scholarly journals Inhibitory Synapses on Pacemaker Neurons in the Heart Ganglion of a Stomatopod, Squilla oratoria

1968 ◽  
Vol 52 (6) ◽  
pp. 908-924 ◽  
Author(s):  
Akira Watanabe ◽  
Shosaku Obara ◽  
Toyohiro Akiyama
Keyword(s):  
Membrane Potential ◽  
Nerve Stimulation ◽  
Membrane Conductance ◽  
Heart Beat ◽  
Inhibitory Synapses ◽  
Pacemaker Cell ◽  
Pacemaker Neurons ◽  
Pacemaker Potential ◽  
Steady Level ◽  
Potential Level

The pacemaker neurons of the Squilla heart ganglion are innervated from the CNS through three pairs of extrinsic nerves. One of them, the α-nerve, is inhibitory to the heart beat. The effect of α-nerve stimulation on the pacemaker potential was examined with intracellular electrodes. Without extrinsic nerve stimulation the membrane potential of the pacemaker cell fluctuated spontaneously. On application of a tetanic train of stimuli to the α-nerve the membrane potential was shifted and fixed to a steady level, which with K2SO4-filled electrodes was near the peak of hyperpolarization after a spontaneous burst, but was less negative with KCl-filled electrodes. The shift of the membrane potential was due to the summated IPSP's. By changing the level of the membrane potential with injection of the polarizing current the IPSP could be reversed in sign, and the size of the IPSP was linearly correlated with the membrane potential level. During inhibition the membrane conductance increased. The increase depended on divalent cation concentrations in the outside medium. In Ca-rich saline the IPSP was greatly enhanced. In Mg-rich saline it was suppressed. The amplitude of antidromic spikes was reduced during inhibition especially when the spike frequency was high.

scholarly journals Acceleratory Synapses on Pacemaker Neurons in the Heart Ganglion of a Stomatopod, Squilla oratoria

1969 ◽  
Vol 54 (2) ◽  
pp. 212-231 ◽  
Author(s):  
Akira Watanabe ◽  
Shosaku Obara ◽  
Toyohiro Akiyama
Keyword(s):  
Direct Action ◽  
Membrane Conductance ◽  
Initial Response ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Late Response ◽  
Local Response ◽  
Pacemaker Neurons ◽  
Pacemaker Potential ◽  
Frequency Stimulation

The pacemaker neurons of the heart ganglion are innervated from the CNS through two pairs of acceleratory nerves. The effect of acceleratory nerve stimulation was examined with intracellular electrodes from the pacemaker cells. The major effects on the pacemaker potential were an increase in the rate of rise of the spontaneous depolarization and in the duration of the plateau. The aftereffect of stimulation could last for minutes. No clear excitatory postsynaptic potential (EPSP) was observed, however. On high frequency stimulation, a small depolarizing response (the initial response) was sometimes observed, but the major postsynaptic event was the following slow depolarization, or the enhancement of the pacemaker potential (the late response). With hyperpolarization the initial response did not significantly change its amplitude, but the late response disappeared, showing that the latter has the property of the local response. The membrane conductance did not increase with acceleratory stimulation. The injection of depolarizing current increased the rate of rise of the spontaneous depolarization, but only slightly in comparison with acceleratory stimulation, and did not increase the burst duration. It is concluded that the acceleratory effect is not mediated by the EPSP but is due to a direct action of the transmitter on the pacemaker membrane.

scholarly journals On The Mechanism of Spontaneous Impulse Generation in the Pacemaker of the Heart

1961 ◽  
Vol 45 (2) ◽  
pp. 317-330 ◽  
Author(s):  
Wolfgang Trautwein ◽  
Donald G. Kassebaum
Keyword(s):  
Sodium Current ◽  
Potassium Conductance ◽  
Rhythmic Activity ◽  
Current Strength ◽  
Heart Beat ◽  
Free Medium ◽  
Pacemaker Potential ◽  
Impulse Generation ◽  
Sodium Conductance ◽  
Voltage Dependent

Rhythmic activity in Purkinje fibers of sheep and in fibers of the rabbit sinus can be produced or enhanced when a constant depolarizing current is applied. When extracellular calcium is reduced successively, the required current strength is less, and eventually spontaneous beating occurs. These effects are believed due to an increase in steady-state sodium conductance. A significant hyperpolarization occurs in fibers of the rabbit sinus bathed in a sodium-free medium, suggesting an appreciable sodium conductance of the "resting" membrane. During diastole, there occurs a voltage-dependent and, to a smaller extent, time-dependent reduction in potassium conductance, and a pacemaker potential occurs as a result of a large resting sodium conductance. It is postulated that the mechanism underlying the spontaneous heart beat is a high resting sodium current in pacemaker tissue which acts as the generator of the heart beat when, after a regenerative repolarization, the decrease in potassium conductance during diastole reestablishes the condition of threshold.

