Noradrenaline-induced afterdepolarization in cat sympathetic preganglionic neurons in vitro

1987 ◽  
Vol 57 (5) ◽  
pp. 1314-1324 ◽  
Author(s):  
M. Yoshimura ◽  
C. Polosa ◽  
S. Nishi
Keyword(s):  
Action Potential ◽  
Slow Component ◽  
Membrane Conductance ◽  
Repetitive Firing ◽  
Ca Channel ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Repolarization Phase

Sympathetic preganglionic neurons of the intermediolateral nucleus were identified by antidromic stimulation in the slice of the T2 or T3 segment of the cat spinal cord. In normal Krebs solution, the action potential of these neurons had a shoulder on the repolarization phase and was followed by a long-lasting afterhyperpolarization (AHP). The AHP had a fast and a slow component. Superfusion of the slice with noradrenaline (NA), 10-50 microM, resulted in depression of the shoulder on the repolarization phase of the action potential, in the appearance of an afterdepolarization (ADP), which was absent in control conditions, and in depression of the slow component of the AHP. These effects were present whether the membrane potential of the sympathetic preganglionic neurons was decreased, increased, or not changed by NA. A typical ADP had time to peak of 50 ms and decay time of 200-500 ms; the amplitude was variable and large ADPs could be suprathreshold, causing repetitive firing. The amplitude and duration of the ADP increased with NA concentration. The appearance of the ADP seemed to be independent of the depressant effect of NA on the slow AHP. The ADP was associated with a decrease in neuron input resistance and was voltage dependent, being depressed in nonlinear fashion by membrane hyperpolarization. The ADP decreased in amplitude or disappeared within a range of membrane potentials from -70 to -90 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM), by low Ca Krebs (0.25 mM), and by iontophoretic injection of ethyleneglycol-bis(B-aminoethyl-ether)-N,N'-tetraacetic acid into the cell. Increasing Ca concentration from 2.5 to 10.0 mM had no effect. The ADP was unaffected by tetrodotoxin, at a concentration blocking the Na spike, but was suppressed in Na-free medium, even when the Ca spike was prolonged by tetraethylammonium 20 mM. Changes in external K concentration from 3.6 to 2.5 or 10.0 mM did not change the ADP. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. It is concluded that the ADP, evoked by NA, is due to an increase in membrane conductance involving Na and Ca ions, possibly a Ca-activated Na conductance. The ADP provides a mechanism with which NA may modulate sympathetic preganglionic neuron responsiveness to excitatory synaptic inputs.

APV-sensitive dorsal root afferent transmission to neonate rat sympathetic preganglionic neurons in vitro

1990 ◽  
Vol 64 (3) ◽  
pp. 991-999 ◽  
Author(s):  
E. Shen ◽  
N. Mo ◽  
N. J. Dun
Keyword(s):  
Receptor Antagonist ◽  
Dorsal Root ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Krebs Solution ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Stimulation Of

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices from neonate (12- to 22-day-old) rats. 2. Electrical stimulation of dorsal roots or dorsal root entry zone elicited in SPNs an excitatory postsynaptic potential (EPSP) or multiple EPSPs of varying latencies. The EPSP could be graded by varying the stimulus intensity and, on reaching the threshold, discharged an action potential. 3. The dorsal root-evoked EPSPs had a mean synaptic latency of 2.6 ms (range: 1.2-11 ms), suggesting a polysynaptic pathway. The EPSPs were characteristically slow in onset with a mean rise time and half-decay time of 8.3 and 23 ms, respectively. 4. At the resting membrane potential of -50 to -60 mV, the amplitude of EPSPs recorded in normal (1.3 mM Mg2+) Krebs solution was reduced by membrane hyperpolarization or depolarization. In Mg2(+)-free solution, EPSPs were potentiated and reached threshold for spike discharge. 5. The EPSPs were suppressed by the nonselective glutamate receptor antagonist kynurenic acid (0.1-0.5 mM) and by the N-methyl-D-aspartate (NMDA) receptor antagonists D-2-amino-5-phosphonovaleric acid (APV; 1-10 microM) and ketamine (5-10 microM), but not by the quisqualate (QA)/kainate (KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1-10 microM). The latter depressed the EPSPs elicited by stimulation of lateral funiculus in the same SPNs. 6. NMDA applied by pressure elicited a depolarization in the SPNs. In normal Krebs solution the response was voltage dependent with the peak amplitude occurring around -60 mV; conditioning depolarization or hyperpolarization diminished the response.(ABSTRACT TRUNCATED AT 250 WORDS)

