Changes of spontaneous miniature excitatory postsynaptic currents in rat hippocampal pyramidal cells induced by aniracetam

1997 ◽  
Vol 435 (2) ◽  
pp. 185-192 ◽  
Author(s):  
M. Ghamari-Langroudi ◽  
M. I. Glavinovi´c
Keyword(s):  
Pyramidal Cells ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Hippocampal Pyramidal Cells

Development of Excitatory Circuitry in the Hippocampus

1998 ◽  
Vol 79 (4) ◽  
pp. 2013-2024 ◽  
Author(s):  
Albert Y. Hsia ◽  
Robert C. Malenka ◽  
Roger A. Nicoll
Keyword(s):  
Synaptic Transmission ◽  
Action Potentials ◽  
Pyramidal Cells ◽  
Excitatory Synaptic Transmission ◽  
Developmental Strategy ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Quantal Size ◽  
Physiological Approach ◽  
Local Circuitry

Hsia, Albert Y., Robert C. Malenka, and Roger A. Nicoll. Development of excitatory circuitry in the hippocampus. J. Neurophysiol. 79: 2013–2024, 1998. Assessing the development of local circuitry in the hippocampus has relied primarily on anatomic studies. Here we take a physiological approach, to directly evaluate the means by which the mature state of connectivity between CA3 and CA1 hippocampal pyramidal cells is established. Using a technique of comparing miniature excitatory postsynaptic currents (mEPSCs) to EPSCs in response to spontaneously occurring action potentials in CA3 cells, we found that from neonatal to adult ages, functional synapses are created and serve to increase the degree of connectivity between CA3-CA1 cell pairs. Neither the probability of release nor mean quantal size was found to change significantly with age. However, the variability of quantal events decreases substantially as synapses mature. Thus in the hippocampus the developmental strategy for enhancing excitatory synaptic transmission does not appear to involve an increase in the efficacy at individual synapses, but rather an increase in the connectivity between cell pairs.

scholarly journals Homeostatic Plasticity Hypothesis and Mechanisms of Neocortical Epilepsies

2005 ◽  
Vol 5 (4) ◽  
pp. 133-135 ◽  
Author(s):  
Jaideep Kapur ◽  
Stacey Trotter
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Activity ◽  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Homeostatic Plasticity ◽  
Excitatory Synapses ◽  
Excitatory Postsynaptic Currents ◽  
Inhibitory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Homeostatic Synaptic Plasticity

Homeostatic Synaptic Plasticity Can Explain Posttraumatic Epileptogenesis in Chronically Isolated Neocortex Houweling AR, Bazhenov M, Timofeev I, Steriade M, Sejnowski TJ Cereb Cortex 2004 [Epub ahead of print] Permanently isolated neocortex develops chronic hyperexcitability and focal epileptogenesis in a period of days to weeks. The mechanisms operating in this model of posttraumatic epileptogenesis are not well understood. We hypothesized that the spontaneous burst discharges recorded in permanently isolated neocortex result from homeostatic plasticity (a mechanism generally assumed to stabilize neuronal activity) induced by low neuronal activity after deafferentation. To test this hypothesis, we constructed computer models of neocortex incorporating a biologically based homeostatic plasticity rule that operates to maintain firing rates. After deafferentation, homeostatic upregulation of excitatory synapses on pyramidal cells, either with or without concurrent downregulation of inhibitory synapses or upregulation of intrinsic excitability, initiated slowly repeating burst discharges that closely resembled the epileptiform burst discharges recorded in permanently isolated neocortex. These burst discharges lasted a few hundred milliseconds, propagated at 1 to 3 cm/s and consisted of large (10–15 mV) intracellular depolarizations topped by a small number of action potentials. Our results support a role for homeostatic synaptic plasticity as a novel mechanism of posttraumatic epileptogenesis. Excitatory and Inhibitory Postsynaptic Currents in a Rat Model of Epileptogenic Microgyria Jacobs KM, Prince DA J Neurophysiol 2005;93:687–696 Developmental cortical malformations are common in patients with intractable epilepsy; however, mechanisms contributing to this epileptogenesis are currently poorly understood. We previously characterized hyperexcitability in a rat model that mimics the histopathology of human four-layered microgyria. Here we examined inhibitory and excitatory postsynaptic currents in this model to identify functional alterations that might contribute to epileptogenesis associated with microgyria. We recorded isolated whole-cell excitatory postsynaptic currents and GABAA receptor–mediated inhibitory currents from layer V pyramidal neurons in the region previously shown to be epileptogenic (paramicrogyral area) and in homotopic control cortex. Epileptiform-like activity could be evoked in 60% of paramicrogyral (PMG) cells by local stimulation. The peak conductance of both spontaneous and evoked inhibitory postsynaptic currents was significantly larger in all PMG cells compared with controls. This difference in amplitude was not present after blockade of ionotropic glutamatergic currents or for miniature (m) inhibitory postsynaptic currents, suggesting that it was due to the excitatory afferent activity driving inhibitory neurons. This conclusion was supported by the finding that glutamatereceptor antagonist application resulted in a significantly greater reduction in spontaneous inhibitory postsynaptic current frequency in one PMG cell group (PMGE) compared with control cells. The frequency of both spontaneous and miniature excitatory postsynaptic currents was significantly greater in all PMG cells, suggesting that pyramidal neurons adjacent to a microgyrus receive more excitatory input than do those in control cortex. These findings suggest that there is an increase in numbers of functional excitatory synapses on both interneurons and pyramidal cells in the PMG cortex, perhaps due to hyperinnervation by cortical afferents originally destined for the microgyrus proper.

