Facilitating effect of CCK on nicotinic neurotransmission in cat pancreatic ganglion

1996 ◽  
Vol 270 (3) ◽  
pp. G526-G534 ◽  
Author(s):  
R. C. Ma ◽  
J. H. Szurszewski
Keyword(s):  
Input Resistance ◽  
Postsynaptic Membrane ◽  
Excitatory Postsynaptic Potential ◽  
Nerve Terminals ◽  
Quantal Content ◽  
Quantal Size ◽  
Postsynaptic Potential ◽  
Ganglion Neurons ◽  
Ganglionic Transmission

Previous studies have demonstrated the presence of cholecystokinin (CCK)-like peptides in nerve terminals surrounding ganglion neurons of the cat pancreas. The present study was undertaken to determine the effect of cholecystokinin octapeptide (CCK-8) on ganglionic transmission. Recordings were made intracellularly in vitro from ganglion neurons in isolated pieces of the pancreas. Sulfated CCK-8 (S-CCK-8) and nonsulfated CCK-8 initiated or increased ongoing fast excitatory postsynaptic potential (fEPSP) activity, an effect antagonized by hexamethonium. Superfusion of S-CCK-8 in concentrations ranging from 10(-11) to 10(-8) M significantly augmented the amplitude of nerve-evoked subthreshold fEPSPs without a significant change in either membrane potential or membrane input resistance. S-CCK-8 (10(-8)M) also increased the quantal content and quantal size of nerve-evoked fEPSPs and increased the response to exogenously applied acetylcholine (ACh). Concentrations of S-CCK-8 higher than 10(-8)M caused depolarization and an increase in membrane input resistance, an effect unaltered by a low-Ca+, high-Mg2+ solution. It was concluded that S-CCK-8 potentiated nicotinic transmission by facilitating release of ACh from preganglionic nerve terminals and by increasing the postsynaptic membrane sensitivity to ACh.

Postnatal Changes in Membrane Properties of Mice Trigeminal Ganglion Neurons

2002 ◽  
Vol 87 (5) ◽  
pp. 2398-2407 ◽  
Author(s):  
Carmen Cabanes ◽  
Mikel López de Armentia ◽  
Félix Viana ◽  
Carlos Belmonte
Keyword(s):  
Postnatal Development ◽  
Trigeminal Ganglion ◽  
Input Resistance ◽  
Membrane Capacitance ◽  
Membrane Properties ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Depolarization Rate ◽  
Ganglion Neurons

Intracellular recordings from neurons in the mouse trigeminal ganglion (TG) in vitro were used to characterize changes in membrane properties that take place from early postnatal stages (P0–P7) to adulthood (>P21). All neonatal TG neurons had uniformly slow conduction velocities, whereas adult neurons could be separated according to their conduction velocity into Aδ and C neurons. Based on the presence or absence of a marked inflection or hump in the repolarization phase of the action potential (AP), neonatal neurons were divided into S- (slow) and F-type (fast) neurons. Their passive and subthreshold properties (resting membrane potential, input resistance, membrane capacitance, and inward rectification) were nearly identical, but they showed marked differences in AP amplitude, AP overshoot, AP duration, rate of AP depolarization, rate of AP repolarization, and afterhyperpolarization (AHP) duration. Adult TG neurons also segregated into S- and F-type groups. Differences in their mean AP amplitude, AP overshoot, AP duration, rate of AP depolarization, rate of AP repolarization, and AHP duration were also prominent. In addition, axons of 90% of F-type neurons and 60% of S-type neurons became faster conducting in their central and peripheral branch, suggestive of axonal myelination. The proportion of S- and F-type neurons did not vary during postnatal development, suggesting that these phenotypes were established early in development. Membrane properties of both types of TG neurons evolved differently during postnatal development. The nature of many of these changes was linked to the process of myelination. Thus myelination was accompanied by a decrease in AP duration, input resistance ( R in), and increase in membrane capacitance (C). These properties remained constant in unmyelinated neurons (both F- and S-type). In adult TG, all F-type neurons with inward rectification were also fast-conducting Aδ, suggesting that those F-type neurons showing inward rectification at birth will evolve to F-type Aδ neurons with age. The percentage of F-type neurons showing inward rectification also increased with age. Both F- and S-type neurons displayed changes in the sensitivity of the AP to reductions in extracellular Ca2+ or substitution with Co2+ during the process of maturation.

