• The Korean Journal of Physiology
• /
• 제29권2호
• /
• pp.309-321
• /
• 1995

In the present study, the relationship between the somatosympathetic reflexes and arterial blood pressure responses to electrical stimulation of the peripheral nerve was investigated in cats anesthetized with ${\alpha}-chloralose$. Single sympathetic postganglionic fiber activities were recorded from the hindlimb muscle and skin nerves and also from the cervical and abdominal sympathetic chains. Effects of the morphine on responses of the sympathetic nerve and arterial blood pressure to activation of the peripheral $A{\delta}-$ and C-afferent nerves were analyzed. The following results were obtained. 1) Arterial blood pressure was depressed by peripheral AS-afferent stimulation (A-response) and was elevated during C-afferent activation (C-response). 2) Intravenously administered morphine enhanced the C-response while the A-response decreased insignificantly, Only the C-response was decreased by intrathecal morphine. 3) All the ten recorded cutaneous sympathetic fibers showed periodic discharge pattern similar to respiratory rhythm and five of them also showed cardiac-related rhythm. However, most of the muscular sympathetic fibers had cardiac-related rhythm and only four fibers showed respiratory rhythm. 4) Morphine decreased the sympathetic C-reflex elicited by the peripheral C-afferent activation and the abdominal sympathetic A-reflex was also decreased by morphine. From the above results, it was concluded that supraspinal mechanisms were involved in the enhanced arterial pressor response to peripheral C-afferent activation by intravenous morphine.

• Molecules and Cells
• /
• 제37권11호
• /
• pp.804-811
• /
• 2014

The protease-activated receptor (PAR)-2 is highly expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although several mechanisms have been suggested to explain PAR-2-induced hypotension, the precise mechanism remains to be elucidated. To investigate this possibility, we investigated the effects of PAR-2 activation on N-type $Ca^{2+}$ currents ($I_{Ca-N}$) in isolated neurons of the celiac ganglion (CG), which is involved in the sympathetic regulation of mesenteric artery vascular tone. PAR-2 agonists irreversibly diminished voltage-gated $Ca^{2+}$ currents ($I_{Ca}$), measured using the patch-clamp method, in rat CG neurons, whereas thrombin had little effect on $I_{Ca}$. This PAR-2-induced inhibition was almost completely prevented by ${\omega}$-CgTx, a potent N-type $Ca^{2+}$ channel blocker, suggesting the involvement of N-type $Ca^{2+}$ channels in PAR-2-induced inhibition. In addition, PAR-2 agonists inhibited $I_{Ca-N}$ in a voltage-independent manner in rat CG neurons. Moreover, PAR-2 agonists reduced action potential (AP) firing frequency as measured using the current-clamp method in rat CG neurons. This inhibition of AP firing induced by PAR-2 agonists was almost completely prevented by ${\omega}$-CgTx, indicating that PAR-2 activation may regulate the membrane excitability of peripheral sympathetic neurons through modulation of N-type $Ca^{2+}$ channels. In conclusion, the present findings demonstrate that the activation of PAR-2 suppresses peripheral sympathetic outflow by modulating N-type $Ca^{2+}$ channel activity, which appears to be involved in PAR-2-induced hypotension, in peripheral sympathetic nerve terminals.

• BMB Reports
• /
• 제54권12호
• /
• pp.620-625
• /
• 2021

Microglia are known to be activated in the hypothalamic paraventricular nucleus (PVN) of rats with cardiovascular diseases. However, the exact role of microglial activation in the plasticity of presympathetic PVN neurons associated with the modulation of sympathetic outflow remains poorly investigated. In this study, we analyzed the direct link between microglial activation and spontaneous firing rate along with the underlying synaptic mechanisms in PVN neurons projecting to the rostral ventrolateral medulla (RVLM). Systemic injection of LPS induced microglial activation in the PVN, increased the frequency of spontaneous firing activity of PVN-RVLM neurons, reduced GABAergic inputs into these neurons, and increased plasma NE levels and heart rate. Systemic minocycline injection blocked all the observed LPS-induced effects. Our results indicate that LPS increases the firing rate and decreases GABAergic transmission in PVN-RVLM neurons associated with sympathetic outflow and the alteration is largely attributed to the activation of microglia. Our findings provide some insights into the role of microglial activation in regulating the activity of PVN-RVLM neurons associated with modulation of sympathetic outflow in cardiovascular diseases.

