Excitatory Synaptic Currents in Lumbosacral Parasympathetic Preganglionic Neurons Evoked by Stimulation of the Dorsal Commissure

2003 ◽  
Vol 89 (1) ◽  
pp. 382-389 ◽  
Author(s):  
Akira Miura ◽  
Masahito Kawatani ◽  
William C. De Groat
Keyword(s):  
Time Constant ◽  
Decay Time ◽  
Fast Component ◽  
Time To Peak ◽  
Current Voltage ◽  
Current Voltage Relationship ◽  
Voltage Relationship ◽  
Stimulation Of

Excitatory pathways from the dorsal commissure (DCM) to L6–S1 parasympathetic preganglionic neurons (PGN) were examined using whole-cell patch-clamp recording techniques in spinal cord slices from neonatal rats. PGN were identified by retrograde axonal transport of a fluorescent dye injected into the intraperitoneal space. Excitatory postsynaptic currents (EPSCs) were evoked in PGN by stimulation of DCM in the presence of bicuculline methiodide (10 μM) and strychnine (1 μM) to block inhibitory pathways. Electrical stimulation of DCM evoked two types of inward currents. In the majority of PGN ( n = 66), currents (mean amplitude, 47.9 ± 4.7 pA) occurred at a short and relatively constant latency (3.8 ± 0.1 ms) and presumably represent monosynaptic EPSCs (Type 1). However, in other neurons ( n = 20), a different type of EPSC (Type 2) was noted, consisting of a fast monosynaptic component followed by a prolonged inward current with superimposed fast transients presumably representing excitatory inputs mediated by polysynaptic pathways. Type 1 EPSCs were pharmacologically dissected into two components. A fast component was blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 5μM) and a slowly decaying component was blocked by 2-amino-5-phosphonovalerate (APV, 50 μM). The fast component of Type 1 EPSCs had a linear current-voltage relationship and reversed at a membrane potential of −7.6 ± 1.3 mV ( n = 5). The fast component of Type 2 EPSCs was also blocked by 5 μM CNQX and the remaining slower component was blocked by 50 μM APV. When the DCM was stimulated in the presence of 50 μM APV, the time to peak and decay time constant in Type 1 EPSCs were 1.9 ± 0.2 and 4.1 ± 0.8 ms, respectively. Examination of the NMDA receptor-mediated component of the EPSCs in the presence of 5 μM CNQX revealed a current-voltage relationship that had a region of negative slope conductance (from −20 to −80 mV), which was abolished in Mg2+-free external solution. The time to peak and decay time constant of this component were 14.2 ± 2.0 and 91.0 ± 12.4 ms, respectively. Type 1 EPSCs in some PGN responded in an all-or-none manner and presumably represented unitary synaptic responses; whereas Type 2 EPSCs always exhibited a graded stimulus intensity–response relationship. Paired-pulse facilitation (50-ms interstimulus intervals; 141 ± 5.6% increase, n = 8) of EPSCs was observed. These results indicate that PGN receive monosynaptic and polysynaptic glutamatergic excitatory inputs from neurons and/or axonal pathways in the DCM.

Gap junction channel gating at bass retinal electrical synapses

1996 ◽  
Vol 13 (6) ◽  
pp. 1049-1057 ◽  
Author(s):  
Chengbiao Lu ◽  
Douglas G. McMahon
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Single Channel ◽  
Horizontal Cells ◽  
Electrical Synapses ◽  
Dependent Inactivation ◽  
Current Voltage ◽  
Voltage Dependent ◽  
Current Voltage Relationship ◽  
Voltage Relationship

