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05F123
O-01
Tetanic stimulation enhances a fraction of fast-releasing synaptic vesicles with
no change in total releasable pool size
Jae Sung Lee, Young-Eun Han, Jeong-Soon Ko, Won-Kyung Ho, Suk-Ho Lee
Cell Physiology Laboratory, Department of Physiology, Seoul National University
College of Medicine, 28 Yongon-Dong, Seoul, 110-799, Korea
Previously we have reported that posttetanic potentiation (PTP) at the calyx of
Held synapse is caused by increases not only in release probability but also in
the readily releasable pool (RRP) size and that the latter is mediated by
calmodulin(CaM)-dependent activation of myosin light chain kinase (MLCK). It
is well known that presynaptic whole-cell recording (WCR) abolishes PTP at
this synapse. Because CaM could be washed out during WCR, we tested
whether the post-tetanic increase in the RRP size can be restored by including
recombinant CaM in the presynaptic patch pipette. Indeed, when when 3 µM
CaM was included in the presynaptic patch pipette, tetanic stimulation (100Hz
for 4 s duration, TS) induced PTP of EPSCs, during which the RRP size
estimated from the plot of cumulative amplitude of 20 EPSCs at 100 Hz,
increased by ~30%. However, increase in release probability, which depends
on mitochondria-derived residual calcium, was significantly smaller than PTP
without presynaptic WCR, probably owing to diffusion of residual calcium into
the patch pipette. The release rates of docked SVs are heterogenous, and the
RRP size estimate based on the cumulative EPSC plot represents only part of
docked SVs. To investigate post-tetanic changes of fast and slow-releasing
SV pool sizes, we estimated quantal release rates before and 40 s after TS by
deconvolving AMPA receptor-mediated EPSCs evoked by a long depolarization
pulse with miniature EPSC. After TS, fast-releasing SV pool (FRP) size
increased by 19.5 ± 3.7% (n = 8, p < 0.01), while slowly releasing SV pool size
decreased by 25.4 ± 5.0% (n = 8, p < 0.01), whereas calcium current
amplitude was not different (2.00 ± 0.17 nA vs. 2.02 ± 0.17 nA, n = 8). Total
RP size did not increase after TS (94.8 ± 1.3% of RP size before TS).
Consistent with our previous study, the post-tetanic increase in the FRP size
was abolished by 100 µM blebbistatin or 5 µM MLCK inhibitor peptide added to
the patch pipette together with CaM.
Key Word : posttetanic potentiation, calmodulin, MLCK, synaptic vesicle
dynamics, calyx of Held
저자 : 이재성, 한영은, 고정순, 호원경, 이석호
소속 : 서울대학교 의과대학 생리학교실
05F036
O-02
AMPA receptor-mediated dendritic Ca²<sup>+</sup> signals in the midbrain
dopamine neurons
Jin Young Jang , Myoung Kyu Park
Department of Physiology, School of Medicine, Sungkyunkwan University Suwon
440-746, South Korea
Glutamate is a major excitatory neurotransmitter in the midbrain dopamine
neurons which activates AMPA- and NMDA-type glutamate receptors.
Dendrites of midbrain dopamine neurons have rare spines and thus do not
possess a clear morphological basis for synapse-specific
compartmentalization. Therefore, in aspiny dendrites of the dopamine neurons,
Ca2+-permeable AMPA receptors (CP-AMPAR) might play a major role in
input-specific synaptic plasticity by confining calcium events within a
microdomain. However, little is known about Ca2+ signals and roles of CPAMPA receptors in dendrites of the midbrain dopamine neurons. Therefore, we
investigated expression of AMPAR and Ca2+ signals in the acutely dissociated
dopamine neurons from the rat midbrain (9-12 days, Sprague-Dawley rat).
Single cell RT-PCR experiments showed that all mRNAs for GluR1, 2, 3 and 4
subtypes were expressed in the thyrosine hydroxylase (TH) positive dopamine
neurons (77.8, 100, 22.2 and 44.4 % expression, respectively).
