• The Korean Journal of Physiology and Pharmacology
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• v.8 no.1
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• pp.7-15
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• 2004

Nitric oxide (NO) system has been implicated in a wide range of physiological functions in the nervous system. However, the role of NO in regulating the neural activity in the gustatory zone of nucleus tractus solitarius (NTS) has not been established. The present study was aimed to investigate the role of NO in the gustatory NTS neurons. Sprague-Dawley rats, weighing about 50 g, were used. Whole cell patch recording and immunohistochemistry were done to determine the electrophysiological characteristics of the rostral gustatory nucleus of the tractus solitaries and distribution of NO synthases (NOS). Neuronal NOS (nNOS) immunoreactivity was strongly detected along the solitary tract extending from rostral to caudal medulla. Resting membrane potentials of NTS neurons were $-49.2{\pm}2\;mV$ and action potential amplitudes were $68.5{\pm}2\;mV$ with a mean duration measured at half amplitude of $1.7{\pm}0.3\;ms$. Input resistance, determined from the response to a 150 ms, -100 pA hyperpolarizing current pulse, was $385{\pm}15\;M{\Omega}$, Superfusion of SNAP or SNP, NO donors, produced either hyperpolarization (68%), depolarization (5%), or no effect (27%). The hyperpolarization was mostly accompanied by a decrease in input resistance. The hyperpolarization caused by SNAP or SNP increased the time to initiate the first action potential, and decreased the number of action potentials elicited by current injection. SNP or SNAP also markedly decreased the number of firing neural discharges of the spontaneous NTS neural activity under zero current. Superfusion of L-NAME, a NOS inhibitor, slightly depolarized the membrane potential and increased the firing rate of NTS neurons induced by current injection. ODQ, a soluble guanylate cyclase inhibitor, ameliorated the SNAP-induced changes in membrane potential, input resistance and firing rates. 8-Br-cGMP, a non-degradable cell-permeable cGMP, hyperpolarized the membrane potential and decreased the number of action potentials. It is suggested that NO in the gustatory NTS has an inhibitory role on the neural activity of NTS through activating soluble guanylate cyclase.

• Korean Journal of Acupuncture
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• v.35 no.4
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• pp.187-202
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• 2018

Objectives : Non-invasive transcranial electrical stimulation is one of therapeutic interventions to change in neural excitability of the cortex. Transcranial electro-acupuncture (TEA) can modulate brain functions through changes in cortical excitability as a model of non-invasive transcranial electrical stimulation. Some composites of fermented Scutellaria baicalenis (FSB) can activate intercellular signaling pathways for activation of brain-derived neurotrophic factor that is critical for formation of neural plasticity in stroke patients. This study was aimed at evaluation of combinatory treatment of TEA and FSB on behavior recovery and cortical neural excitability in rodent focal stroke model. Methods : Focal ischemic stroke was induced by photothrombotic injury to the motor cortex of adult rats. Application of TEA with 20 Hz and $200{\mu}A$ in combination with daily oral treatment of FBS was given to stroke animals for 3 weeks. Motor recovery was evaluated by rotating bean test and ladder working test. Electrical activity of cortical pyramidal neurons of stroke model was evaluated by using multi-channel extracellular recording technique and thallium autometallography. Results : Compared with control stroke group who did not receive any treatment, Combination of TEA and FSB treatment resulted in more rapid recovery of forelimb movement following focal stroke. This combination treatment also elicited increase in spontaneous firing rate of putative pyramidal neurons. Furthermore expression of metabolic marker for neural excitability was upregulated in peri-infract area under thallium autometallography. Conclusions : These results suggest that combination treatment of TEA and FSB can be a possible remedy for motor recovery in focal stroke.

• The Korean Journal of Physiology
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• v.22 no.2
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• pp.219-230
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• 1988

The effect of glycine, structurally the most simple amino acid was investigated on the electrophysiological characteristics of the isolated superfused atrial muscle and sinus node cells of the rabbit heart. Superfusion of the sinus node cell with glycine solution (3, 5 and 8 mM) produced concentration-dependent increments of OS (overshoot potential) and MDP (maximum diastolic potential). Generally action potential amplitude increased as a result of greater increment of OS than that of MDP. The changes in action potential of the sinus node cell peaked in $7{\sim}10{\;}minutes$ after onset of superfusioin. On the contrary to the response to intravenously administered glycine, the rate of spontaneous firing of sinus node cell was invariably increased following superfusion with glycine. Action potential duration manifested as $APD_{60}$ (time to 60% repolarization) was significantly shortened by glycine. And the electrophysiological effects of glycine on the atrial muscle cell were similar to that on the sinus node cells. The results of present study suggest that glycine can exert direct effects on the atrial muscle and sinus node cells of the rabbit heart.