• 한국감성과학회:학술대회논문집
• /
• 한국감성과학회 1999년도 춘계학술발표논문집 논문집
• /
• pp.127-132
• /
• 1999

Cardiovascular, respiratory and electrodermal responses to acute stress episodes modeled by combined presentation of intense white noise and performance of word recognition task with noise background were studied in 15 college students. Experimental procedure consisted in sessions with white noise, word recognition task presentation with noise background and test with noise background. Recorded physiological variables were analyzed in terms of their sensitivity to detect activation of sympathetic and parasympathetic branches of autonomic nervous system and thus reflect autonomic arousal level during shout-term stress-inducing experimental manipulations. It was shown that performance of effortful mental task with noise background elicited significant physiological responses typical for active coping behavior, namely electrodermal arousal and increased cardiovascular activity. this response profile was more profound as compared to white noise only or attending task in noise background. However, all physiological responses were mostly phasic, without long-term tonic changes, since almost all variables recovered to their initial baseline levels, suggesting that dominant autonomic mechanisms in transient acute stress episodes were of parasympathetic nature (withdrawal in stress with subsequent activation in restoration period), while sympathetic contribution was not long-lasting. Nevertheless, increased number of stressors and their longer exposure may result in higher profile of tonic sympathetic arousal and reduced functional role of vagal mechanisms in autonomic balance regulation.

• 대한의생명과학회지
• /
• 제12권2호
• /
• pp.113-118
• /
• 2006

Major pelvic ganglia (MPG) in rats are an unique autonomic ganglia, containing both sympathetic and parasympathetic neurons related with the function of bladder, penis and bowel. It has been widely known that ionotropic $GABA_A$ receptors are the molecular target of $\gamma$-aminobutric acid (GABA), a major inhibitory neurotransmitter in central nervous system. However, their functions and regulations of $GABA_A$ receptors expressed in autonomic ganglia have been poorly understood. 1 examined the modulatory role of adenylyl cyclase (AC) and protein kinase A(PKA) on $GABA_A$-induced inward currents in the neurons of rat MPG. $GABA_A$ receptors were identified using immunofluorescent labeling in the rat major pelvic ganglion. Electrophysiological experiments were performed to record the activities of $GABA_A$ receptors. $GABA_A$ receptors were expressed only in sympathetic neurons. GABA induced marked inward currents in a concentration-dependent manner. Mucimol ($5{\mu}M$), a $GABA_A$ receptor agonist induced inward currents were significantly reduced in the presence of SQ 225361 $20{\mu}M$, a AC inhibitor and myristoylated PKA inhibitor 100 nM. In addition, forskolin ($1{\mu}M$), AC activator, augmented the GABA induced currents. The activation of AC/PKA-dependent pathway could involve in the regulation $GABA_A$ receptors, expressed only in sympathetic neurons of rat MPG. These findings are helpful for the better understanding the function of various pelvic organs innervated by MPG.

• The Journal of Korean Physical Therapy
• /
• 제22권1호
• /
• pp.61-66
• /
• 2010

Purpose: The purpose of this study was to investigate the change in sympathetic nervous system responses of healthy adult women with changes in stimulus intensity of high frequency transcutaneous electrical nerve stimulation. Methods: Twenty-four healthy subjects (women) received high frequency electrical stimulation of the forearm. The subjects were randomly assigned to one of two groups; a low intensity stimulation group (n=12) and a high intensity stimulation group (n=12). The electrode attachment was arranged on the forearm of the dominant arm and the electricity stimulus time was 20 minutes. Measured items included skin conductance, pulse rate, skin temperature, and respiration rate. Each was measured at 4 times. Results: Skin conductance and skin temperature showed significant group by time interactions, though there were no significant group and time effects. There were no significant differences according to time, group effect, and a group by time interaction in pulse and respiration rates. Conclusion: High frequency and high intensity electrical stimulation may be helpful for the improvement of sudomotor function through the activation of the sympathetic nervous system. Also, high frequency and low intensity electrical stimulation may be helpful for the reduction of sudomotor function via inhibition of the sympathetic nervous system.

• The Korean Journal of Physiology and Pharmacology
• /
• 제18권6호
• /
• pp.489-495
• /
• 2014

Protease-activated receptor (PAR)-2 is expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although some reports have suggested involvement of a neurogenic mechanism in PAR-2-induced hypotension, the accurate mechanism remains to be elucidated. To examine this possibility, we investigated the effect of PAR-2 activation on smooth muscle contraction evoked by electrical field stimulation (EFS) in the superior mesenteric artery. In the present study, PAR-2 agonists suppressed neurogenic contractions evoked by EFS in endothelium-denuded superior mesenteric arterial strips but did not affect contraction elicited by the external application of noradrenaline (NA). However, thrombin, a potent PAR-1 agonist, had no effect on EFS-evoked contraction. Additionally, ${\omega}$-conotoxin GVIA (CgTx), a selective N-type $Ca^{2+}$ channel ($I_{Ca-N}$) blocker, significantly inhibited EFS-evoked contraction, and this blockade almost completely occluded the suppression of EFS-evoked contraction by PAR-2 agonists. Finally, PAR-2 agonists suppressed the EFS-evoked overflow of NA in endothelium-denuded rat superior mesenteric arterial strips and this suppression was nearly completely occluded by ${\omega}$-CgTx. These results suggest that activation of PAR-2 may suppress peripheral sympathetic outflow by modulating activity of $I_{Ca-N}$ which are located in peripheral sympathetic nerve terminals, which results in PAR-2-induced hypotension.