Immunocytochemistry results showed that the expression of CP-AMPA
receptors along a dendrite increases with distance from the soma. Application
of glutamate and AMPA evoked inward currents at -60 mV membrane potential
together with increases in cytosolic Ca2+ levels at dendrites, which were
significantly inhibited by an AMPA/KA receptor blocker, CNQX. Philanthotoxin433 (PhTX), a specific CP-AMPAR blocker, also inhibited the AMPA-induced
Ca2+ rises. From these results, we conclude that, although GluR2 subunits
were abundantly expressed in all dopamine neurons, contribution of CP-AMPA
receptors to the glutamate-induced currents and Ca2+ influx along a dendrite
increases with distance from the soma in the SNc dopamine neurons.
Key Word : Dopamine neuron, Glutamate receptor, CP-AMPA
저자 : 장진영, 박명규
소속 : 성균관대학교 의과대학 생리학교실
05F159
O-03
L-type Ca2+ channel, Cav1.3 is required for Histamine induced Ca2+ increase in
the suprachiasmatic nucleus neurons.
Yoon Sik Kim¹, C. Justin Lee², Yang In Kim¹
¹ Department of Physiology and Neuroscience Research Institute, Korea
University, College of Medicine Seoul 136-705, Republic of Korea ²Center for
Neural Science, Korea Institute of Science and Technology, Seoul 136-791,
Republic of Korea.
The master circadian clock in mammals is located in the suprachiasmatic
nucleus (SCN) of the hypothalamus. Studies have indicated that many
neurotransmitters regulate the function of circadian clock, which governs
various physiological, endcrinological, and behavioral circadian rhythms.
Histamine is a neurotransmitter implicated in the control of sleep and arousal. It
is reported that histamine induces a phase delay at early night, and a phase
advance at late night, just as the light impulses and glutamate treatment.
However, the mechanisms of histamine-induced circadian phase shift remain
unknown. Here we report that histamine causes Ca2+ increase in SCN neurons
by activating Histamine 1 receptors (H1 receptors). Interestingly we discovered
that H1 receptor activation does not lead to conventional, IP3-mediated
release of Ca2+ from intracellular stores, but instead leads to an activation of
L-type Ca2+ channels. Further, we found that most H1 receptors colocalize
with L-type Ca2+ channel subunit Cav1.3, which contribute to most of L-type
current, but not with Cav1.2 that contributes minimally to L-type current. These
results indicate that histamine by activating H1 receptors lead to Ca2+ influx
through Cav1.3 L-type Ca2+ channels. We speculate that this Ca2+ increase
may be responsible for histamine-induced circadian phase-shift , considering
that L-type Ca2+ channel activation is crucial for glutamate –induced phase
shifts of circadian clock in the SCN (Do Young Kim et al, 2005, EJN, Vol. 21,
p1215-1222).
Key Word : Histamine, Cav1.3, SCN, Circadian clock.
저자 : 김윤식¹ 이창준², 김양인¹
소속 : 고려대학교 의과대학 생리학교실
05F038
O-04
Modulation of spinally- and meduallary-projecting PVN neurons via
glucocorticoid and mineralocorticoid receptors in rats
Seung Yub Shin, Tae Hee Han, So Yeong Lee, Pan Dong Ryu
Laboratory of Veterinary Pharmacology, College of Veterinary Medicine, Seoul
National University
The hypothalamic paraventricular nucleus (PVN) is well known integrative center
for autonomic responses to stressors. To study whether corticosterone (CORT)
can act directly to the pre-sympathetic neurons in the PVN which modulate
sympathetic outflow, we aimed to show the effect of CORT on spontaneous
firing activity of pre-sympathetic PVN neurons. The pre-sympathetic neurons in
the PVN were identified by the retrograde tracer injection into the
intermediolateral cell column (IML) of spinal cord or rostral ventrolateral medulla
(RVLM). Then, using single cell RT-PCR and immunohistochemistry, the
presence of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR)
mRNAs as well as proteins were shown in the retrogradely-labeled neurons.