Serotonin has different effects on two classes of Betz cells from the cat

1994 ◽  
Vol 72 (4) ◽  
pp. 1925-1937 ◽  
Author(s):  
W. J. Spain
Keyword(s):  
Firing Rate ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Constant Current ◽  
Repetitive Firing ◽  
Calcium Dependent ◽  
Constant Current Stimulation ◽  
Ionic Mechanisms ◽  
Betz Cells

1. Intracellular recording from cat Betz cells in vitro revealed a strong correlation between the dominant effect of serotonin (5-HT) and the Betz cell subtype in which it occurred. In large Betz cells that show posthyperpolarization excitation (termed PHE cells), 5-HT evoked a long-lasting membrane depolarization, whereas 5-HT evoked an initial hyperpolarization of variable duration in smaller Betz cells that show posthyperpolorization inhibition (termed PHI cells). 2. Voltage-clamp studies revealed that 5-HT caused a depolarizing shift of activation of the cation current Ih, which resulted in the depolarization in PHE cells, whereas the hyperpolarization in PHI cells is caused by an increase in a resting potassium conductance. 3. The effect of 5-HT on firing properties during constant current stimulation also differed consistently in the two types of Betz cells. In PHE cells the initial firing rate increased after 5-HT application, but the steady firing was unaffected. The depolarizing shift of Ih activation caused the increase of initial firing rate. 4. In PHI cells 5-HT caused a decrease in spike frequency adaptation. The decrease in adaptation was caused by a combination of two conductance changes. First, 5-HT caused a slow afterdepolarization in PHI cells that could trigger repetitive firing in the absence of further stimulation. The sADP depended on calcium entry through voltage-gated channels and was associated with a decrease in membrane conductance. Second, 5-HT caused reduction of a slow calcium-dependent potassium current that normally contributes to slow adaptation. 5. In conclusion, the effect of 5-HT on excitability differs systematically in Betz cell subtypes in part because they have different dominant ionic mechanisms that are modulated. If we assume that PHE cells and PHI cells represent fast and slow pyramidal tract (PT) neurons respectively, 5-HT will cause early recruitment of fast PT cells and delay recruitment of slow PT cells during low levels of synaptic excitation.

Synaptic and intrinsic responses of medical entorhinal cortical cells in normal and magnesium-free medium in vitro

1988 ◽  
Vol 59 (5) ◽  
pp. 1476-1496 ◽  
Author(s):  
R. S. Jones ◽  
U. Heinemann
Keyword(s):  
Entorhinal Cortex ◽  
Action Potentials ◽  
Membrane Conductance ◽  
Nmda Receptor Antagonist ◽  
Field Potentials ◽  
Cortical Cells ◽  
Medial Entorhinal Cortex ◽  
Membrane Hyperpolarization