The stimulant action of acetylcholine and catecholamines on the uterus

1973 ◽  
Vol 265 (867) ◽  
pp. 149-156 ◽  
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Membrane Conductance ◽  
Primary Effect ◽  
Force Of Contraction ◽  
Chloride Permeability ◽  
Duration Of Action ◽  
Spike Discharge ◽  
Calcium Permeability

The α action of catecholamines on oestrogen dominated guinea-pig uterus is stimulant. The cell membrane is depolarized, membrane conductance is increased, spike discharge is accelerated and tension develops. This action resembles that of acetylcholine though catecholamines are less potent, and, in equiactive concentrations, catecholamines have a longer latency and a longer duration of action. Evidence, obtained by modifications of the ionic environment, indicates that the depolarization by acetylcholine is due to an increase in sodium and calcium permeability and that acetylcholine can release calcium from intracellular stores. The depolarization by catecholamines is due to an increase in chloride permeability and, in addition, sodium is required for the ensuing increase of spike discharge. Catecholamines produce an increase in the force of contraction, long outlasting their immediate stimulation. Moreover, their effect on membrane potential and membrane conductance persists in the presence of lanthanum. These results suggest that Ca release from intracellular stores may be the primary effect produced by the α action of catecholamines and that the increase in the cytoplasmic Ca 2+ concentration may cause the changes at the cell membrane.

Voltage-dependent modulation of GABAA receptor channel desensitization in rat hippocampal neurons

1994 ◽  
Vol 71 (6) ◽  
pp. 2151-2160 ◽  
Author(s):  
K. W. Yoon
Keyword(s):  
Membrane Potential ◽  
Hippocampal Neurons ◽  
Membrane Conductance ◽  
Cell Voltage ◽  
Chloride Conductance ◽  
Membrane Voltage ◽  
Hippocampal Cell Culture ◽  
Voltage Dependent ◽  
Agonist Concentration ◽  
Rate Of Recovery

1. The mechanism of the time-dependent decline in gamma-amino-butyric acid (GABA)-induced chloride conductance, referred to as desensitization, was studied in dissociated rat hippocampal cell culture with the use of a whole-cell voltage-clamp recording. 2. In most cells the gradual decline of membrane conductance was dependent simultaneously on the agonist concentration and membrane voltage. Even in the continued presence of GABA, desensitization could be prevented by holding the membrane potential > 0 mV in a near symmetrical chloride gradient across the cell membrane. 3. The “recovery” from desensitization occurred after removal of the agonist with a time constant of approximately 35 s. The rate of recovery from desensitization was independent of membrane voltage. 4. When the membrane potential was jumped from a negative to a positive membrane potential during steady state of desensitization, the GABA-induced chloride conductance gradually “relaxed” to the undesensitized state. This phenomenon of gradual increase in chloride conductance or “reactivation” from desensitization was both voltage and agonist dependent. 5. The process of recovery of the GABA ionophore from the desensitized state is distinct from the process of reactivation, which is dependent both on the voltage and agonist. 6. These observations suggest that the ligand-bound GABA receptor has two alternate states, i.e., permissive (activated) and desensitized. The rates of transition between these two states are voltage dependent.

Effect of a spider toxin (JSTX) on excitatory postsynaptic current at neuromuscular synapse of spiny lobster

1987 ◽  
Vol 58 (2) ◽  
pp. 319-326 ◽  
Author(s):  
A. Miwa ◽  
N. Kawai ◽  
M. Saito ◽  
H. Pan-Hou ◽  
M. Yoshioka
Keyword(s):  
Membrane Potential ◽  
Neuromuscular Junction ◽  
Time Constant ◽  
Spiny Lobster ◽  
Neuromuscular Synapse ◽  
Ionic Channel ◽  
Excitatory Postsynaptic Potential ◽  
Excitatory Postsynaptic Current ◽  
Steady Level ◽  
The Relationship

1. We studied the blocking properties of a spider (Nephila clavata) toxin (JSTX) purified from venom on the spiny lobster neuromuscular junction. 2. When a small amount of JSTX was applied to the neuromuscular junction, the excitatory postsynaptic potential (EPSP) was partially suppressed. The amplitude of EPSPs remained at a steady level for several hours during the washing of the preparation, showing that the action of JSTX is irreversible. 3. We recorded the excitatory postsynaptic current (EPSC) from synaptic site using a macro-patch electrode. The amplitude of EPSC increased linearly with hyperpolarization of the membrane potential in the presence and absence of JSTX. 4. The decay phase time constant of EPSC and spontaneous EPSC was decreased by hyperpolarizing the membrane potential both in the absence and in the presence of JSTX. The relationship between the decay time constant and the membrane potential was not modified by JSTX. 5. It is suggested that JSTX irreversibly blocks EPSC by acting on the site that is apart from the ionic channel of the glutamate receptor molecule.