Patch clamp recordings showed the firing pattern and rate of RVLM-projecting
PVN neurons were affected by CORT. After in vitro slice incubation of the brain
slices from adrenalectomized rats, either in vehicle or CORT or CORT with the
GR or MR antagonist, the neuronal populations for tonic regular (T-R) or tonic
irregular (T-IR) firings was changed by which receptor was activated among
GR and MR. T-R was the major firing pattern in CORT with MR antagonist
treated group (89%). On the contrary, T-IR was the major firing pattern in
CORT with GR antagonist treated group (83%). The mean firing rate was also
significantly different between these two groups (3.35 0.72 Hz in CORT + MR
antagonist vs 1.21 0.44 Hz in CORT + GR antagonist). The firing rate of T-R
neurons was significantly higher than T-IR neurons (4.95 0.44 Hz vs 1.02
0.19 Hz). Collectively, this study suggests the presence of functionally working
corticosteroid receptors (GR and MR) on the pre-sympathetic neurons in the
PVN. The results implicate that CORT can directly modulate the sympathetic
outflow by regulating neuronal activity of pre-sympathetic PVN neurons at the
level of hypothalamus.
Key Word : spontaneous firing, RVLM, IML, tonic regular, tonic irregular
저자 : 신승엽, 한태희, 이소영, 류판동
소속 : 서울대학교 수의과대학 약리학교실
05F005
O-05
Developmental changes of chloride transporters, KCC2 and NKCC1, in LSO
neurons of circling mice
Myeung Ju Kim¹, Ki Sup Park¹, D Maskey¹, J Pradhan², Seung Cheol Ahn²
Department of Anatomy¹, Department of Physiology², College of Medicine,
Dankook University
The glycine receptors, one of main pathways of chloride ion, do not develop
normally in lateral superior olive (LSO) neurons in developing homozygous
(cir/cir) circling mice, animal model for congenital deafness, which suggests
the possibility that other apparatus regulating chloride concentration of LSO
neurons might not develop well in homozygous (cir/cir) circling mice. The aim
of this study is to evaluate whether the known chloride transporters, potassium
chloride co-transporter: KCC2, sodium-potassium-2 chloride cotrasnporter:
NKCC1, are functioning normally in developing homozygous (cir/cir) or
heterozygous (+/cir) circling mice. Using voltage clamp technique, we tested
whether chloride reversal potentials recorded in LSO neurons were changed by
bumetanide, a NKCC1 blocker or furosemide, a KCC2 blocker in mice younger
than P5 or older than P9. In homozygous (cir/cir) mice, we could not find any
effects of bumetanide or furosemide on chloride reversal potentials in both
younger and older mice groups. In heterozygous (+/cir) mice younger than P5,
chloride reversal potentials were shifted to hyperpolarization by bumetanide
(from -59.2±3.0 mV to -66.7±3.5 mV) with no significant effects by following
application of furosemide (from -66.7±3.5 mV to -66.0±3.9 mV, n = 8).
However, in heterozygous (+/cir) mice older than P9, chloride reversal
potentials shifted to hyperpolarization by bumetanide (from -54.5±2.8 mV to 65.2±2.0 mV) were restored by following application of furosemide (from 65.2±2.0 mV to -53.3±4.0 mV, n=9). These data indicate that NKCC1 and
KCC2 develop normally in heterozygous (+/cir) circling mice, while those
transporters are not functioning or developing normally in homozygous (cir/cir)
circling mice.