AbstractTo further characterize the properties of retinal horizontal cell electrical synapses, we have studied the gating characteristics of gap junctions between cone-driven horizontal cells from the hybrid striped bass retina using double whole-cell voltage-clamp techniques. In a total of 105 cell pairs, the macroscopic conductance ranged from 0.4–100 nS with most cell pairs exhibiting junctional conductances between 10 and 30 nS. The junctional current-voltage relationship showed that peak or instantaneous currents (Iinst) were linear within the Vj range of ±100 mV and that steady-state junctional currents (Iss) exhibited rectification with increasing voltage beginning around ±30–40 mV Vj. The normalized junctional current-voltage relationship was well fit by a two-state Boltzmann distribution, with an effective gating charge of 1.9 charges/channel, a half-maximal voltage of approximately ±55 mV, and a normalized residual conductance of 0.28. The decay of junctional current followed a single exponential time course with the time constant decreasing with increasing Vj. Recovery of junctional current from voltage-dependent inactivation takes about 1 s following a pulse of 80 mV, and is about five times slower than the inactivation time course at the same Vj. Single-channel analysis showed that the unitary conductance of junctional channels is 50–70 pS. The overall open probability decreased in a voltage-dependent manner. Both the mean channel open time and the frequency of channel opening decreased, while the channel closure time increased. The ratio of closed time/total recording time significantly increased as Vj increased. Increased Vj reduced the number of events at all levels and shifted the unitary conductance to a lower level. Kinetic analysis of channel open duration showed that the distribution of channel open times was best fit by two exponentials and increased Vj significantly reduced the slower time constant. These results indicate that bass retina horizontal cells exhibit voltage-dependent inactivation of macroscopic junctional current. The inactivation occurs at the single-channel level mainly by increasing the rate of closure of voltage-sensitive channels.

Stimulation of the slow calcium current in bullfrog skeletal muscle fibers by cAMP and cGMP

1993 ◽  
Vol 265 (1) ◽  
pp. C47-C53 ◽  
Author(s):  
T. G. Kokate ◽  
J. A. Heiny ◽  
N. Sperelakis
Keyword(s):  
Skeletal Muscle ◽  
Cardiac Muscle ◽  
Cyclic Nucleotides ◽  
Muscle Fibers ◽  
Cyclic Monophosphate ◽  
Current Voltage ◽  
Current Voltage Relationship ◽  
Camp And Cgmp ◽  
Voltage Relationship ◽  
Stimulation Of

The effects of adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP) on slow calcium currents (ICa) were investigated using the Vaseline-gap voltage-clamp technique in bullfrog skeletal muscle cut fibers. Both cAMP and cGMP induced a pronounced increase in the amplitude of ICa when applied to the cut ends of fibers. Both cyclic nucleotides also decreased time to peak current at all membrane potentials. The current-voltage relationship was shifted toward more negative potentials by cAMP as well as cGMP. The potentiating effects of cAMP and cGMP on ICa were additive. 8-Bromo analogues of both nucleotides had similar effects on ICa. The beta-adrenergic agonist isoproterenol, applied extracellularly, also produced an increase in the amplitude of ICa and produced a leftward shift in the current-voltage relationship. These results suggest that both cAMP and cGMP modulate calcium slow channels in bullfrog skeletal muscle fibers, causing stimulation of the ICa. The effect of cyclic nucleotides on ICa in bullfrog skeletal muscle contrasts with that in mammalian cardiac muscle, in which the same nucleotides produce opposite effects on the slow ICa, i.e., in cardiac muscle cAMP stimulates, and cGMP inhibits, the slow ICa.

scholarly journals Plasticity of calcium-permeable AMPA glutamate receptors in Pro-opiomelanocortin neurons

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Shigetomo Suyama ◽  
Alexandra Ralevski ◽  
Zhong-Wu Liu ◽  
Marcelo O Dietrich ◽  
Toshihiko Yada ◽  
...  
Keyword(s):  
Food Deprivation ◽  
High Fat Diet ◽  
Receptor Complex ◽  
High Fat ◽  
Fasted State ◽  
Linear Current ◽  
Current Voltage ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship

POMC neurons integrate metabolic signals from the periphery. Here, we show in mice that food deprivation induces a linear current-voltage relationship of AMPAR-mediated excitatory postsynaptic currents (EPSCs) in POMC neurons. Inhibition of EPSCs by IEM-1460, an antagonist of calcium-permeable (Cp) AMPARs, diminished EPSC amplitude in the fed but not in the fasted state, suggesting entry of GluR2 subunits into the AMPA receptor complex during food deprivation. Accordingly, removal of extracellular calcium from ACSF decreased the amplitude of mEPSCs in the fed but not the fasted state. Ten days of high-fat diet exposure, which was accompanied by elevated leptin levels and increased POMC neuronal activity, resulted in increased expression of Cp-AMPARs on POMC neurons. Altogether, our results show that entry of calcium via Cp-AMPARs is inherent to activation of POMC neurons, which may underlie a vulnerability of these neurons to calcium overload while activated in a sustained manner during over-nutrition.