scholarly journals Effects of PKA and PKC on Miniature Excitatory Postsynaptic Currents in CA1 Pyramidal Cells

1998 ◽  
Vol 80 (5) ◽  
pp. 2797-2800 ◽  
Author(s):  
Reed C. Carroll ◽  
Roger A. Nicoll ◽  
Robert C. Malenka
Keyword(s):  
Protein Kinase ◽  
Pyramidal Cells ◽  
Synaptic Strength ◽  
Dependent Protein Kinase ◽  
Excitatory Postsynaptic Currents ◽  
Ca1 Pyramidal Cells ◽  
Postsynaptic Currents ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein ◽  
Glur1 Subunit

Carroll, Reed C., Roger A. Nicoll, and Robert C. Malenka. Effects of PKA and PKC on miniature excitatory postsynaptic currents in CA1 pyramidal cells. J. Neurophysiol. 80: 2797–2800, 1998. Protein kinases play an important role in controlling synaptic strength at excitatory synapses on CA1 pyramidal cells. We examined the effects of activating cAMP-dependent protein kinase or protein kinase C (PKC) on the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) with perforated patch recording techniques. Both forskolin and phorbol-12,13-dibutryate (PDBu) caused a large increase in mEPSC frequency, but only PDBu increased mEPSC amplitude, an effect that was not observed when standard whole cell recording was performed. These results support biochemical observations indicating that PKC, similar to calcium/calmodulin-dependent protein kinase II, has an important role in controlling synaptic strength via modulation of AMPA receptor function, potentially through the direct phosphorylation of the GluR1 subunit.

Large Amplitude Miniature Excitatory Postsynaptic Currents in Hippocampal CA3 Pyramidal Neurons Are of Mossy Fiber Origin

1997 ◽  
Vol 77 (3) ◽  
pp. 1075-1086 ◽  
Author(s):  
Darrell A. Henze ◽  
J. Patrick Card ◽  
German Barrionuevo ◽  
Yezekiel Ben-Ari
Keyword(s):  
Rise Time ◽  
Large Amplitude ◽  
Mossy Fiber ◽  
Pyramidal Cells ◽  
Peak Amplitude ◽  
Γ Irradiation ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
The Mean ◽  
Ca3 Pyramidal Cells