• The Korean Journal of Physiology
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• v.18 no.1
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• pp.19-35
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• 1984

Since the first report of Drury and $Szent-Gy{\ddot{o}}rgyi$ in 1929, the inhibitory influences of adenosine on the heart have repeatedly been described by many investigators. These studies have shown that adenosine and adenine nucleotides have overall depressant effects, similar to those of acetylcholine. Heart beats become slow and weak. It is also well known that adenosine is a potent endogenous coronary vasodilator. Many investigations on the working mechanisms of adenosine have been focused mainly on the effects of the coronary blood flow. However, the cellular mechanisms underlying the inhibitory action of adenosine on sinus node are not well understood yet. Thus, this study was undertaken to examine the behavior of rabbit SA node under influence of adenosine. In these series of experiments three kinds of preparations were used: whole atrial pair, left atrial strip, and isolated SA node preparations. The electrical activity of SA node was recorded with conventional glass microelectrodes 30 to 50 $M{\Omega}$. The preparations were superfused with bicarbonate-buffered Tyrode solution of pH 7.35 and aerated with a gas mixture of $3%\;CO_2-97%\;O_2$ at $35^{\circ}C$. In whole atrial pair, adenosine suppressed sinoatrial rhythm in a dose-dependent manner. Effect of adenosine on atrial rate appeared at the concentration of $10^{-5}M$ and was enhanced in parallel with the increase in adenosine concentration. Inhibitory action of adenosine on pacemaker activity was more prominent in the preparation pretreated with norepinephrine, which can steepen the slope of pacemaker potential by increasing permeability of $Ca^{+2}$. Calcium ions in perfusate slowly produced a marked change in sinoatrial rhythm. Elevation of the calcium concentration from 0.3 to 8 mM increased the atrial rate from 132 to 174 beats/min, but over 10 mM $Ca^{+2}$ decreased. The inhibitory effect of adenosine on sinoatrial rhythm developed very rapidly. Atrial rate was recovered promptly from the adenosine-induced suppression by the addition of norepinephrine, but extra $Ca^{+2}$ was less suitable to restore the suppression of atrial rate. Adenosine suppressed also atrial contractility in the same dosage range that restricted pacemaker activity, even in the reserpinized preparation. In isolated SA node preparation, spontaneous firing rate of SA node at $35^{\circ}C$(mean{\pm}SEM, n=16) was $154{\pm}3.3\;beats/min. The parameters of action potentials were: maximum diastolic potential(MDP), $-73{\pm}1.7\;mV: overshoot(OS), $9{\pm}1.4\;mV: slope of pacemaker potential(SPP), $94{\pm}3.0\;mV/sec. Adenosine suppressed the firing rate of SA node in a dose-dependent manner. This inhibitory effect appeared at the concentration of $10^{-6}M$ and was in parallel with the increase in adenosine concentration. Changes in action potential by adenosine were dose-dependent increase of MDP and decrease of SPP until $10^{-4}M$. Above this concentration, however, the amplitude of action potential decreased markedly due to the simultaneous decrease of both MDP and OS. All these effects of adenosine were not affected by pretreatment of atropine and propranolol. Lowering extra $Ca^{2+}$ irom 2 mM to 0.3 mM resulted in a marked decrease of OS and SPP, but almost no change of MDP. However, increase of perfusate $Ca^{2+}$ from 2 mM to 6 or 8 mM produced a prominent decrease of MDP and a slight increase of OS and SPP. Dipyridamole(DPM), which is known to block the adenosine transport across the cell membrane, definately potentiated the action of adenosine. The results of this experiment suggest that adenosine suppressed pacemaker activity and atrial contractility simultaneously and directly, by decreasing $Ca^{2+}-permeability$ of nodal and atrial cell membranes.