxytryptamine (5-HT). 4. Superfusion with gamma-aminobutyric acid (GABA) and excitatory amino acid receptor antagonists were used to block "fast" synaptic potentials that preceded the IPSP such that it could be studied in isolation. Blockade of the GABA-mediated synaptic potentials increased the amplitude of the IPSP by 1.3-fold. The amplitude of the IPSP was reduced by 30% after blockade of the excitatory amino acid-mediated synaptic potential. 5. The results indicate that the IPSP recorded in dorsal raphe neurons was caused by 5-HT released at least in part from indirect (synaptically induced) excitation of 5-HT-containing cells within the slice.

Ammonia does not selectively block IPSPs in rat hippocampal pyramidal cells

1983 ◽  
Vol 49 (6) ◽  
pp. 1381-1391 ◽  
Author(s):  
B. E. Alger ◽  
R. A. Nicoll
Keyword(s):  
Reversal Potential ◽  
Pyramidal Cells ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials ◽  
Calcium Dependent ◽  
Nonspecific Effects ◽  
Chloride Pump ◽  
High Concentrations ◽  
Conductance Increase ◽  
Potassium Response

Intracellular recordings from CA1 pyramidal cells in the rat hippocampal slice preparation have been used to study the action of ammonia on inhibitory postsynaptic potentials (IPSPs). Concentrations of ammonia less than 2 mM had little effect on IPSPs or the action of iontophoretically applied gamma-aminobutyric acid (GABA). This concentration has been reported to be fully effective in blocking hyperpolarizing IPSPs in spinal cord and neocortex. Concentrations above 2 mM did cause a depolarizing shift in the IPSP and GABA reversal potentials, but this effect was accompanied by several generalized effects. The conductance increase during the IPSP but not during the GABA response was depressed, indicating that ammonia has a presynaptic depressant effect on the IPSP. Ammonia also depressed excitatory postsynaptic potentials (EPSPs), presynaptic fiber potentials, and pyramidal cell population spikes. In addition, the calcium-dependent potassium response elicited by depolarizing current pulses was depressed. This depression was due, in part, to a depolarizing shift in the reversal potential for this response. Responses recorded with potassium-sensitive microelectrodes indicate that ammonia releases potassium into the extracellular space. The possibility is discussed that the shifts in IPSP reversal potential seen with high concentrations of ammonia are a consequence of generalized nonspecific effects. We conclude that the relative insensitivity of hippocampal IPSPs to blockade by ammonia suggests that a mechanism fundamentally unlike an ammonia-sensitive chloride pump must maintain the hippocampal IPSP gradient.

Role of HCO3- ions in depolarizing GABAA receptor-mediated responses in pyramidal cells of rat hippocampus

1993 ◽  
Vol 69 (5) ◽  
pp. 1541-1555 ◽  
Author(s):  
L. M. Grover ◽  
N. A. Lambert ◽  
P. A. Schwartzkroin ◽  
T. J. Teyler
Keyword(s):  
Gabaa Receptor ◽  
Gabab Receptor ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Gamma Aminobutyric Acid ◽  
Free Medium ◽  
Postsynaptic Potentials ◽  
Ca1 Pyramidal Cells ◽  
Ionic Basis