1. Extracellular recordings were made from slices of hippocampus plus parahippocampal regions maintained in vitro. Field potentials, recorded in the entorhinal cortex after stimulation in the subiculum, resembled those observed in vivo. 2. Washout of magnesium from the slices resulted in paroxysmal events which resembled those occurring during sustained seizures in vivo. These events were greatest in amplitude and duration in layers IV/V of the medial entorhinal cortex and could occur both spontaneously and in response to subicular stimulation. Spontaneous seizure-like events were not prevented by severing the connections between the hippocampus and entorhinal cortex, but much smaller and shorter events occurring in the dentate gyrus were stopped by this manipulation. Both spontaneous and evoked paroxysmal events were blocked by perfusion with the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-amino-5-phosphonovalerate (2-AP5). 3. Neurons in layers IV/V were characterized by intracellular recording. Injection of depolarizing current in most cells evoked a train of nondecrementing action potentials with only weak spike frequency accommodation and little or no posttrain after hyperpolarization. 4. A small number of cells displayed burst response when depolarized by positive current. The burst consisted of a slow depolarization with superimposed action potentials which decreased in amplitude and increased in duration during the discharge. The burst was terminated by a strong after hyperpolarization and thereafter, during prolonged current pulses a train of nondecrementing spikes occurred. The burst response remained if the cell was held at hyperpolarized levels but was inactivated by holding the cell at a depolarized level. 5. Depolarizing synaptic potentials could be evoked by stimulation in the subiculum. A delayed and prolonged depolarization clearly decremented with membrane hyperpolarization and, occasionally, increased with depolarization. 6. Washout of magnesium from the slices resulted in an enhancement of the late depolarization and a reversal of its voltage dependence. Eventually a single shock to the subiculum evoked a large all-or-none paroxysmal depolarization associated with a massive increase in membrane conductance. Similar events occurred spontaneously in all cells tested. The paroxysmal depolarizations, both spontaneous and evoked, were rapidly blocked by 2-AP5. 7. It is concluded that medial entorhinal cortical cells possess several intrinsic and synaptic properties which confer an extreme susceptibility to generation of sustained seizure activity.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Two Components of the Cardiac Action Potential

1969 ◽  
Vol 54 (5) ◽  
pp. 607-635 ◽  
Author(s):  
Antonio Paes de Carvalho ◽  
Brian Francis Hoffman ◽  
Marilene de Paula Carvalho
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Slow Component ◽  
Slow Inward Current ◽  
Equilibrium Potential ◽  
Slow Phase ◽  
Positive Equilibrium ◽  
Cardiac Action

Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (V, V or phase-plane display). Acetylcholine was applied to the recording site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the relative magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (c) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow component, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current having a positive equilibrium potential, coupled to a decrease in the resting potassium conductance. According to the hypothesis, SA and AV nodal action potentials are due entirely or almost entirely to the slow component and can therefore be expected to exhibit unique electrophysiological and pharmacological properties.

Hydrogen peroxide increases the activity of rat sympathetic preganglionic neurons in vivo and in vitro

Neuroscience ◽  
2003 ◽  
Vol 121 (3) ◽  
pp. 641-647 ◽  
Author(s):  
H.H Lin ◽  
C.-H Chen ◽  
W.-K Hsieh ◽  
T.H Chiu ◽  
C.-C Lai
Keyword(s):  
Hydrogen Peroxide ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons

Afterdepolarization mechanism in the in vitro, cesium-loaded, sympathetic preganglionic neuron of the cat

1987 ◽  
Vol 57 (5) ◽  
pp. 1325-1337 ◽  
Author(s):  
M. Yoshimura ◽  
C. Polosa ◽  
S. Nishi
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Time Course ◽  
Choline Chloride ◽  
Membrane Potentials ◽  
Ca Channel ◽  
Krebs Solution ◽  
Similar Time ◽  
K Concentration

