scholarly journals The effects of neurotransmitters on the integrative properties of spinal neurons in the lamprey

1993 ◽  
Vol 175 (1) ◽  
pp. 89-114
Author(s):  
L. E. Moore ◽  
J. T. Buchanan
Keyword(s):  
Amino Acids ◽  
Spinal Cord ◽  
Voltage Clamp ◽  
Excitatory Amino Acids ◽  
Neuronal Model ◽  
Spinal Neurons ◽  
Current Clamp ◽  
Impedance Function ◽  
Central Neurons ◽  
Voltage Dependent

1. The integrative behavior of lamprey central neurons was analyzed by white noise frequency domain methods and simulated with a minimal, non-linear neuronal model consisting of two voltage-dependent processes: (i) a depolarizing inwardly directed conductance carrying calcium and monovalent ions and (ii) a repolarizing outwardly directly conductance representing a generalized potassium conductance. In addition to normal properties, the effects of neurotransmitters were interpreted with the model. Specifically, N-methyl-D-aspartate (NMDA)-induced properties were simulated under conditions where the intrinsic voltage dependence of the potassium channels was constrained by properties of lamprey neurons. However, the NMDA channel kinetics were fixed by the single-channel properties of other neurons. The effects of focally applied neurotransmitters on the membrane properties of intact spinal cord neurons were quantitatively described with a reduced neuronal model that was also used to simulate transmitter-induced responses. In addition, transmitters were also released synaptically by KCl depolarization of projecting neurons. 2. Both synaptically released transmitters and focally applied putative excitatory or inhibitory transmitters directly applied to the spinal cord generally resulted in a decrease in the magnitude of the impedance function that was modeled by a decrease in membrane resistance (shunting effect). 3. Local application of the inhibitory neurotransmitters glycine or gamma-aminobutyric acid (GABA) led to small voltage responses when recorded near the resting potential. However, large decreases in the magnitude of the impedance function were observed in both current-clamp or voltage-clamp recording modes. 4. The excitatory amino acids quisqualate, kainate and glutamate evoked depolarizations in current clamp that activated intrinsic voltage-dependent conductances and obscured the direct effects of the transmitters. Under voltage-clamp conditions these transmitters caused a small decrease in the impedance magnitude that could be modeled by a shunt. 5. In contrast to the other excitatory amino acids, NMDA elicited large increases, rather than decreases, in both the magnitude and the phase lag of the impedance function. These changes were modeled by a negative conductance (a voltage-dependent conductance that produces an inward current). 6. The reduced neuron model provides an experimentally based description of the highly oscillatory and non-linear responses observed during NMDA activation of the spinal neurons involved in the pattern generation of locomotion. Simulations of sustained oscillatory behaviors consistent with experimental observations were carried out to illustrate the NMDA-induced integrative properties of central neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

Serotonin Modulates Dendritic Calcium Influx in Commissural Interneurons in the Mouse Spinal Locomotor Network

2007 ◽  
Vol 98 (4) ◽  
pp. 2157-2167 ◽  
Author(s):  
Manuel Díaz-Ríos ◽  
Daniel A. Dombeck ◽  
Watt W. Webb ◽  
Ronald M. Harris-Warrick
Keyword(s):  
Spinal Cord ◽  
Voltage Clamp ◽  
Neuronal Excitability ◽  
Calcium Influx ◽  
Active Role ◽  
Calcium Currents ◽  
Detectable Effect ◽  
Lumbar Region ◽  
Fictive Locomotion ◽  
Voltage Dependent