• The Korean Journal of Physiology
• /
• 제26권1호
• /
• pp.75-88
• /
• 1992

It is well established that neurons in ventrolateral medulla play a key role in determining the vasomotor tone. The purpose of present study is to identify sympathetic related, medullospinal tract neurons in ventrolateral medulla and to show that these mediate somato-sympathetic reflex. Medullospinal tract cells were identified by antidromic stimulation to intermediolateral nucleus (IML) of the second thoracic ($T_2$) spinal cord in anesthetized cats. Peripheral nerves were stimulated for orthodromic activation of these cells and peripheral receptive fields were determined. Post R wave histogram of unit and spike triggered averaging of sympathetic nerve discharge (SND) were used to define sympathetic related cell. A total of 113 neurons was recorded in ventrolateral medulla that had the axonal projections to $T_2$ spinal cord. Thirty four of these medullospinal cells showed spontaneous discharges and the others not. Between these two groups, rostro-caudal coordinate of the distribution from obex [$4.7{\pm}0.2\;$ (mean S.E.) mm, 4.1 0.1 mm], depth from dorsal surface ($5.5{\pm}0.2mm,\;4.9{\pm}0.1mm$ and conduction velocity ($9.9{\pm}1.7m/sec,\;16.7{\pm}1.9\;m/sec$) were significantly different (p<0.05). In spontaneously discharging group, characteristics of rostral and caudal groups were significantly different and we demonstrated that cells in rostral group mediate somatosympathetic reflex. From these results, we conclude that a certain portion of spontaneously discharging medullospinal tract cells in rostral ventrolateral medulla comprise the efferent outputs of somatosympathetic reflex to sympathetic preganglion neurons.

• The Korean Journal of Physiology and Pharmacology
• /
• 제28권1호
• /
• pp.93-103
• /
• 2024

Satellite glial cells (SGCs), a major type of glial cell in the autonomic ganglia, closely envelop the cell body and even the synaptic regions of a single neuron with a very narrow gap. This structurally unique organization suggests that autonomic neurons and SGCs may communicate reciprocally. Glial Ca²⁺ signaling is critical for controlling neural activity. Here, for the first time we identified the machinery of store-operated Ca²⁺ entry (SOCE) which is critical for cellular Ca²⁺ homeostasis in rat sympathetic ganglia under normal and pathological states. Quantitative realtime PCR and immunostaining analyses showed that Orai1 and stromal interaction molecules 1 (STIM1) proteins are the primary components of SOCE machinery in the sympathetic ganglia. When the internal Ca²⁺ stores were depleted in the absence of extracellular Ca²⁺, the number of plasmalemmal Orai1 puncta was increased in neurons and SGCs, suggesting activation of the Ca²⁺ entry channels. Intracellular Ca²⁺ imaging revealed that SOCE was present in SGCs and neurons; however, the magnitude of SOCE was much larger in the SGCs than in the neurons. The SOCE was significantly suppressed by GSK7975A, a selective Orai1 blocker, and Pyr6, a SOCE blocker. Lipopolysaccharide (LPS) upregulated the glial fibrillary acidic protein and Toll-like receptor 4 in the sympathetic ganglia. Importantly, LPS attenuated SOCE via downregulating Orai1 and STIM1 expression. In conclusion, sympathetic SGCs functionally express the SOCE machinery, which is indispensable for intracellular Ca²⁺ signaling. The SOCE is highly susceptible to inflammation, which may affect sympathetic neuronal activity and thereby autonomic output.

• 한국감성과학회:학술대회논문집
• /
• 한국감성과학회 1999년도 추계학술대회 논문집
• /
• pp.216-221
• /
• 1999

A mental task combined with noise background is an effective model of laboratory stress for study of psychophysiology of the autonomic nervous system (ANS). The intensity of the background noise significantly affects both a subjective evaluation of experienced stress level during test and the physiological responses associated with mental load in noisy environments. Providing tests of similar difficulties we manipulated the background noise intensity as a main factor influencing a psychophysiological outcome and the analyzed reactivity along withe the noise intensity dimension. The goal of this study was to identify the patterns of ANS responses and the relevant subjective stress scores during performance of word recognition tasks on the background of white noise (WN) of the different intensities (55, 70 and 85 dB). Subjects were 27 college students (19-24 years old). BIOPAC, Grass Neurodata System and AcqKnowlwdge 3.5 software were used to record ECG, PPG, SCL, skin temperature, and respiration. Experimental manipulations were effective in producing subjective and physiological responses usually associated with stress. The results suggested that the following potential autonomic mechanisms might be involved in the mediation of the observed physiological responses: A sympathetic activation with parasympathetic withdrawal during mild 55 and 70dB noise (featured by similar profiles) and simultaneous activation of sympathetic and parasympathetic systems during intense 85dB WN. The parasympathetic activation in this case might be a compensatory effect directed to prevent sympathetic domination and to maintain optimal arousal state for the successful performance on mental stress task. It should be mentioned that obtained results partially support Gellhorn's (1960; 1970) "tuning phenomenon" as a possible mechanism underlying stress response.