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro

1994 ◽  
Vol 72 (4) ◽  
pp. 1993-2003 ◽  
Author(s):  
R. A. Warren ◽  
A. Agmon ◽  
E. G. Jones
Keyword(s):  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Initial Response ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential ◽  
Synaptic Interactions ◽  
Gabaa Receptor Antagonist

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

Extracellular Magnesium Ion Modifies the Actions of Volatile Anesthetics in Area CA1 of Rat Hippocampus In Vitro 

2002 ◽  
Vol 96 (3) ◽  
pp. 681-687 ◽  
Author(s):  
Rika Sasaki ◽  
Koki Hirota ◽  
Sheldon H. Roth ◽  
Mitsuaki Yamazaki
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hippocampal Slices ◽  
Volatile Anesthetics ◽  
Population Spike ◽  
Magnesium Ion ◽  
Excitatory Postsynaptic Potential ◽  
Aspartate Receptor ◽  
Postsynaptic Potential

Background Magnesium ion (Mg2+) is involved in important processes as modulation of ion channels, receptors, neurotransmitter release, and cell excitability in the central nervous system. Although extracellular Mg2+ concentration ([Mg2+]o) can be altered during general anesthesia, there has been no evidence for [Mg2+]o-dependent modification of anesthetic actions on neural excitability in central nervous system preparations. The purpose of current study was to determine whether the effects of volatile anesthetics are [Mg2+]o-dependent in mammalian central nervous system. Methods Extracellular electrophysiologic recordings from CA1 neurons in rat hippocampal slices were used to investigate the effects of [Mg2+]o and anesthetics on population spike amplitude and excitatory postsynaptic potential slope. Results The depression of population spike amplitudes and excitatory postsynaptic potential slopes by volatile anesthetics were significantly dependent on [Mg2+]o. The effects were attenuated in the presence of a constant [Mg2+]o/extracellular Ca2+ concentration ratio. However, neither N-methyl-d-aspartate receptor antagonists nor a non-N-methyl-d-aspartate receptor antagonist altered the [Mg2+]o-dependent anesthetic-induced depression of population spikes. Volatile anesthetics produced minimal effects on input-output (excitatory postsynaptic potential-population spike) relations or the threshold for population spike generation. The effects were not modified by changes in [Mg2+]o. In addition, the population spike amplitudes, elicited via antidromic (nonsynaptic) stimulation, were not influenced by [Mg2+]o in the presence of volatile anesthetics. Conclusions These results provide support that alteration of [Mg2+]o modifies the actions of volatile anesthetics on synaptic transmission and that the effects could be, at least in part, a result of presynaptic Ca2+ channel-related mechanisms.

Effects of low concentrations of 4-aminopyridine on CA1 pyramidal cells of the hippocampus

1989 ◽  
Vol 61 (5) ◽  
pp. 953-970 ◽  
Author(s):  
P. Perreault ◽  
M. Avoli
Keyword(s):  
High Frequency ◽  
Hippocampal Slices ◽  
Extracellular Recording ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Peak Latency ◽  
Excitatory Postsynaptic Potential ◽  
Average Value ◽  
Bath Application

1. Intracellular and extracellular recording techniques were used to study the effects of bath application of 4-aminopyridine (4-AP) on pyramidal cells of the CA1 subfield of rat hippocampal slices maintained in vitro. The concentration of 4-AP used in most experiments was 50 microM. However, similar results were obtained with a concentration ranging from 5 to 100 microM. 2. Following 4-AP application, cells impaled with K-acetate-filled microelectrodes hyperpolarized by an average of 2.6 mV (from -68.7 to -71.3 mV, P less than or equal to 0.01). This change was accompanied by the appearance of high-frequency spontaneous hyperpolarizations. Conversely, when KCl-filled microelectrodes were used, an average depolarization of 5.8 mV [from -73.1 to -67.3 mV, not significant (NS)] associated with the occurrence of repetitive depolarizing potentials was observed. In both cases, these changes were concomitant with a small decrease in membrane input resistance, which was statistically significant only for cells impaled with K-acetate-filled microelectrodes. When synaptic transmission was blocked by tetrodotoxin (TTX), 4-AP induced in cells studied with K-acetate microelectrodes an average depolarization of 2.4 mV (from -62.8 to -60.4 mV, P less than or equal to 0.01) accompanied by a small increase in input resistance (from 32.0 to 35.8 M omega, P less than or equal to 0.05). High-frequency spontaneous potentials failed to occur under these conditions. During 4-AP application, the threshold and the latency of action potentials elicited by a depolarizing current pulse increased in 36% of the neurons studied (n = 14). 3. The amplitude of the stratum (s.) radiatum-induced excitatory postsynaptic potential (EPSP) was augmented by 4-AP. Both the early and late inhibitory postsynaptic potentials (IPSPs) evoked by orthodromic stimuli were also increased in amplitude and duration. In addition, a late (peak latency, 150-600 ms) and long-lasting (duration, 600-1,500 ms) depolarizing potential appeared between the early and the late IPSPs and progressively increased until it partially masked these hyperpolarizations. This long-lasting depolarization (LLD) could also be induced by antidromic stimulation, although in this case it was preceded by an additional, fast-rising, brief depolarization. 4. A similar brief depolarization preceded the orthodromically induced LLD in 69% of the neurons bathed in the presence of 4-AP. The average value of the peak latency of this potential was 62 +/- 27 (SD) ms for orthodromic and 110 +/- 70 ms for antidromic responses.(ABSTRACT TRUNCATED AT 400 WORDS)