Commissural interneurons (CINs) help to coordinate left–right alternating bursting activity during fictive locomotion in the neonatal mouse spinal cord. Serotonin (5-HT) plays an active role in the induction of fictive locomotion in the isolated spinal cord, but the cellular targets and mechanisms of its actions are relatively unknown. We investigated the possible role of serotonin in modifying dendritic calcium currents, using a combination of two-photon microscopy and patch-clamp recordings, in identified CINs in the upper lumbar region. Dendritic calcium responses to applied somatic voltage-clamp steps were measured using fluorescent calcium indicator imaging. Serotonin evoked significant reductions in voltage-dependent dendritic calcium influx in about 40% of the dendritic sites studied, with no detectable effect in the remaining sites. We also detected differential effects of serotonin in different dendritic sites of the same neuron; serotonin could decrease voltage-sensitive calcium influx at one site, with no effect at a nearby site. Voltage-clamp studies confirmed that serotonin reduces the voltage-dependent calcium current in CINs. Current-clamp experiments showed that the serotonin-evoked decreases in dendritic calcium influx were coupled with increases in neuronal excitability; we discuss possible mechanisms by which these two seemingly opposing results can be reconciled. This research demonstrates that dendritic calcium currents are targets of serotonin modulation in a group of spinal interneurons that are components of the mouse locomotor network.

Voltage-clamp analysis of a Ca2+- and voltage-dependent chloride conductance in cultured mouse spinal neurons

1986 ◽  
Vol 55 (6) ◽  
pp. 1115-1135 ◽  
Author(s):  
D. G. Owen ◽  
M. Segal ◽  
J. L. Barker
Keyword(s):  
Voltage Clamp ◽  
Reversal Potential ◽  
Gamma Aminobutyric Acid ◽  
Spinal Neurons ◽  
Exponential Process ◽  
Voltage Clamp Analysis ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Ca 50 ◽  
O 10

Current and voltage-clamp recordings were made at room temperature from cultured mouse spinal neurons using conventional two-electrode voltage-clamp techniques and electrodes filled with either 3 M KCl, 3 M CsCl, or 3 M Cs2SO4. In the presence of tetraethylammonium and tetrodotoxin, “fast” (rapidly rising and falling) action potentials (FAP) of variable duration were recorded in most neurons. “Slow” (slowly rising and falling) depolarizing potentials (SDP) occurred in 23% of the cells, when using KCl-filled electrodes, and in 82% of the cells with CsCl-filled electrodes. The SDP was frequently preceded by an FAP, although in some cells activation of the SDP occurred before the FAP threshold was reached and in a graded fashion. Both the FAP and SDP were abolished by Cd2+ and other Ca2+ antagonists. In cells exhibiting SDPs, voltage-clamp analysis revealed a sustained (noninactivating) inward current (Isin) during depolarizing steps to potentials more positive than -45 mV. Repolarizing steps resulted in slowly decaying inward tail currents (Itail). Both Isin and Itail were abolished in solutions nominally free of Cao2+, or containing Ca2+-channel antagonists. Bao2+ did not support Isin. The data indicated a U-shaped activation curve for Isin, peaking at about -10 mV. Activation of Isin occurred exponentially with a time constant of approximately 140 ms at -23 mV, becoming faster at more depolarized potentials (ca. 50 ms at -2 mV). Deactivation was slow, giving rise to tail currents lasting seconds. In some cases deactivation could be described by a single exponential process, although frequently the kinetics were more complex. Deactivation was faster at hyperpolarized potentials and sensitive to extracellular ([Ca2+]o), duration of activating voltage steps, and the degree of activation of Isin. Using CsCl-filled electrodes, the reversal potential (Erev) for Isin was -1.7 mV (SEM 3.5 mV, n = 20). Erev always corresponded to the reversal potential for gamma-aminobutyric acid-evoked currents in the same cell. In experiments in which Cs2SO4-filled electrodes were used, Erev was estimated to be -44 mV (SEM 2.3 mV, n = 9). Neither complete substitution of Nao+ with choline ions nor elevation of [K+]o 10-fold significantly affected the estimated Erev. However, substitution of Cl0- with isethionate or methanesulphonate increased the amplitude of inward currents (recorded with CsCl-filled electrodes) and shifted Erev to more depolarized potentials. The results indicate that Cl- are the primary charge carriers for this current and that Cai2+ is required for its activation, leading us to identify it as ICl(Ca).(ABSTRACT TRUNCATED AT 400 WORDS)