1. Activation of GABAA receptors can produce both hyperpolarizing and depolarizing responses in CA1 pyramidal cells. The hyperpolarizing response is mediated by a Cl- conductance, but the ionic basis of the depolarizing response is not clear. We compared the GABAA receptor-mediated depolarizations induced by synaptically released gamma-aminobutyric acid [GABA; depolarizing inhibitory postsynaptic potentials (dIPSPs)] with those produced by exogenous GABA (depolarizing GABA responses). Short trains of high-frequency (200 Hz) stimuli were used to generate dIPSPs. We found that dIPSPs generated by trains of stimuli and depolarizing responses to exogenous GABA were accompanied by a conductance increase and had a similar reversal potential, indicating a similar ionic basis for both responses. 2. We wished to determine whether an HCO3- current contributed to the GABAA-mediated depolarizations. We found that dIPSPs and depolarizing GABA responses were sensitive to perfusion with HCO3(-)-free medium. Interpretation of these data was complicated by the mixed nature of the responses: dIPSPs were invariably accompanied by conventional, Cl(-)-mediated fast hyperpolarizing IPSPs (fIPSPs), and response to exogenous GABA usually consisted of biphasic hyperpolarizing and depolarizing responses. However, it was sometimes possible to elicit responses to GABA that appeared purely depolarizing (monophasic depolarizing GABA responses). 3. We analyzed monophasic depolarizing GABA responses and found no change in reversal potential when slices were perfused with HCO(3-)-free medium. We also made whole-cell recordings from CA1 pyramidal cells, attempting to reduce [HCO3-]i, and compared the reversal potential for monophasic depolarizing GABA responses with similar responses recorded with fine intracellular microelectrodes. We found no difference in reversal potential. We also examined effects of the carbonic anhydrase inhibitor acetazolamide (ACTZ) on depolarizing GABA responses. ACTZ reduced these responses but did not change their reversal potential. 4. Effects of HCO(3-)-free medium were not specific to GABAA receptor-mediated responses. GABAB receptor-mediated slow IPSPs (sIPSPs) were also reduced, as were excitatory postsynaptic potentials (EPSPs). Analyses of field potentials and spontaneous fIPSPs suggested a decrease in presynaptic excitability during perfusion with HCO(3-)-free medium. In addition, pyramidal cells showed decreased input resistance when perfused with HCO(3-)-free medium. 5. The sensitivity of GABAA receptor-mediated depolarizations to HCO(3-)-free medium can be explained by a decrease in presynaptic excitability and an increased resting conductance in postsynaptic neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Actions of bicuculline on cell body and neuropilar membranes of identified insect neurones

1994 ◽  
Vol 186 (1) ◽  
pp. 235-244
Author(s):  
S. D. Buckingham ◽  
B. Hue ◽  
D. B. Sattelle
Keyword(s):  
Cell Body ◽  
Nicotinic Acetylcholine Receptors ◽  
Gaba Receptors ◽  
Acetylcholine Receptors ◽  
Periplaneta Americana ◽  
Neuronal Nicotinic Acetylcholine Receptors ◽  
Gamma Aminobutyric Acid ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Motor Neurones

Bicuculline and its methochloride salt block inhibitory postsynaptic potentials recorded from giant interneurone 2 (GI 2) of the cockroach Periplaneta americana following stimulation of cercal nerve X, but fail to block the response to gamma-aminobutyric acid (GABA) when this neurotransmitter is ionophoresed or pressure-injected onto the fine branches of GI 2 within the neuropile of the terminal abdominal ganglion. Bicuculline is similarly ineffective in blocking the response recorded when GABA is ionophoresed onto the cell body membrane of GI 2. The cell body membranes of cockroach GI 2 and fast coxal depressor motor neurones have been used to show that bicuculline blocks cell body (extrasynaptic) neuronal nicotinic acetylcholine receptors. Pressure-injection of acetylcholine into the neuropile results in a depolarization of GI 2 that is blocked by bicuculline. Therefore, the block by bicuculline of inhibitory postsynaptic potentials recorded from GI 2 may result in part from actions at sites other than synaptic GABA receptors. Alternatively, there may exist a population of synaptic GABA receptors on GI 2 that, unlike GI 2 cell body GABA receptors, are sensitive to bicuculline.

scholarly journals Inhibitory Postsynaptic Potentials in Lumbar Motoneurons Remain Depolarizing After Neonatal Spinal Cord Transection in the Rat

2006 ◽  
Vol 96 (5) ◽  
pp. 2274-2281 ◽  
Author(s):  
Céline Jean-Xavier ◽  
Jean-François Pflieger ◽  
Sylvie Liabeuf ◽  
Laurent Vinay
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Time Window ◽  
Reversal Potential ◽  
Perinatal Period ◽  
Spinal Cord Transection ◽  
Resting Potential ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
The Brain