Key Word : circling mouse, congenital deafness, LSO, KCC2, NKCC1
저자 : 김명주¹, 박기섭¹, D Maskey¹, J Pradhan², 안승철²
소속 : Department of Physiology, College of Medicine, Dankook University
05F168
O-06
Neuregulin-1 rescues the neurotoxicities and impairment of LTP induced by
amyloidβ
Jinhua An¹, Ran-SooK Woo², Seung Hon Han¹, Jaeyong Yee¹, Chan Kim¹, Geun
Hee Seol³, Sun Seek Min¹
Department of ¹Physiology and Biophysics, School of Medicine, Eulji University,
²Department of Anatomy and Neuroscience, School of Medicine, Eulji University,
³Department of Basic Nursing Science, School of Nursing, Korea University
Neuregulin-1 (NRG-1) signaling adjusts synaptic activity of target cell and the
expression of other neurotransmitter receptors and survival of satellite cells,
Schwann cells and oligodendrocytes in the brain. However, little is known
about its role in Alzheimer’s disease. Cerebral accumulation of amyloid βprotein is generally accepted to play a negative role in the pathogenesis of
Alzheimer’s disease (AD). In the present study, we found that NRG1 attenuates
the neurotoxicities and impairment of long-term potentiation induced by
amyloid peptide (Aβ₁-₄₂) treatment and the expression of a Swedish
mutation of amyloid precursor protein (Swe-APP) and the C-terminal fragments
of APP (APP-CTs) in neurons. These effects were blocked by AG1478, the
inhibitor of ErbB4 receptors, suggesting the involvement of ErbB4, a key NRG1
receptor. We also show that NRG1 reduces production of reactive oxygen
species and attenuates mitochondrial membrane potential loss. Together, these
results demonstrate the neuroprotective effects of NRG1 in the in vitro AD
model. Our findings further indicate that NRG1 could be used as a therapeutic
agent for Alzheimer patients.
Key Word : neuregulin-1, synaptic plasticity, Long-term potentiation,
Alzheimer’s disease, neurotoxicity
저자 : 안금화¹, 우란숙², 한승호¹, 이재용¹, 김찬¹, 설근희³, 민선식¹
소속 : Department of Physiology and Biophysics, School of Medicine, Eulji
University
05F181
O-07
COCAINE REGULATES ERM PROTEINS AND RHOA SIGNALING IN THE NUCLEUS
ACCUMBENS
W. Y. Kim¹, S. R. Shin¹, S. Kim¹, S. Jeon²,J. -H. Kim¹
¹Department of Physiology, Brain Korea 21 Project for Medical Science, Yonsei
University College of Medicine, Seoul, ²Dongguk University Research Institute of
Biotechnology, Medical Science Research Center, Goyang-si, Gyeonggi-do,
South Korea
Drug addiction can be viewed as a form of neuronal plasticity that involves
structural as well as functional changes of target areas or molecules to the
drugs. The ezrin-radixin-moesin (ERM) proteins have been implicated in cellshape determination by crosslinking F-actin to plasma membranes. Here we
show that the phosphorylation levels of ERM protein are dose- and timedependently decreased in the NAcc by a single injection of cocaine (15 or 30
mg/kg, i.p.). Further, we show that the amount of active RhoA, a small GTPase
protein, is significantly reduced in the NAcc by cocaine, while the
phosphorylation levels of ERM protein are also decreased by bilateral
microinjections in this site of the Rho kinase inhibitors, Y27632 (1.0 or 10.0
μg/0.5 µl/side) or RKI II (0.5 or 2.0 μg/0.5 µl/side). Together, these results
suggest that cocaine reduces phosphorylated ERM levels in the NAcc by
making down-regulation of RhoA-Rho kinase signaling, which may importantly
contribute to initiate synaptic morphological changes in the NAcc leading to
drug addiction.
