Excitatory postsynaptic potentials recorded from regular-spiking cells in layers II/III of rat sensorimotor cortex

1992 ◽  
Vol 67 (3) ◽  
pp. 728-737 ◽  
Author(s):  
G. G. Hwa ◽  
M. Avoli
Keyword(s):  
Nmda Receptor Antagonist ◽  
Short Latency ◽  
Neuronal Membrane ◽  
Dependent Manner ◽  
Excitatory Postsynaptic Potentials ◽  
Normal Medium ◽  
Postsynaptic Potentials ◽  
Extracellular Stimuli ◽  
Relationship Of

1. Intracellular recording techniques were used to investigate the physiological and pharmacological properties of stimulus-induced excitatory postsynaptic potentials (EPSPs) recorded in regular-spiking cells located in layers II/III of rat sensorimotor cortical slices maintained in vitro. 2. Depending on the strength of the extracellular stimuli, a pure EPSP or an EPSP-inhibitory postsynaptic potential sequence was observed under perfusion with normal medium. The EPSPs displayed short latency of onset [2.4 +/- 0.7 (SD) ms] and were able to follow repetitive stimulation (tested less than or equal to 5 Hz). Variation of the membrane potential (Vm) revealed two types of voltage behavior for the short-latency EPSP. The first type decreased in amplitude with depolarization and increased in amplitude with hyperpolarization. In contrast, the second type behaved anomalously by increasing and decreasing in size after depolarization and hyperpolarization, respectively. 3. Several experimental procedures were carried out to investigate the mechanism underlying the anomalous voltage behavior of the EPSP. Results indicated that this type of Vm dependency could be mimicked by an intrinsic response evoked by a brief pulse of depolarizing current and could be abolished by N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (50 mM). Furthermore, the EPSP was not sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP, 10 microM). Thus the anomalous voltage relationship of the neuronal membrane. 4. The involvement of non-NMDA receptors in excitatory synaptic transmission was investigated with their selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 1-10 microM). This drug greatly reduced or completely blocked the EPSP in a dose-dependent manner (1-10 microM). The IC50 for the CNQX effect was approximately 2 microM. In the presence of CNQX (10 microM) and glycine (10 microM), synaptic stimulation failed to elicit firing of action potential. However, a CPP-sensitive EPSP was observed. 5. When synaptic inhibition was reduced by low concentration of bicuculline methiodide (BMI, 1-2 microM), extracellular stimulation revealed late EPSPs (latency to onset: 10-30 ms) that were not discernible in normal medium. Similar to the short-latency EPSP, the Vm dependency displayed by this late EPSP could be modified by inward membrane rectifications. The late EPSP appeared to be polysynaptic in origin because 1) its latency of onset was long and variable and 2) it failed to follow repetitive stimuli delivered at a frequency that did not depress the short-latency EPSP.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Excitatory postsynaptic potentials in rat neocortical neurons in vitro. III. Effects of a quinoxalinedione non-NMDA receptor antagonist

1990 ◽  
Vol 64 (4) ◽  
pp. 1282-1290 ◽  
Author(s):  
J. J. Hablitz ◽  
B. Sutor
Keyword(s):  
Nmda Receptor ◽  
Action Potentials ◽  
Nmda Antagonist ◽  
Nmda Receptor Antagonist ◽  
Cortical Layer ◽  
Bipolar Electrode ◽  
Dependent Manner ◽  
Excitatory Postsynaptic Potentials ◽  
Postsynaptic Potentials

1. Intracellular microelectrodes were used to obtain recordings from neurons in layer II/III of rat frontal cortex. A bipolar electrode positioned in layer IV of the neocortex was used to evoke postsynaptic potentials. Graded series of stimulation were employed to selectively activate different classes of postsynaptic responses. The sensitivity of postsynaptic potentials and iontophoretically applied neurotransmitters to the non-N-methyl-D-asparate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) was examined. 2. As reported previously, low-intensity electrical stimulation of cortical layer IV evoked short-latency early excitatory postsynaptic potentials (eEPSPs) in layer II/III neurons. CNQX reversibly antagonized eEPSPs in a dose-dependent manner. Stimulation at intensities just subthreshold for activation of inhibitory postsynaptic potentials (IPSPs) produced long-latency (10 to 40-ms) EPSPs (late EPSPs or 1EPSPs). CNQX was effective in blocking 1EPSPs. 3. With the use of stimulus intensities at or just below threshold for evoking an action potential, complex synaptic potentials consisting of EPSP-IPSP sequences were observed. Both early, Cl(-)-dependent and late, K(+)-dependent IPSPs were reduced by CNQX. This effect was reversible on washing. This disinhibition could lead to enhanced excitability in the presence of CNQX. 4. Iontophoretic application of quisqualate produced a membrane depolarization with superimposed action potentials, whereas NMDA depolarized the membrane potential and evoked bursts of action potentials. At concentrations up to 5 microM, CNQX selectively antagonized quisqualate responses. NMDA responses were reduced by 10 microM CNQX. D-Serine (0.5-2 mM), an agonist at the glycine regulatory site on the NMDA receptor, reversed the CNQX depression of NMDA responses.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Nicotinic and Muscarinic Reduction of Unitary Excitatory Postsynaptic Potentials in Sensory Cortex; Dual Intracellular Recording In Vitro