Milk Ejection Burst-Like Electrical Activity Evoked in Supraoptic Oxytocin Neurons in Slices From Lactating Rats

2004 ◽  
Vol 91 (5) ◽  
pp. 2312-2321 ◽  
Author(s):  
Yu-Feng Wang ◽  
Glenn I. Hatton
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Membrane Conductance ◽  
Peak Level ◽  
Sudden Increase ◽  
Milk Ejection ◽  
Peak Rate ◽  
Vasopressin Neurons

To examine the mechanisms underlying milk-ejection bursts of oxytocin (OT) neurons during suckling, both in vivo and in vitro studies were performed on supraoptic OT neurons from lactating rats. The bursts were first recorded extracellularly in anesthetized rats. Burst-related electrical parameters were essentially the same as previous reports except for a trend toward transient decreases in basal firing rates immediately preceding the burst. From putative OT neurons in slices with extracellular recordings, bursts that closely mimicked the in vivo bursts were elicited by phenylephrine, an α1-adrenoceptor agonist, in a low-Ca2+ medium. Moreover, in whole cell patch-clamp recordings, the in vitro bursts were recorded from immunocytochemically identified OT neurons. After a transient decrease in the basal firing rate, the in vitro bursts started with a sudden increase in the firing rate, quickly reaching a peak level, then gradually decaying, and ended with a postburst inhibition. A brief depolarization of the membrane potential and an increase in membrane conductance appeared after the onset of the burst. Spikes during a burst were characterized by a significant increase in the duration and decrease in the amplitude around the peak rate firing. These bursts were significantly different from short-lasting burst firing of vasopressin neurons in membrane potential changes, time to reach peak firing rate, spike amplitude and duration during peak rate firing. Our extensive analysis of these results suggests that the in vitro burst is a useful model for further study of mechanisms underlying milk-ejection bursts of OT neurons in vivo.

scholarly journals CaMKII inhibition hyperpolarizes membrane and blocks nitrergic IJP by closing a Cl− conductance in intestinal smooth muscle

2012 ◽  
Vol 303 (2) ◽  
pp. G240-G246 ◽  
Author(s):  
Xue-Dao He ◽  
Raj K. Goyal
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Membrane Conductance ◽  
Electrical Field Stimulation ◽  
Intestinal Smooth Muscle ◽  
Membrane Potential Change ◽  
Ion Conductance ◽  
Active Conductance ◽  
Dependent Protein ◽  
Cell Changes

The ionic basis of nitrergic “slow'” inhibitory junction potential (sIJP) is not fully understood. The purpose of the present study was to determine the nature and the role of calmodulin-dependent protein kinase II (CaMKII)-dependent ion conductance in nitrergic neurotransmission at the intestinal smooth muscle neuromuscular junction. Studies were performed in guinea pig ileum. The modified Tomita bath technique was used to induce passive hyperpolarizing electrotonic potentials (ETP) and membrane potential change due to sIJP or drug treatment in the same cell. Changes in membrane potential and ETP were recorded in the same smooth muscle cell, using sharp microelectrode. Nitrergic IJP was elicited by electrical field stimulation in nonadrenergic, noncholinergic conditions and chemical block of purinergic IJP. Modification of ETP during hyperpolarization reflected active conductance change in the smooth muscle. Nitrergic IJP was associated with decreased membrane conductance. The CAMKII inhibitor KN93 but not KN92, the Cl− channel blocker niflumic acid (NFA), and the KATP-channel opener cromakalim hyperpolarized the membrane. However, KN93 and NFA were associated with decreased and cromakalim was associated with increased membrane conductance. After maximal NFA-induced hyperpolarization, hyperpolarization associated with KN93 or sIJP was not seen, suggesting a saturation block of the Cl− channel signaling. These studies suggest that inhibition of CaMKII-dependent Cl− conductance mediates nitrergic sIJP by causing maximal closure of the Cl− conductance.

Effects of Ultraviolet Radiation on the Plasma Membranes of Chara corallina. I The Hyperpolarized State

1976 ◽  
Vol 3 (5) ◽  
pp. 677
Author(s):  
C.J Doughty ◽  
A.B Hope
Keyword(s):  
Membrane Potential ◽  
Ultraviolet Radiation ◽  
Ultraviolet Irradiation ◽  
Plasma Membranes ◽  
Membrane Conductance ◽  
Chara Corallina ◽  
Potential Difference ◽  
Electrogenic Pump ◽  
Chloride Permeability ◽  
Membrane Potential Difference

Effects of 254 nm ultraviolet irradiation on the plasmalemma potential difference and conductance in C, corallina have been further analysed. Following an increase in passive chloride permeability, revealed from previous studies, and which is manifested as a depolarization of membrane potential difference and an increase in membrane conductance, a secondary depolarization was prominent at pH 7 and is attributed to u.v.-induced inhibition of an electrogenic pump. The secondary depolarization was usually accompanied by a decrease in membrane conductance. For doses of u.v. of 1400 J m-2, these effects were almost reversible within about 1 h

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