Key Word : cocaine, ERM, RhoA, nucleus accumbens
저자 : 김화영¹, 신소라¹, 김승우¹, 전송희², 김정훈¹
소속 : 연세대학교 의과대학 생리학교실
05F025
O-08
Early treatment with dexamethasone attenuates p38 MAPK activation induced by
mal-positioned dental implants in rats
Seung Ro Han, Min Kyung Lee, Min Kyoung Park, Kyoung Ae Won, Min Ji Kim,
Jin Sook Ju, Dong Ho Youn, Dong Kuk Ahn
Department of Oral Physiology and BrainKorea21, School of Dentistry,
Kyungpook National University, Daegu, 700-412, Korea
We have previously reported a novel animal model for trigeminal neuropathic
pain induced by mal-positioned dental implants in rats. In this animal model,
we showed that mal-position of dental implants produced the prolonged
nociceptive behavior in the trigeminal territory. In the present study, we
examined effects of dexamethasone treatment on nociceptive behavior and the
expression of p-p38 MAPK in the trigeminal subnucleus caudalis following
mal-positioned dental implants in rats. The left mandibular second molars of
male Sprague-Dawley rats (220 - 240 g) were extracted and this was followed
by the placement of a mini dental implant to induce injury to the inferior alveolar
nerve. Mechanical allodynia was observed on postoperative day 1 and
sustained over postoperative day 42. We found that p-p38 MAPK were
significantly increased in the trigeminal subnucleus caudalis following nerve
injury. It was also shown that p-p38 only co-localized with OX-42, a marker for
microglia. The rats received dexamethasone (2.5, 25 and 50 mg/kg, i.p.) on
postoperative day 1 showed anti-allodynic effects which produced transient
inhibition of mechanical allodynia. However, treatment with dexamethasone on
postoperative day 3 after injury failed to prevent mechanical allodynia.
Moreover, increased p-p38 MAPK expression was reduced by dexamethasone
treatment on postoperative day 1 but not on postoperative day 3. The current
results demonstrate that early treatment with dexamethasone attenuates not
only mechanical allodynia but also expression of p-p38 MAPK induced by malpositioned dental implants in rats. Thus, the appropriate treatment with
dexamethasone might be therapeutically beneficial for trigeminal neuropathic
pain caused by mal-positioned dental implants. "This study was supported by a
grant of the Korea Healthcare technology R&D Project, Ministry for Health,
Welfare and Family Affairs, Republic of Korea. (A080028)"
Key Word : Dental Implant, Dexamethasone, Inferior Alveolar Nerve, p38 MAPK,
Trigeminal Neuropathic Pain
저자 : 한승로, 이민경, 박민경, 원경애, 김민지, 주진숙, 윤동호, 안동국
소속 : 경북대학교 치과대학 구강생리학교실
05F007
O-09
Behavioral Alterations in Adrenal Clock-Disrupted Middle-Aged Female Mice:
Effect of Voluntary Exercise
Tae-Soo Kim1, Dong-Hee Han1, Yeon-Ju Lee1, Gi Hoon Son2, Kyungjin Kim2,
Chang-Ju Kim1, Sehyung Cho1
1Department of Physiology, Kyung Hee University School of Medicine; 2School
of Biological Sciences, Seoul National University, Seoul, Korea
Glucocorticoid, synthesized in and secreted from the adrenal cortex, plays
crucial roles in diverse physiological functions including stress-related
behavior, metabolism, reproduction, cardiovascular function, immunity and
inflammation. We recently established an adrenal clock-disrupted transgenic
mouse line (BMAS) where murine BMAL1 antisense RNA is stably expressed
under the control of adrenal-specific MC2R promoter. The BMAS mice with
adrenal clock disruption exhibit a dampened rhythm of corticosterone secretion
and show reduced amplitude of day/night activity. In the present study, using a
computerized monitoring system that allows long-term simultaneous
measurement of voluntary wheel running (VWR), home cage activity (HCA) and
body temperature (BT) in freely moving animals, we examined the effects of
VWR on daily HCA and BT rhythms both in middle-aged (11-12 mo) wild-type
(WT) and BMAS female mice. We observed that BMAS females are reluctant to
wheel running and, even when they are inclined to VWR, show much reduced
VWR activity during the dark (active) phase. VWR itself increases the
robustness and amplitude of both BT and HCA rhythms in WT, but not in BMAS
mice, by lowering the daytime but elevating the nighttime BT and HCA. In the
absence of wheel, daily BT and HCA waveforms are similar in both genotypes
while the HCA rhythm is significantly dampened in BMAS mice. Surprisingly,
VWR alters the HCA waveform of BMAS females in a way that preferentially
increases the late nighttime (ZT21~ZT24) HCA. Estrous cyclicity was virtually
unaffected in both genotypes regardless of the presence of wheel even though
the infradian nighttime BT amplitude was a bit reduced in BMAS animals. These
results indicate that adrenal clock disruption in middle-aged female mice alters
BT and HCA rhythmic variables and makes the animals respond differently to
the voluntary exercise cue.