Intracellular recordings were performed in Cs-loaded sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus, identified by antidromic stimulation, in the slice of the T2 or T3 segment of the cat spinal cord. Loading the neurons with Cs resulted in broadening of the action potential, depression of the fast component of the afterhyperpolarization (AHP), and appearance of an afterdepolarization (ADP). A typical ADP in a Cs-loaded neuron had time to peak of 45-110 ms, half-decay time of 70-250 ms, and amplitude of 2-10 mV at membrane potentials between -60 and -70 mV and at a Ca and K concentration of 2.5 and 3.6 mM, respectively, in the superfusion medium. The ADP was associated with a decrease in neuron input resistance and increased in magnitude with hyperpolarization of the cell membrane. The relation between peak ADP amplitude and membrane potential was linear within the range of membrane potentials from -60 to -100 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM) or by low Ca Krebs solution (0.25 mM). Superfusion with BaCl2 (1.0 mM) or tetraethylammonium (TEA) (10-20 mM) caused an increase in amplitude of the ADP and an increase in action potential duration. Hyperpolarizing pulses, delivered during the course of the spike shoulder, resulted in a decrease of spike duration and ADP amplitude. The ADP was not affected by tetrodotoxin, at a dose blocking the Na-spike, and was enhanced, in association with an increase in action potential duration, when NaCl in the Krebs solution was replaced with choline chloride. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. Changes in external K concentration from 3.6 to 10 or 0.36 mM increased and decreased, respectively, the amplitude of the ADP. In the absence of Cs, and ADP, with similar time course to that recorded in Cs-loaded SPNs, was recorded when CaCl2 was replaced by BaCl or NaCl was replaced by TEAC1. It is concluded that the SPN afterpotential includes a Ca-dependent inward current, in addition to the already described fast and slow outward K currents of the AHP.

Adrenergic receptors (α1 and α2) modulate different potassium conductances in sympathetic preganglionic neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S92-S97 ◽  
Author(s):  
Hiroe Inokuchi ◽  
Megumu Yoshimura ◽  
Canio Polosa ◽  
Syogoro Nishi
Keyword(s):  
Spinal Cord ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Extracellular Potassium ◽  
Thoracic Spinal Cord ◽  
Membrane Hyperpolarization ◽  
Sympathetic Preganglionic Neurons ◽  
Preganglionic Neurons ◽  
Thoracic Spinal ◽  
Spinal Cord Segment

Intracellular recordings were made from 168 sympathetic preganglionic neurons in the slice of the second or third thoracic spinal-cord segment of the adult cat to study the actions of noradrenaline on these neurons. Noradrenaline, applied by superfusion (0.5–50 μM), produced membrane depolarization in 73 neurons and membrane hyperpolarization in 39 neurons. In 26 neurons noradrenaline produced a biphasic response (depolarization–hyperpolarization or vice versa). The depolarization was blocked by prazosin, while the hyperpolarization was blocked by yohimbine. The noradrenaline-induced depolarization was associated with an increase in neuron input resistance, while the noradrenaline-induced hyperpolarization was associated with a decrease in neuron input resistance. Both responses decreased in amplitude with membrane hyperpolarization and were nullified at around the potassium equilibrium potential EK. The null potential of both responses became more and less negative with a decrease and an increase, respectively, in the extracellular potassium concentration. When the membrane potential was made more negative than EK, the noradrenaline-induced hyperpolarization reversed to depolarization in all cases, whereas in only 4 of 12 cases did the noradrenaline-induced depolarization reverse to hyperpolarization. These data suggest that the noradrenaline-induced depolarization is a result of a decrease, while the noradrenaline-induced hyperpolarization is a result of an increase in K+ conductance. Cobalt (2 mM), low calcium – high magnesium, and intracellular EGTA markedly reduced or abolished the noradrenaline-induced depolarization but had no significant effect on the noradrenaline-induced hyperpolarization. Barium (2 mM) depressed both responses. Tetraethylammonium (10–30 mM), 4-aminopyridine (3 mM), and cesium (2 mM) had no effect on either response. These data suggest that the noradrenaline-induced depolarization is a result of an inactivation of a background calcium-sensitive K+ conductance, while the noradrenaline-induced hyperpolarization is due to activation of a calcium-insensitive potassium conductance.Key words: K+ conductances, catecholamines, Ca2+ dependent, K+ current, spinal cord.

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