2006 ◽  
Vol 95 (4) ◽  
pp. 2155-2166 ◽  
Author(s):  
Robert B. Levy ◽  
Alex D. Reyes ◽  
Chiye Aoki
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Receptor Activation ◽  
Nmda Receptor Antagonist ◽  
Excitatory Postsynaptic Potentials ◽  
Postsynaptic Potentials ◽  
Sensory Activity

We studied the cholinergic modulation of glutamatergic transmission between neighboring layer 5 regular-spiking pyramidal neurons in somatosensory cortical slices from young rats (P10-P26). Brief bath application of 5–10 μM carbachol, a nonspecific cholinergic agonist, decreased the amplitude of evoked unitary excitatory postsynaptic potentials (EPSPs). This effect was blocked by 1 μM atropine, a muscarinic receptor antagonist. Nicotine (10 μM), in contrast to carbachol, reduced EPSPs in nominally magnesium-free solution but not in the presence of 1 mM Mg+2, indicating the involvement of NMDA receptors. Likewise, when the postsynaptic cell was depolarized under voltage clamp to allow NMDA receptor activation in the presence of 1 mM Mg+2, synaptic currents were reduced by nicotine. Nicotinic EPSP reduction was prevented by the NMDA receptor antagonist d-AP5 (50 μM) and by the nicotinic receptor antagonist mecamylamine (10 μM). Both carbachol and nicotine reduced short-term depression of EPSPs evoked by 10 Hz stimulation, indicating that EPSP reduction happens via reduction of presynaptic glutamate release. In the case of nicotine, several possible mechanisms for NMDAR-dependent EPSP reduction are discussed. As a result of NMDA receptor dependence, nicotinic EPSP reduction may serve to reduce the local spread of cortical excitation during heightened sensory activity.

scholarly journals A Novel Kartogenin-Releasing Polymer Scaffold Promotes Wounded Rat Achilles Tendon Enthesis Healing

2018 ◽  
Vol 3 (3) ◽  
pp. 2473011418S0053
Author(s):  
Jianying Zhang ◽  
Daibang Nie ◽  
Guangyi Zhao ◽  
Susheng Tan ◽  
MaCalus Hogan ◽  
...  
Keyword(s):  
Achilles Tendon ◽  
Saline Group ◽  
Future Research ◽  
Dependent Manner ◽  
Polymer Scaffold ◽  
Normal Medium ◽  
Post Surgery ◽  
Tendon Stem Cells

Category: Hindfoot Introduction/Purpose: Entheses have a special fibrocartilage transition zone where tendons and ligaments attach to bone. Enthesis injury is very common, and the reattachment of tendon to bone is a great challenge because healing takes place between a soft tissue (tendon) and a hard tissue (bone). We have now developed a kartogene (KGN)-containing polymer scaffold (KGN-P) that can precisely deliver KGN to damaged enthesis area. The effects of the KGN-containing polymer on the healing of wounded TBJ were investigated in vitro and in vivo. Methods: The proliferation and chondrogenesis of rat Achilles tendon stem cells (TSCs) grown in four conditions were measured: normal medium (Control); normal medium with 100 nM KGN (KGN); lysine diisocyanate (LDI)-glycerol scaffold with normal medium (LDI-P); LDI-glycerol-KGN scaffold with normal medium (KGN-P).A wound (1 mm) was created on each hind leg Achilles enthesis of all 8 rats (3 months old). The wounds were then treated either with 10 ul saline (Wound); or 10 ul of 10 uM KGN (KGN); or LDI polymer scaffold (LDI-P); or KGN-containing polymer scaffold (KGN-P). The rats were sacrificed on day 15 and 30 post-surgery, and their Achilles entheses were collected for gross inspection and histochemical analysis. Results: KGN-containing polymers have sponge-like structures (Fig. 1A-D), and release KGN in a time- and temperature-dependent manner (Fig. 1E). KGN-P scaffold induced chondrogenesis of TSCs (Fig. 2D, 2H) without changing cell proliferation (Fig. 2I), and enhanced fibrocartilage-like tissue formation (Fig. 3E). KGN (Fig. 3C) and LDI-P (Fig. 3D) treated groups exhibited unhealed wound areas as in saline group (Fig. 3B). Finally, KGN-P and KGN treated rat TSCs underwent chondrogenesis by upregulating collagen II, aggrecan, and SOX-9 expression (Fig. 3F). Conclusion: Our results showed that KGN-containing polymer scaffold enhanced wounded enthesis healing by inducing TSC chondrogenesis and promoting the formation of the fibrocartilage in the wound site. The KGN-P may be used for regeneration of wounded entheses in clinical settings. Future research will focus on optimizing KGN concentration and releasing rate in the polymer scaffold during enthesis healing.