Key Word : adrenal clock, exercise, biological rhythm, body temperature, home
cage activity
저자 : 김태수 1, 한동희 1, 이연주 1, 손기훈 2, 김경진 2, 김창주 1, 조세형 1
소속 : 경희대학교 의과대학 생리학교실
05F053
O-10
NF-kB activation stimulates osteogenic differentiation on human adipose tissue
derived mesenchymal stem cells through increase of TAZ expression
Keun Koo Shin¹²³, Hyun Hwa Cho¹², Yeon Jeong Kim¹², Ji Sun Song¹²³, Jong
Myung Kim¹²³, Yong Chan Bae⁴, Jin Sup Jung¹²³*
¹Department of Physiology, School of Medicine, Pusan National University,
²Medical Research Center for Ischemic Tissue Regeneration, ³BK21 Medical
Science Education Center, School of Medicine, ⁴Department of Plastic Surgery,
School of Medicine, Pusan National University * Medical Research Institute,
Pusan National University, Yangsan, 626-870, Korea.
TNF-α is a skeletal catabolic agent that stimulates osteoclastogenesis and
inhibits osteoblast function. Although TNF-α inhibits the mineralization of
osteoblasts, the effect of TNF-α on mesenchymal stem cells is not clear. In
this study, we determined the effect of TNF-α on osteogenic differentiation of
stromal cells derived from human adipose tissue (hADSC) and the role of NFκB activation on TNF-α activity. TNF-α treatment dose-dependently increased
osteogenic differentiation over the first 3 days of treatment. TNF-α activated
ERK and increased NF-κB promoter activity. PDTC, an NF-κB inhibitor,
blocked the osteogenic differentiation induced by TNF-α and TLR-ligands, but
U102, an ERK inhibitor, did not. Overexpression of miR-146a inhibited basal,
TNF-α- and TLR ligand-induced osteogenic differentiation. TNF-α and TLR
ligands increased the expression of transcriptional coactivator with PDZbinding motif (TAZ), which was inhibited by the addition of PDTC. A ChIP assay
showed that p65 was bound to the TAZ promoter. TNF-α also increased
osteogenic differentiation of human aortic smooth muscle cells. Our data
indicate that TNF-α enhances osteogenic differentiation of hADSC via the
activation of NF-κB and a subsequent increase of TAZ expression.
Key Word : TNF-α, NF-kB, TAZ, human adipose tissue
저자 : 신근구¹²³, 조현화¹², 김연정¹², 송지선¹²³, 김종명¹²³, 배용찬⁴, 정진섭¹²³*
소속 : 부산대학교 의과대학 생리학교실
05F081
O-11
Mechanism of Anorexia Induced by Metformin in the Hypothalamus of Rats
Chang Koo Lee, Jung Yoon Huh, Yoon Jung Choi, So Young Park, Jong Yeon
Kim, Yong Woon Kim
Department of Physiology, School of Medicine, Yeungnam University, Daegu,
705-717, Korea
Metformin, an oral biguanide insulin-sensitizing agent, decreases appetite and
adiposity in obese adults and reduces serum leptin concentration even without
affecting body fat content in normal weight men. This phenomenon, however,
has not yet been clearly explained. Kim et al (2006) suggested that the
anorexic effect of metformin resulted from the leptin sensitizing effect of
metformin. It has been reported that metformin activates AMP-activating
protein kinase (AMPK) in muscle and liver, however, there is little literature that
evaluates the effect of metformin in the brain. In this study, to evaluate whether
metformin induces anorexia via hypothalamus directly and if so, whether leptin
is involved in the anorexic effect of metformin, various concentrations of
metformin were infused into lateral ventricle through chronically implanted
catheter and food intake for 24 hours was measured. The hypothalamic
neuropeptides associated with regulation of food intake were also analysed
following 1 hour of intracerebroventricular (i.c.v.) metformin injection.
