• The Korean Journal of Physiology and Pharmacology
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• v.7 no.4
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• pp.193-198
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• 2003

In the present study, the vestibularly evoked activity of inferior olive (IO) neurons was examined to investigate the vertical vestibular information transmitted through the vestibulo-olivo-cerebellar climbing fiber pathway. The extracellular recording was made in 74 neurons of the IO of cats, while animals were sinusoidally rotated. Most of vestibularly activated IO neurons responded to the vertical rotation (roll) test and were found in or near the ${\beta}$ subnuclei $(IO{\beta})$. The vestibular IO neurons were activated, when the animal was rotated to the side contralateral to the recording site. In contrast to the observation that the gain of responses of yaw sensitive cells (YSC) was not changed by the rotation frequency, that of the roll-sensitive cells (RSC) decreased as the rotation frequency was increased. Regardless of RSC or HSC, IO neurons showed the tendency of phase-lag in their responses. The alternating excitatory and inhibitory phases of responses of RSC were dependent on the direction of head orientation, the characteristics of which are the null response plane (NRP) and the optimal response plane (ORP). The analysis based on the NRP of RSC showed that vestibular inputs from the ipsilateral anterior semicircular canal induced the NRP of the RSC response at about 45 degree counterclockwise to the longitudinal axis of the animal, and that those inputs were distributed to RSC in the rostral part of $IO{\beta}$. On the other hand, those from the posterior semicircular canal were related with the NRP at about 45 degree clockwise and with the caudal part of the $IO{\beta}$. These results suggest that IO neurons receive and encode the vestibular information, the priority of which seems to be the vertical component of the body movement rather than the horizontal ones.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.9-19
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• 1998

The present study was primarily carried out to characterize the properties of the spinomesencephalic tract (SMT) neurons that project from the upper cervical spinal segments to the midbrain. It was also investigated whether these neurons received convergent afferent inputs from other sources in addition to cervical inputs. Extracellular single unit recordings were made from neurons antidromically activated by stimulation of midbrain. Recording sites were located in lamina $I{\sim}VIII\;of\;C1{\sim}C3$ segments of spinal cord. Receptive field (RF) and response properties to mechanical stimulation were studied in 71 SMT neurons. Response profiles were classified into six groups: complex (Comp, n=9), wide dynamic range (WDR, n=16), low threshold (LT, n=5), high threshold (HT, n=6), deep/tap (Deep, n=10), and non- responsive (NR, n=25). Distributions of stimulation and recording sites were not significantly different between SMT groups classified upon their locations and/or response profiles. Mean conduction velocity of SMT neurons was $16.7{\pm}1.28\;m/sec$. Conduction velocities of SMTs recorded in superficial dorsal horn (SDH, n=15) were significantly slower than those of SMTs recorded in deep dorsal horn (DDH, n=18), lateral reticulated area (LRA, n=21), and intermediate zone and ventral horn (IZ/VH, n=15). Somatic RFs for SMTs in LRA and IZ/VH were significantly larger than those in SDH and DDH. Five SMT units (4 Comps and 1 HT) had inhibitory somatic RFs. About half (25/46) of SMT units have their RFs over trigeminal dermatome. Excitabilities of 5/12 cells and 9/13 cells were modulated by stimulation of ipsilateral phrenic nerve and vagus nerve, respectively. These results suggest that upper cervical SMT neurons are heterogenous in their function by showing a wide range of variety in location within the spinal gray matter, in response profile, and in convergent afferent input.

• The Korean Journal of Pharmacology
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• v.27 no.2
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• pp.99-108
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• 1991

The effect of racemic Ketamine HCl was observed on excitable membranes of sciatic nerve fibres and toe muscles from frog. Ketamine significantly depressed the amplitude of the action potential, maximum rate of rise and that of fall of action potentials of sciatic nerve by dose-dependent and time-course manner, and also it produced the inhibition of $K^+-contracture$ in toe muscle. We used two different ways of sucrose gap method to to obtain the better results from sciatic nerve. We observed and compared the effect of ketamine on sciatic nerve with naloxone, 4-AP (4-aminopyridine) and TEA (Tetraethylammonium). Naloxone significantly but not totally blocked the effect of ketamine both on nerve and on skeletal muscle. 4-AP or TEA by itself had a significant depressant effect on the action potentials on nerve by central perfusion (extracellular perfusion), but both of these drugs did not much affect the action of Ketamine on nerve. The reversibility of effect of Ketamine (10 mM) was observed both on nerve and on skeletal muscles when exposed to drug for short duration. The effects of racemic ketamine described may provide to support that one of the mechanisms of the action of Ketamine on nerve and on muscles of frog might be related to non-specifically effect on receptors within the ion channels $(K^+-channel,\;Na^+-channel\;or\;slow\;Ca^{++}\;channel)$ at higher dose which produces anesthetic effect and also it interacts specifically with one of the opioid receptors or subtype of these receptors which is sensitive to Naloxone at lower dose which produces analgesia.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.3
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• pp.213-221
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• 2001