The Role of Excitatory Amino Acids in Hypothermic Injury to Mammalian Spinal Cord Neurons

1996 ◽  
Vol 13 (12) ◽  
pp. 809-818 ◽  
Author(s):  
GEERT CRAENEN ◽  
SRDIJA JEFTINIJA ◽  
IVETA GRANTS ◽  
JEN HILL LUCAS
Keyword(s):  
Amino Acids ◽  
Spinal Cord ◽  
Excitatory Amino Acids ◽  
Spinal Cord Neurons ◽  
Hypothermic Injury

Excitatory amino acids rise to toxic levels upon impact injury to the rat spinal cord

1991 ◽  
Vol 547 (2) ◽  
pp. 344-348 ◽  
Author(s):  
Danxia Liu ◽  
Wipawan Thangnipon ◽  
David J. McAdoo
Keyword(s):  
Amino Acids ◽  
Spinal Cord ◽  
Excitatory Amino Acids ◽  
Rat Spinal Cord ◽  
Impact Injury

scholarly journals Intracellular QX-314 Causes Depression of Membrane Potential Oscillations in Lamprey Spinal Neurons During Fictive Locomotion

2002 ◽  
Vol 87 (6) ◽  
pp. 2676-2683 ◽  
Author(s):  
Guo-Yuan Hu ◽  
Zoltán Biró ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Dendritic Tree ◽  
Cell Voltage ◽  
Fictive Locomotion ◽  
Spinal Neurons ◽  
Potential Oscillations ◽  
Short Pulses ◽  
Voltage Dependent ◽  
Membrane Potential Oscillations

Spinal neurons undergo large cyclic membrane potential oscillations during fictive locomotion in lamprey. It was investigated whether these oscillations were due only to synaptically driven excitatory and inhibitory potentials or if voltage-dependent inward conductances also contribute to the depolarizing phase by using N-(2,6-dimethylphenyl carbamoylmethyl)triethylammonium bromide (QX-314) administered intracellularly during fictive locomotion. QX-314 intracellularly blocks inactivating and persistent Na+ channels, and in some neurons, effects on certain other types of channels have been reported. To detail the effects of QX-314 on Na+ and Ca2+ channels, we used dissociated lamprey neurons recorded under whole cell voltage clamp. At low intracellular concentrations of QX-314 (0.2 mM), inactivating Na+ channels were blocked and no effects were exerted on Ca2+ channels (also at 0.5 mM). At 10 mM QX-314, there was, however a marked reduction of I Ca. In the isolated spinal cord of the lamprey, fictive locomotion was induced by superfusing the spinal cord with Ringer's solution containing N-methyl-d-aspartate (NMDA), while recording the locomotor activity from the ventral roots. Simultaneously, identified spinal neurons were recorded intracellularly, while infusing QX-314 from the microelectrode. Patch electrodes cannot be used in the intact spinal cord, and therefore “sharp” electrodes were used. The amplitude of the oscillations was consistently reduced by 20–25% in motoneurons ( P < 0.05) and unidentified spinal neurons ( P < 0.005). The onset of the effect started a few minutes after impalement and reached a stable level within 30 min. These effects thus show that QX-314 causes a reduction in the amplitude of membrane potential oscillations during fictive locomotion. We also investigated whether QX-314 could affect glutamate currents by applying short pulses of glutamate from an extracellular pipette. No changes were observed. We also found no evidence for a persistent Na+ current in dissociated neurons, but these cells have a much-reduced dendritic tree. The results indicate that there is an inward conductance, which is sensitive to QX-314, during membrane potential oscillations that “boosts” the synaptic drive during fictive locomotion. Taken together, the results suggest that inactivating Na+ channels contribute to this inward conductance although persistent Na+channels, if present on dendrites, could possibly also contribute to shaping the membrane potential oscillations.

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