Henze, Darrell A., J. Patrick Card, German Barrionuevo, and Yezekiel Ben-Ari. Large amplitude miniature excitatory postsynaptic currents in hippocampal CA3 pyramidal neurons are of mossy fiber origin. J. Neurophysiol. 77: 1075–1086, 1997. Neonatal (P0) γ-irradiation was used to lesion selectively the mossy fiber (MF) synaptic input to CA3 pyramidal cells. This lesion caused a >85% reduction in the MF input as determined by quantitative assessment of the number of dynorphin immunoreactive MF boutons. Theγ-irradiation lesion caused a reduction in the mean number of miniature excitatory postsynaptic currents (mEPSCs) recorded from CA3 pyramidal cells (2,292 vs. 1,429/3-min period; n = 10). The lesion also caused a reduction in the mean mEPSC peak amplitude from 19.1 ± 0.45 to 14.6 ± 0.49 pA (mean ± SE; peak conductance 238.8 ± 5.6 to 182.0 ± 6.1 pS). Similarly, there was a reduction in the mean 10–85% rise time from 1.72 ± 0.02 ms to 1.42 ± 0.04 ms. The effects of the γ-irradiation on both mEPSC amplitude and 10–85% rise time were significant at P < 0.002 and P < 0.005 (2-tailed Kolmogorov-Smirnov test). Based on the selectivity of the γ-irradiation, MF and non-MF mEPSC amplitude and 10–85% rise-time distributions were calculated. Both the amplitude and 10–85% rise-time distributions showed extensive overlap between the MF and non-MF mediated mEPSCs. The MF mEPSC distributions had a mean peak amplitude of 24.6 pA (307.5 pS) and a mean 10–85% rise time of 2.16 ms. The non-MF mEPSC distributions had a mean peak amplitude of 12.2 pA (152.5 pS) and 10–85% rise time of 1.26 ms. The modes of the amplitude distributions were the same at 5 pA (62 pS). The MF and non-MF mEPSC amplitude and 10–85% rise-time distributions were significantly different at P ≪ 0.001 (1-tailed, large sample Kolmogorov-Smirnov test). The data demonstrate that the removal of the MF synaptic input to CA3 pyramidal cells leads to the absence of the large amplitude mEPSCs that are present in control recordings.

Neuropeptide Y2 receptors inhibit the frequency of spontaneous but not miniature EPSCs in CA3 pyramidal cells of rat hippocampus

1996 ◽  
Vol 76 (5) ◽  
pp. 3159-3168 ◽  
Author(s):  
A. R. McQuiston ◽  
W. F. Colmers
Keyword(s):  
Glutamate Release ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Rat Hippocampus ◽  
Excitatory Postsynaptic Currents ◽  
Synaptic Excitation ◽  
Postsynaptic Currents ◽  
Y2 Receptor ◽  
Ca3 Pyramidal Cells

1. Neuropeptide Y (NPY) inhibits synaptic excitation in hippocampal area CA3. We studied its site of action with the use of whole cell patch-clamp recordings from CA3 pyramidal cells of rat hippocampal slices in vitro. 2. Spontaneous excitatory postsynaptic currents (sEPSCs) were isolated with picrotoxin, to block gamma-aminobutyric acid-A receptors, whereas miniature excitatory postsynaptic currents (mEPSCs) were isolated by additionally treating the slice with tetrodotoxin (TTX) and/or Cd2+, sEPSCs and mEPSCs were eliminated by the excitatory amino acid antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (10 microM) and DL-2-amino-5-phosphonovaleric acid (50 microM), and were thus solely attributable to glutamate release. 3. The interval and amplitude distributions of sEPSCS and (TTX-isolated) mEPSCS were analyzed. Either NPY or the rapidly reversible, Y2-receptor-selective agonist [6-aminohexanoic5-24] NPY, ([ahx5-24]NPY) sharply increased the inter-sEPSC intervals in 16 of 16 neurons tested. In 11 of these cells, these agonists also simultaneously shifted the sEPSC amplitude distribution to somewhat smaller amplitudes, whereas in the remaining 5 cells, no concurrent effect on amplitudes was observed. By contrast, in 15 separate neurons treated with 1 microM TTX, neither NPY nor [ahx5-24]NPY altered either mEPSC amplitude or interval distributions of the mEPSCs. 4. To directly compare the effects of Y2 receptor activation on sEPSC and mEPSC properties, we applied [ahx5-24]NPY to the same cell in the absence and presence of TTX (n = 7). sEPSC intervals were characteristically increased by the Y2 agonist in all cells; in six of seven cells the sEPSC distribution was also shifted to smaller amplitudes. TTX application reduced the mean amplitude of the synaptic events more than did [ahx5-24]NPY, while increasing their intervals. [ahx5-24]NPY had no effect in TTX. 5. NPY, acting on a Y2 receptor, inhibits impulse-dependent synaptic excitation of CA3 pyramidal cells of the rat hippocampus by an entirely presynaptic action.