The amygdala is known as a site for inducing analgesia, but its action on the trigeminal nucleus has not been known well. Little information is available on the effect of dynorphin on NMDA receptor-mediated electrophysiological events in the trigeminal nucleus. The purpose of this study was to investigate the changes in the single neuron spikes at the trigeminal nucleus caused by the amygdala and the action of dynorphin on the trigeminal nucleus. In the present study, extracellular single unit recordings were made in the dorsal horn of the medulla (trigeminal nucleus caudalis) and the effects of microiontophoretically applied compounds were examined. When [D-Ala2, N-Me-Phe4, Glys5-ol]enkephalin (DAMGO, 10-25 mM), a ${\mu}-opioid$ receptor agonist, was infused into the amygdala, the number of NMDA-evoked spikes at the trigeminal nucleus decreased. However, the application of naloxone into the trigeminal nucleus while DAMGO being infused into the amygdala increased the number of spikes. Low dose (1 mM) of dynorphin in the trigeminal nucleus produced a significant decrease in NMDA-evoked spikes of the trigeminal nucleus but the NMDA-evoked responses were facilitated by a high dose (5 mM) of dynorphin. After the ${\kappa}$ receptors were blocked with naloxone, dynorphin induced hyperalgesia. After the NMDA receptors were blocked with AP5, dynorphin induced analgesia. In conclusion, dynorphin A exerted dose-dependent dual effects (increased & decreased spike activity) on NMDA-evoked spikes in the trigeminal nucleus. The inhibitory effect of the dynorphin at a low concentration was due to the activation of ${\kappa}$ receptors and the excitatory effect at a high concentration was due to activation of NMDA receptors in the trigeminal neurons.

• The Korean Journal of Physiology and Pharmacology
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• v.28 no.5
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• pp.413-422
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• 2024

Group I metabotropic glutamate receptors (mGluRs) modulate postsynaptic neuronal excitability and epileptogenesis. We investigated roles of group I mGluRs on low extracellular Mg²⁺ concentration ([Mg²⁺]_o)-induced epileptiform activity and neuronal cell death in the CA1 regions of isolated rat hippocampal slices without the entorhinal cortex using extracellular recording and propidium iodide staining. Exposure to Mg²⁺-free artificial cerebrospinal fluid can induce interictal epileptiform activity in the CA1 regions of rat hippocampal slices. MPEP, a mGluR 5 antagonist, significantly inhibited the spike firing of the low [Mg²⁺]_o-induced epileptiform activity, whereas LY367385, a mGluR1 antagonist, did not. DHPG, a group 1 mGluR agonist, significantly increased the spike firing of the epileptiform activity. U73122, a PLC inhibitor, inhibited the spike firing. Thapsigargin, an ER Ca²⁺-ATPase antagonist, significantly inhibited the spike firing and amplitude of the epileptiform activity. Both the IP₃ receptor antagonist 2-APB and the ryanodine receptor antagonist dantrolene significantly inhibited the spike firing. The PKC inhibitors such as chelerythrine and GF109203X, significantly increased the spike firing. Flufenamic acid, a relatively specific TRPC 1, 4, 5 channel antagonist, significantly inhibited the spike firing, whereas SKF96365, a relatively non-specific TRPC channel antagonist, did not. MPEP significantly decreased low [Mg²⁺]_o DMEM-induced neuronal cell death in the CA1 regions, but LY367385 did not. We suggest that mGluR 5 is involved in low [Mg²⁺]_o-induced interictal epileptiform activity in the CA1 regions of rat hippocampal slices through PLC, release of Ca²⁺ from intracellular stores and PKC and TRPC channels, which could be involved in neuronal cell death.

• Journal of Ginseng Research
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• v.24 no.3
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• pp.134-137
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• 2000

Spontaneous bursting activity was studied in rat thalamocortical slices using extracellular field potential recording to test the potential utilization of ginsenoside Rb$_1$ in controlling overactivated neural systems. In order to induce bursting activity, slices were perfused with Mg$\^$2+/-free artificial cerebrospinal fluid (ACSF). Two major types of spontaneous bursting activity, simple thalamocortical burst complexes (sTBCs) and complex thalamocortical burst complexes (cTBCs), were recorded in Mg$\^$2+/ -free ACSF. Ginsenoside Rb$_1$ selectively suppressed cTBCs. Duration and occurrence rate of cTBCs were reduced by 87.3${\pm}$10.2% and 85.3${\pm}$ 14.7% in the presence of 90 ${\mu}$M ginsenoside Rb$_1$ respectively, while amplitude and intraburst frequency were slightly changed by ginsenoside Rb$_1$. In contrast, ginsenoside Rb$_1$was much less effective in reducing duration and occurrence rate of sTBCs. We also tested effects of ginsenoside Rb$_1$ on bursting activity in the presence of a GABA$\sub$A/ receptor antagonist, bicuculline methiodide (BMI). Ginsenoside Rb$_1$ had no effect in suppressing BMI-induced bursting activities. These results suggest that ginsenoside Rbi may be useful in controlling seizure-like bursting activity under pathological conditions.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.113-122
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• 1994