Capsaicin and nicotine both activate a subset of rat trigeminal ganglion neurons

1996 ◽  
Vol 270 (6) ◽  
pp. C1807-C1814 ◽  
Author(s):  
L. Liu ◽  
S. A. Simon
Keyword(s):  
Trigeminal Ganglion ◽  
Acetylcholine Receptors ◽  
Ganglion Cells ◽  
Whole Cell Patch Clamp ◽  
Current Voltage ◽  
Trigeminal Ganglion Neurons ◽  
Ganglion Neurons ◽  
Relationship Of ◽  
Current Voltage Relationship ◽  
Voltage Relationship

Nicotine and capsaicin produce many similar physiological responses that include pain, irritation, and vasodilation. To determine whether neuronal nicotine acetylcholine receptors (nAChR) are present on capsaicin-sensitive neurons, whole cell patch-clamp recordings were performed on rat trigeminal ganglion cells. It was found that approximately 20% of the total number of neurons tested was activated by both 100 microM nicotine and 1 nM capsaicin. Other subsets of neurons were activated by only one of these compounds, whereas a fourth subset was not activated by either compound. At -60 mV, the magnitude of the capsaicin-activated currents was about three times larger than the magnitude of the nicotine-activated currents. The current-voltage relationship of the nAChR exhibited marked rectification, such that for voltages > or = 0 mV the current was essentially zero. In contrast, the current-voltage relationship of the capsaicin-activated current was ohmic from +/- 60 mV. These data indicate the existence of subsets of capsaicin-sensitive afferent neurons.

Simulation of Na/K Pump Current-Voltage Relationship

1992 ◽  
Vol 671 (1 Ion-Motive AT) ◽  
pp. 449-451 ◽  
Author(s):  
X.-Y. LIU ◽  
T. A. KINARD ◽  
J. R. STIMERS
Keyword(s):  
Pump Current ◽  
Current Voltage ◽  
Current Voltage Relationship ◽  
Voltage Relationship

scholarly journals Ionic Basis of Membrane Potential and of Acetylcholine-evduced Currents in the Cell Body of the Cockroach Fast Coxal Depressor Motor Neurone

1990 ◽  
Vol 151 (1) ◽  
pp. 21-39 ◽  
Author(s):  
JONATHAN A. DAVID ◽  
DAVID B. SATTELLE
Keyword(s):  
Cell Body ◽  
Outward Current ◽  
Motor Neurone ◽  
Resting Potential ◽  
Inward Current ◽  
Current Voltage ◽  
Low K ◽  
Current Voltage Relationship ◽  
Ionic Basis ◽  
Voltage Relationship

The ionic basis of the resting potential and of the response to acetylcholine (ACh) has been investigated in the cell body membrane of the fast coxal depressor motor neurone in the metathoracic ganglion of the cockroach Periplaneta americana. By means of ion-sensitive microelectrodes, intracellular concentrations of three ion species were estimated (mmoll−1): [K+]i, 1443; [Na+]i, 9±1; [Cl−], 7±1. The resting potential of continuously superfused cells was −75.6±1.9mV at 22° C. A change in resting potential of 42.0±2.5mV accompanied a decade change in [K+]o. Experiments with (10−4moll−1) ouabain, Na+ injection, low temperature (10°C) and non-superfused cells indicated the presence of an electrogenic sodium pump. Under current-clamp, the cell body membrane was depolarized by sequentially applied, ionophoretic pulses (500ms duration) of ACh. Under voltage-clamp, such doses of ACh resulted in an inward current which was abolished in low-Na+ saline. Ion-sensitive electrodes revealed an increase in [Na+]i but no change in [Cl−1]j in response to externally applied ACh. The ACh-induced current-voltage relationship was shifted in a negative direction by low-K+ saline. The AChinduced inward current was usually followed by a delayed outward current which reversed at Ek. Low-K+ saline had the same effect on this outward component as depolarizing the membrane. This suggests that the outward current component is carried by K+. The ACh-induced inward current and the delayed outward current were potentiated either when [Ca2+]i was lowered by injecting the calcium chelator BAPTA or by exposure of the cell to low-Ca2+ saline. High-Ca2+ saline reduced the inward component of the response and produced a negative shift in the AChinduced current-voltage relationship. The amplitude of the delayed outward

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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