GABA and glycine are excitatory in the immature spinal cord and become inhibitory during development. The shift from depolarizing to hyperpolarizing inhibitory postsynaptic potentials (IPSPs) occurs during the perinatal period in the rat, a time window during which the projections from the brain stem reach the lumbar enlargement. In this study, we investigated the effects of suppressing influences of the brain on lumbar motoneurons during this critical period for the negative shift of the reversal potential of IPSPs ( EIPSP). The spinal cord was transected at the thoracic level on the day of birth [postnatal day 0 (P0)]. EIPSP, at P4–P7, was significantly more depolarized in cord-transected than in cord-intact animals ( EIPSP above and below resting potential, respectively). EIPSP at P4–P7 in cord-transected animals was close to EIPSP at P0–P2. K-Cl cotransporter KCC2 immunohistochemistry revealed a developmental increase of staining in the area of lumbar motoneurons between P0 and P7 in cord-intact animals; this increase was not observed after spinal cord transection. The motoneurons recorded from cord-transected animals were less sensitive to the experimental manipulations aimed at testing the functionality of the KCC2 system, which is sensitive to [K+]o and blocked by bumetanide. Although bumetanide significantly depolarized EIPSP, the shift was less pronounced than in cord-intact animals. In addition, a reduction of [K+]o affected EIPSP significantly only in cord-intact animals. Therefore influences from the brain stem may play an essential role in the maturation of inhibitory synaptic transmission, possibly by upregulating KCC2 and its functionality.

Inhibitory Interactions Between Ferret Thalamic Reticular Neurons

2002 ◽  
Vol 87 (5) ◽  
pp. 2571-2576 ◽  
Author(s):  
Yousheng Shu ◽  
David A. McCormick
Keyword(s):  
Reversal Potential ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Inhibitory Input ◽  
Inhibitory Interaction ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Reticular Neurons ◽  
Inhibitory Interactions

The thalamic reticular nucleus (nRt) provides an important inhibitory input to thalamic relay nuclei and is central in the generation of both normal and abnormal thalamocortical activities. Although local inhibitory interactions between these neurons may play an important role in controlling thalamocortical activities, the physiological features of this interaction have not been fully investigated. Here we sought to establish the nature of inhibitory interaction between nRt neurons with intracellular and extracellular recordings in slices of ferret nRt maintained in vitro. In many nRt neurons, intracellular recordings revealed spontaneous inhibitory postsynaptic potentials (IPSPs). In addition, the local excitation of nRt cells with glutamate led to the generation of IPSPs in the intracellularly recorded nRt neuron. These evoked IPSPs exhibited an average reversal potential of −72 mV and could be blocked by picrotoxin, a GABAA-receptor antagonist. These results indicate that nRt neurons interact locally through the activation of GABAA receptor-mediated inhibitory postsynaptic potentials. This lateral inhibition may play an important role in controlling the responsiveness of these cells to cortical and thalamic excitatory inputs in both normal and abnormal thalamocortical function.

GABA-induced chloride current in rat isolated Purkinje cells

1989 ◽  
Vol 256 (6) ◽  
pp. C1153-C1159 ◽  
Author(s):  
M. Kaneda ◽  
M. Wakamori ◽  
N. Akaike
Keyword(s):  
Purkinje Cells ◽  
Reversal Potential ◽  
External Solution ◽  
Hill Coefficient ◽  
Equilibrium Potential ◽  
Maximal Response ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Concentration Jump ◽  
The Hill