The present study was carried out to characterize the functional properties of spinomesencephalic tract (SMT) neurons in the lumbar spinal cord of urethane anesthetized rats. Extracellular single unit recordings were made from neurons antidromically activated by stimulation of the midbrain area, including the deep layers of superior colliculus, periaqueductal gray and midbrain reticular formation. Recording sites were located in laminae I-VII of spinal cord segments of L2-L5. Receptive field properties and responses to calibrated mechanical stimulation were studied in 78 SMT cells. Mean conduction velocity of SMT neurons was $19.1{\pm}1.04\;m/sec$. SMT units were classified according to their response profiles into four groups: wide dynamic range (58%), deep/tap (23%), high threshold (9%) and low threshold (3%). A simple excitatory receptive field was found for most SMT neurons recorded in superficial dorsal horn (SDH). Large complex inhibitory and/or excitatory receptive fields were found for cells in lateral reticulated area which usually showed long after-discharge. Most of SMT cells received inputs from $A{\delta}$ and C afferent fiber types. These results suggest that sensory neurons in the rat SMT may have different functional roles according to their location in the spinal cord in integrating and processing sensory inputs including noxious mechanical stimuli.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.303-306
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• 2003

Metabotropic glutamate receptors (mGluRs), classified into three groups (group I, II, III), play a critical role in modulation of synaptic transmission at central and peripheral synapses. In the present study, extracellular field potential recording techniques were used to investigate effects of mGluR agonists on excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala. The non-selective mGluR agonist t-ACPD ($100{\mu}M$) produced reversible, short-term depression, but the group III mGluR agonist L-AP4 ($50{\mu}M$) did not have any significant effects on amygdala synaptic transmission, suggesting that group I and/or II mGluRs are involved in the modulation by t-ACPD. The group I mGluR agonist DHPG ($100{\mu}M$) produced reversible inhibition as did t-ACPD. Unexpectedly, the group II mGluR agonist LCCG-1 ($10{\mu}M$) induced long-term as well as short-term depression. Thus, our data suggest that activation of group I or II mGluRs produces short-term, reversible depression of excitatory synaptic transmission at thalamic input synapses onto the lateral amygdala. Considering the long-term effect upon activation of group II mGluRs, lack of long-term effects upon activation of group I and II mGluRs may indicate a possible cross-talk among different groups of mGluRs.

• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.26 no.3
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• pp.262-269
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• 2000

말초 미각계 및 중추 미각계에서 산화질소의 역할과 그것의 합성효소의 존재는 아직 규명되지 않고 있다. 본 연구는 말초미각계인혀와 미각구심성신경 그리고 중추미각계인 뇌간고속핵에서 산화질소 합성효소의 분포 및 면역조직화학 방법과 고삭신경의 extracellular recording 뇌간고속핵 절편 whole cell patch 방법으로 조사하였다. 신경성 산화질소 합성효소는 혀의 전방에 위치한 심상유두와 유곽유두에 약하게 존재하였으며 미뢰주위와 결체조직에 존재하는 신경섬유 및 혀의 상피층에 풍부하게 존재하였다. 혀에 소금물을 가하여 증가된 고삭신경의 복합전위는 산화질소 유리제인 SNP에 의해 증가되었으며 내인성 산화질소 합성효소 억제제인 L-NAME와 soluble guanylate cyclase 억제제인 ODQ에 의해 억제되었다. 문측 연수에 존재한 문측 고속핵과 진전핵에서 nNOS가 풍부하게 존재하였다. 문측 고속핵의 신경들은 안정막전위가 $-48{\pm}52mV$였고 활동전위의 크기는 $74{\pm}11mV$였다. SNP에 의해 뇌간 고속핵 신경들이 탈분극되었으며 current clamp하였을 때 활동전압의 빈도가 증가하였다. 또한 SNP에 의한 문측 고속핵의 탈분극과 활동전압 빈도증가는 L-NAME와 ODQ에 의해 감소되었다. 이상의 실험결과는 산화질소 합성효소가 혀와 뇌간고속핵에 존재하며 여기서 유리된 내인성 산화질소가 말초성 및 중추성 미각기전에 관여하리라 사료된다.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.1
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• pp.13-17
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• 2006

Experimentally induced cortical disorganization exhibits many anatomical features which are characteristic of cortical malformations in children with early-onset epilepsy. We used an immunocytochemical technique and extracellular field potential recordings from the dorsal hippocampus to determine whether the excitability of the CA1 pyramidal cells was enhanced in rats with exnerimentallv induced hippocampal dysplasia. Compared with control rats, the MAM-treated rats displayed a decrease of paired pulse inhibition. When $GABA_A$ receptor antagonists were blocked with $10{\mu}M$ bicuculline the amplitude of the second population spike of the MAM-treated of rats was similar to that of the first population spike, as was in the control rats. The MAM-treated rats had fewer somatostatin and parvalbumin-immunoreactive neurons than the control rats. These results suggest that the enhanced neuronal responsiveness of the in vivo recording of the CA1 in this animal model may involve a reduction of CA1 inhibition.