Excitatory and Inhibitory Postsynaptic Currents in a Rat Model of Epileptogenic Microgyria

2005 ◽  
Vol 93 (2) ◽  
pp. 687-696 ◽  
Author(s):  
K. M. Jacobs ◽  
D. A. Prince
Keyword(s):  
Rat Model ◽  
Pyramidal Neurons ◽  
Intractable Epilepsy ◽  
Pyramidal Cells ◽  
Excitatory Input ◽  
Inhibitory Neurons ◽  
Cell Group ◽  
Excitatory Postsynaptic Currents ◽  
Postsynaptic Currents ◽  
Layer V

Developmental cortical malformations are common in patients with intractable epilepsy; however, mechanisms contributing to this epileptogenesis are currently poorly understood. We previously characterized hyperexcitability in a rat model that mimics the histopathology of human 4-layered microgyria. Here we examined inhibitory and excitatory postsynaptic currents in this model to identify functional alterations that might contribute to epileptogenesis associated with microgyria. We recorded isolated whole cell excitatory postsynaptic currents and GABAA receptor-mediated inhibitory currents (EPSCs and IPSCs) from layer V pyramidal neurons in the region previously shown to be epileptogenic (paramicrogyral area) and in homotopic control cortex. Epileptiform-like activity could be evoked in 60% of paramicrogyral (PMG) cells by local stimulation. The peak conductance of both spontaneous and evoked IPSCs was significantly larger in all PMG cells compared with controls. This difference in amplitude was not present after blockade of ionotropic glutamatergic currents or for miniature (m)IPSCs, suggesting that it was due to the excitatory afferent activity driving inhibitory neurons. This conclusion was supported by the finding that glutamate receptor antagonist application resulted in a significantly greater reduction in spontaneous IPSC frequency in one PMG cell group (PMGE) compared with control cells. The frequency of both spontaneous and miniature EPSCs was significantly greater in all PMG cells, suggesting that pyramidal neurons adjacent to a microgyrus receive more excitatory input than do those in control cortex. These findings suggest that there is an increase in numbers of functional excitatory synapses on both interneurons and pyramidal cells in the PMG cortex perhaps due to hyperinnervation by cortical afferents originally destined for the microgyrus proper.

Effects of Halothane on Glutamate Receptor-mediated Excitatory Postsynaptic Currents

1995 ◽  
Vol 83 (1) ◽  
pp. 109-119. ◽  
Author(s):  
Misha Perouansky ◽  
Dimitri Baranov ◽  
Michael Salman ◽  
Yoel Yaari
Keyword(s):  
Glutamate Receptor ◽  
Glutamate Release ◽  
Pyramidal Cells ◽  
Receptor Subtype ◽  
Excitatory Postsynaptic Currents ◽  
Ca1 Pyramidal Cells ◽  
Postsynaptic Currents ◽  
High Concentrations

Background The effects of halothane on excitatory synaptic transmission in the central nervous system of mammals have been studied in vivo and in vitro in several investigations with partially contradicting results. Direct measurements of the effects of halothane on isolated glutamate receptor-mediated (glutamatergic) excitatory postsynaptic currents (EPSCs), however, have not been reported to date. Methods The effects of halothane on glutamatergic EPSCs were studied in vitro by using tight-seal, whole-cell recordings from CA1 pyramidal cells in thin slices from the adult mouse hippocampus. The EPSCs were pharmacologically isolated into their non-N-methyl-D-aspartate (non-NMDA) and NMDA receptor-mediated components by using selective antagonists. The effects of halothane on EPSC amplitude and kinetics were analyzed at various membrane potentials and were compared with its effects on currents evoked by exogenously applied glutamatergic agonists. Results Halothane (0.2-5.1%; 0.37-2.78 mM) reversibly blocked non-NMDA and NMDA EPSCs. This effect was voltage independent; concentrations producing 50% inhibition were 0.87% (0.66 mM) and 0.69% (0.57 mM), respectively. Currents induced by bath-applied glutamatergic agonists were not affected even by the high concentrations of halothane. Conclusions Halothane depresses glutamatergic EPSCs irrespective of receptor subtype, most likely by inhibition of glutamate release.

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