Electrical and pharmacological properties of the gamma-aminobutyric acid (GABA)-induced current in the rat isolated cerebellar Purkinje cell bodies were studied using a concentration-jump method, which is termed as a "concentration-clamp" technique. This technique enables the rapid exchange of external solution around the neurons to be perfused internally under a voltage-clamp condition. The peak amplitude of GABA response increased sigmoidally with the increase of the concentration of GABA. The value of the GABA concentration that evokes a half-maximal response (Ka) was 5 X 10(-5) M, and the Hill coefficient was 1.8. The current-voltage relationship for the GABA response showed nonlinearity at membrane potentials more negative than -40 mV. The reversal potential of GABA-evoked current was close to the equilibrium potential of Cl- (ECl), indicating that the current elicited by GABA is carried by Cl-. Both the activation and inactivation phases of GABA-induced Cl- current (ICl) consisted of fast and slow components. These time constants in both phases decreased as the concentration of GABA increased. Strychnine and bicuculline inhibited the GABA-induced ICl in a dose-dependent manner, and the inhibition of the GABA response by bicuculline was competitive. Pentobarbital sodium augmented the GABA response and modified the inactivation phase. The augmentation of the GABA response by pentobarbital was more profound at lower concentrations of GABA and was accompanied by a change in the Hill coefficient from 2 to 1. The properties of the GABA response in cerebellar Purkinje cells were thought to be basically similar to those previously reported in other preparations.

Characterization of spontaneous and evoked inhibitory postsynaptic potentials in rat supraoptic neurosecretory neurons in vitro

1986 ◽  
Vol 56 (6) ◽  
pp. 1703-1717 ◽  
Author(s):  
J. C. Randle ◽  
C. W. Bourque ◽  
L. P. Renaud
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Reversal Potential ◽  
Chloride Ions ◽  
Membrane Potentials ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Neurosecretory Neurons ◽  
The Mean ◽  
Mean Time

Intracellular recordings from 52 supraoptic nucleus neurosecretory neurons in perfused explants of rat hypothalamus revealed abundant spontaneous inhibitory postsynaptic potentials (sIPSPs) and a compound evoked inhibitory postsynaptic potential (eIPSP) following electrical stimulation in the diagonal band of Broca (DBB). These IPSPs were characterized in terms of the magnitude and ionic specificity of the underlying current and in terms of the transmitter responsible for their activation. sIPSPs rose rapidly to peak within 3-5 ms and decayed exponentially with a mean time constant of 20.2 +/- 1.9 ms (mean +/- SE), a value 1.6-fold greater than the mean cell time constant of 13.8 +/- 1.0 ms. The eIPSPs rose rapidly to peak within 3-10 ms and decayed exponentially over 60-100 ms with a mean time constant of 37.0 +/- 2.8 ms, which is 2.6-fold greater than the mean cell time constant. These features imply a brief persistence of the conductance underlying the IPSPs. In recordings with KAcetate-filled micropipettes, sIPSPs were hyperpolarizing at membrane potentials in the range of -50 to -70 mV and reversed polarity when the membrane was hyperpolarized beyond -80 mV. The mean reversal potential (EsIPSP) was -72.4 +/- 1.1 mV. eIPSPs were hyperpolarizing at resting membrane potential and could be reversed by membrane hyperpolarization beyond a mean reversal potential (EIPSP) of -67.4 +/- 1.4 mV. In recordings with KCl-filled micropipettes, sIPSPs were depolarizing at all membrane potentials more negative than -50 mV. Under these conditions, EsIPSP was estimated at -44 mV. sIPSPs were absent when chloride ions were removed from the perfusion medium. eIPSPs were depolarizing at all membrane potentials and often evoked action potentials; mean EeIPSP was 43.2 mV. Reversal potentials of spontaneous and evoked IPSPs were similar. At a given membrane potential, sIPSP amplitudes varied widely between 1 and 20 mV. The conductance increase underlying individual sIPSPs was estimated to vary between 0.17 and 3.0 nS (avg 0.6 nS) against a mean resting input conductance of 3.78 +/- 0.41 nS. Estimates of the conductance underlying eIPSPs varied widely between cells, from 0.8 to 22.0 nS (mean 72 nS). Accordingly, the ratio of evoked to spontaneous IPSP conductance varied from 1.6 to 43.7 (mean 13.1). The reversal potential of evoked IPSPs shifted with the extracellular concentration of Cl- ions ([Cl-]0) with a mean slope of 41 mV/log [Cl-]0.(ABSTRACT TRUNCATED AT 400 WORDS)

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