Similar Electrophysiological Changes in Axotomized and Neighboring Intact Dorsal Root Ganglion Neurons

2003 ◽  
Vol 89 (3) ◽  
pp. 1588-1602 ◽  
Author(s):  
Chao Ma ◽  
Yousheng Shu ◽  
Zheng Zheng ◽  
Yong Chen ◽  
Hang Yao ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Receptive Fields ◽  
Input Resistance ◽  
Spinal Nerve ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Ganglion Neurons

We investigated electrophysiological changes in chronically axotomized and neighboring intact dorsal root ganglion (DRG) neurons in rats after either a peripheral axotomy consisting of an L5 spinal nerve ligation (SNL) or a central axotomy produced by an L5 partial rhizotomy (PR). SNL produced lasting hyperalgesia to punctate indentation and tactile allodynia to innocuous stroking of the foot ipsilateral to the injury. PR produced ipsilateral hyperalgesia without allodynia with recovery by day 10. Intracellular recordings were obtained in vivo from the cell bodies (somata) of axotomized and intact DRG neurons, some with functionally identified peripheral receptive fields. PR produced only minor electrophysiological changes in both axotomized and intact somata in L5 DRG. In contrast, extensive changes were observed after SNL in large- and medium-sized, but not small-sized, somata of intact (L4) as well as axotomized (L5) DRG neurons. These changes included (in relation to sham values) higher input resistance, lower current and voltage thresholds, and action potentials with longer durations and slower rising and falling rates. The incidence of spontaneous activity, recorded extracellularly from dorsal root fibers in vitro, was significantly higher (in relation to sham) after SNL but not after PR, and occurred in myelinated but not unmyelinated fibers from both L4 (9.1%) and L5 (16.7%) DRGs. We hypothesize that the changes in the electrophysiological properties of axotomized and intact DRG neurons after SNL are produced by a mechanism associated with Wallerian degeneration and that the hyperexcitability of intact neurons may contribute to SNL-induced hyperalgesia and allodynia.

scholarly journals Electrophysiological Properties and Synaptic Responses of Cells in the Trigeminal Principal Sensory Nucleus of Postnatal Rats

1999 ◽  
Vol 82 (5) ◽  
pp. 2765-2775 ◽  
Author(s):  
Fu-Sun Lo ◽  
William Guido ◽  
Reha S. Erzurumlu
Keyword(s):  
Brain Stem ◽  
Stimulus Intensity ◽  
Input Resistance ◽  
Excitatory Postsynaptic Potential ◽  
Epsp Amplitude ◽  
Postsynaptic Potential ◽  
Stepwise Increase ◽  
Sensory Nucleus ◽  
Postnatal Rats ◽  
Synaptic Responses

In the rodent brain stem trigeminal complex, select sets of neurons form modular arrays or “barrelettes,” that replicate the patterned distribution of whiskers and sinus hairs on the ipsilateral snout. These cells detect the patterned input from the trigeminal axons that innervate the whiskers and sinus hairs. Other brain stem trigeminal cells, interbarrelette neurons, do not form patterns and respond to multiple whiskers. We examined the membrane properties and synaptic responses of morphologically identified barrelette and interbarrelette neurons in the principal sensory nucleus (PrV) of the trigeminal nerve in early postnatal rats shortly after whisker-related patterns are established. Barrelette cell dendritic trees are confined to a single barrelette, whereas the dendrites of interbarrelette cells span wider territories. These two cell types are distinct from smaller GABAergic interneurons. Barrelette cells can be distinguished by a prominent transient A-type K+ current ( I A) and higher input resistance. On the other hand, interbarrelette cells display a prominent low-threshold T-type Ca2+ current ( I T) and lower input resistance. Both classes of neurons respond differently to electrical stimulation of the trigeminal tract. Barrelette cells show either a monosynaptic excitatory postsynaptic potential (EPSP) followed by a large disynaptic inhibitory postsynaptic potential (IPSP) or just simply a disynaptic IPSP. Increasing stimulus intensity produces little change in EPSP amplitude but leads to a stepwise increase in IPSP amplitude, suggesting that barrelette cells receive more inhibitory input than excitatory input. This pattern of excitation and inhibition indicates that barrelette cells receive both feed-forward and lateral inhibition. Interbarrelette cells show a large monosynaptic EPSP followed by a small disynaptic IPSP. Increasing stimulus intensity leads to a stepwise increase in EPSP amplitude and the appearance of polysynaptic EPSPs, suggesting that interbarrelette cells receive excitatory inputs from multiple sources. Taken together, these results indicate that barrelette and interbarrelette neurons can be identified by their morphological and functional attributes soon after whisker-related pattern formation in the PrV.

Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. I. Electrophysiology

1990 ◽  
Vol 64 (2) ◽  
pp. 532-540 ◽  
Author(s):  
D. H. Edwards
Keyword(s):  
Reverse Bias ◽  
Membrane Conductance ◽  
Input Resistance ◽  
Postsynaptic Membrane ◽  
Delayed Rectifier ◽  
Excitatory Postsynaptic Potential ◽  
Gamma Aminobutyric Acid ◽  
Resistance Change ◽  
Inward Current ◽  
Electrode Current

1. Mechanisms of depolarizing synaptic inhibition were investigated at the crayfish giant motor synapse with the use of two-electrode current- and voltage-clamp techniques. Depolarizing inhibitory postsynaptic potentials (d-IPSPs) of between 5 and 15 mV in amplitude are produced there in the motor giant motoneuron (MoG) by motor giant inhibitor (MoGI) interneurons. 2. Three mechanisms of inhibition are activated by the d-IPSP: inactivation of a voltage-sensitive inward current (probably sodium), activation of the delayed rectifier, and reverse bias of the electrically rectifying giant motor synapse (GMS). These mechanisms supplement the inhibition produced by a gamma-aminobutyric acid (GABA)-mediated increase in postsynaptic conductance. 3. The d-IPSP is produced by a fast-rising increase in postsynaptic membrane conductance that peaks at 10 microS and lasts nearly 100 ms. 4. An 8-ms, 10-mV depolarizing prepulse inactivated 90% of the inward current evoked by a subsequent step to 33 mV above rest potential, which was -70 mV. d-IPSPs having similar amplitudes should have similar effects on the inward current evoked by an excitatory postsynaptic potential (EPSP). 5. The input resistance of MoG decreased by greater than 60% when the cell was depolarized to 11 mV above rest. This resistance change corresponds to delayed rectification, which should also contribute to the increase in input conductance during a d-IPSP. 6. Depolarization of MoG by 10 mV reduced the excitatory postsynaptic current through the GMS by up to 30%. The reduction in synaptic current occurs because postsynaptic depolarization reduces the transynaptic driving force and increases the reverse bias of the electrically rectifying synapse.(ABSTRACT TRUNCATED AT 250 WORDS)

Kynurenic acid antagonizes the excitatory postsynaptic potential elicited in neostriatal neurons in the in vitro slice of the rat

1989 ◽  
Vol 480 (1-2) ◽  
pp. 290-293 ◽  
Author(s):  
John P. Walsh ◽  
Chester D. Hull ◽  
Michael S. Levine ◽  
Nathaniel A. Buchwald
Keyword(s):  
Kynurenic Acid ◽  
Excitatory Postsynaptic Potential ◽  
Postsynaptic Potential

Neurophysiological consequences of nitroxide antioxidants

1995 ◽  
Vol 73 (3) ◽  
pp. 399-403 ◽  
Author(s):  
Stephen M. Hahn ◽  
Anne Marie DeLuca ◽  
James B. Mitchell ◽  
Dennis L. Lepinski ◽  
Terry C. Pellmar
Keyword(s):  
Central Nervous System ◽  
Epileptiform Activity ◽  
Antioxidant Compounds ◽  
Excitatory Postsynaptic Potential ◽  
Toxic Compound ◽  
Postsynaptic Potential ◽  
Potential Spike ◽  
The Central Nervous System

Nitroxides are antioxidant compounds that have been shown to provide radioprotection in vivo and in vitro. Radioprotection in vivo is limited by toxicity, which appears to be neurologic in nature. To further evaluate the toxicity of these compounds, three representative nitroxides, Tempol, Tempamine, and Tempo, were examined in slices of guinea pig hippocampus. Each nitroxide increased the population spike and caused potentiation of excitatory postsynaptic potential – spike coupling. Repetitive activity and epileptiform activity were observed at the highest concentrations of Tempo and Tempamine. Tempol was the least toxic compound in this system, followed by Tempamine and Tempo. Additional studies are necessary to further define the effects of nitroxides on the central nervous system and to develop strategies to mitigate these effects.Key words: nitroxides, brain, neurophysiology, toxicity, antioxidants.

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