Excitatory Postsynaptic Potentials Trigger a Plateau Potential in Rat Subthalamic Neurons at Hyperpolarized States

2001 ◽  
Vol 86 (4) ◽  
pp. 1816-1825 ◽  
Author(s):  
Takeshi Otsuka ◽  
Fujio Murakami ◽  
Wen-Jie Song
Keyword(s):  
Basal Ganglia ◽  
Membrane Properties ◽  
Dependent Manner ◽  
Excitatory Postsynaptic Potentials ◽  
Plateau Potentials ◽  
Postsynaptic Potentials ◽  
Plateau Potential ◽  
Voltage Dependent ◽  
Subthalamic Neurons ◽  
The Stability

The subthalamic nucleus (STN) directly innervates the output structures of the basal ganglia, playing a key role in basal ganglia function. It is therefore important to understand the regulatory mechanisms for the activity of STN neurons. In the present study, we aimed to investigate how the intrinsic membrane properties of STN neurons interact with their synaptic inputs, focusing on their generation and the properties of the long-lasting, plateau potential. Whole cell recordings were obtained from STN neurons in slices prepared from postnatal day 14 (P14) to P20 rats. We found that activation of glutamate receptor-mediated excitatory synaptic potentials (EPSPs) evoked a plateau potential in a subpopulation of STN neurons ( n = 13/22), in a voltage-dependent manner. Plateau potentials could be induced only when the cell was hyperpolarized to more negative than about −75 mV. Plateau potentials, evoked with a depolarizing current pulse, again only from a hyperpolarized state, were observed in about half of STN neurons tested ( n = 162/327). Only in neurons in which a plateau potential could be evoked by current injection did EPSPs evoke plateau potentials. L-type Ca2+ channels, Ca2+-dependent K+ channels, and TEA-sensitive K+ channels were found to be involved in the generation of the potential. The stability of the plateau potential, tested by the injection of a negative pulse current during the plateau phase, was found to be robust at the early phase of the potential, but decreased toward the end. As a result the early part of the plateau potential was resistant to membrane potential perturbations and would be able to support a train of action potentials. We conclude that excitatory postsynaptic potentials, evoked in a subpopulation of STN neurons at a hyperpolarized state, activate L-type Ca2+ and other channels, leading to the generation of a plateau potential. Thus about half of STN neurons can transform short-lasting synaptic excitation into a long train of output spikes by voltage-dependent generation of a plateau potential.

Effect of substance P on colonic mechanoreceptors, motility, and sympathetic neurons

1982 ◽  
Vol 243 (4) ◽  
pp. G259-G267 ◽  
Author(s):  
J. Krier ◽  
J. H. Szurszewski
Keyword(s):  
Substance P ◽  
Synaptic Transmission ◽  
Sympathetic Neurons ◽  
Colonic Motility ◽  
Input Resistance ◽  
Intraluminal Pressure ◽  
Excitatory Postsynaptic Potentials ◽  
Postsynaptic Potentials ◽  
Recording Techniques

Intracellular recording techniques were used in vitro to analyze the effects of substance P (SP) on synaptic transmission and electrical properties of sympathetic neurons in the inferior mesenteric ganglion (IMG) of the guinea pig. Intraluminal pressure-recording techniques were used to study the effects of SP on colonic motility. Superfusion of the ganglia with SP (10(-7) to 10(-6) M) depolarized the cell soma (2--12 mV) and increased cell input resistance (8--11 M omega). These effects converted synchronous excitatory postsynaptic potentials, in response to electrical stimulation of preganglionic nerves, and asynchronous excitatory postsynaptic potentials, in response to activation of colonic mechanoreceptors, to action potentials. Administration of SP to only the colon increased basal intraluminal pressure and the frequency and amplitude of phasic changes in intraluminal pressure. These changes increased mechanoreceptor synaptic input to neurons in the IMG. We conclude that SP facilitates synaptic transmission along noradrenergic pathways and increases colonic motility.

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