Treatment of i.c.v. metformin decreased food intake in a dose dependent
manner in unrestrained conscious rats. The anorexic effect of metformin was
also found in chronically (1 week) infused rats model, however, the food intake
returned to normal level after disconnection of infusion line. The hypothalamic
phosphorylated signal transducer and activator of transcription3 (pSTAT3) was
increased by 3 μg of metfromin treatment, however, there was no further
increase in pSTAT3 level following increases of metformin dosage. The
hypothalamic pAMPK increased by 3 μg of metfromin treatment, however, there
was no further increase with increases in metformin dosage. The increase of
pSTAT3 by metformin was blocked by treatment with leptin antagonist.
Hypothalamic proopimelanocortin was elevated with metformin treatment, while
neuropeptide Y was not significantly changed. These results suggest that
metformin induces anorexia via a direct action in the hypothalamus and the
increase in pSTAT3, at least in part, is involved in that process. However,
hypothalamic pAMPK is not involved in metformin induced appetite reduction
in, at least, normal rat. Further study for evaluating new pathway connecting
metformin and feeding regulation is needed.
Key Word : Hypothalamus, metformin, anorexia, leptin, AMPK
저자 : 이창구,허정윤,최윤정,박소영,김종연,김용운
소속 : 영남대학교 의과대학 생리학교실
05F126
O-12
Characterization of MOB Single Unit Responses to Different Odors in
Anesthetized Rats.
HG Ham, XM Jin, CK Im, YR Lang, HJ Lee, HC Shin
Hallym University, College of Medicine, Dept. of Physiol., Chuncehon, Gangwon,
South Korea #200-702
Multi-channel extracelluar single unit recordings were done from the
mitral/tufted cells in the main olfactory bulb (MOB) of anesthetized (urethane,
1.5g/kg, IP) SD rats (n=5, 250~400g) to compare any differences of neural
responses to various odors. Tungsten micro-wire (50μm, A-M system inc.
USA) electrodes (32 channels) were implanted in the MOB. Unit recordings
(Plexon inc. USA) were done near the midline of the dorsal surface of the
olfactory bulb. Methyl methacrylate (MMA, 10%), isoamyl acetate (IAA, 10%),
methyl ethyl ketone (MEK, 10%) were used as odorants, which were prepared
by dissolving into mineral oil. Each substances was exposed in front of rat's
nose in random sequence for 4 sec with 2 min of resting interval. Each smelling
substance was tested for 5~10 times. Spontaneous activity of the lab air
stimulation was 8.4±0.5 Hz. Spontaneous activities of either mineral oil
(10.7±0.9 Hz) or MEK (11.7±0.7 Hz) stimulation were significantly elevated.
Averaged mean % change of the stimulation-induced evoked response during
fresh air stimulation was 163.9±4.3% above spontaneous activity. All odors
except MEK (169.0±4.3%) exhibited significant changes of evoked responses
(%, mineral oil: 150.3±3.8, MMA: 219.1±6.4, IAA: 217.5±6.6) compared to
fresh air stimulation. Maximum response peak after fresh air stimulation was
observed at 4.9±0.2 sec after initiation of stimulation. Peak responses after all
three odors were not significantly different from that after air stimulation. Peak
width at half height for air stimulation was 1.5±0.8 sec. Those for either MMA
(1.8±0.1 sec) or IAA (2.1±0.1 sec) were significantly increased. Out of 517
single units recorded. 14.31% did not show responses to any scents, while
26.50% of them exhibited responses to all three odors. About 50~60% of units
showed responsiveness to one of three substances. 23% exhibited responses
to all three chemicals, while 12.7%, 3.43%, 0.66% responded exclusively to
MMA, IAA, MEK, respectively. The results of this study suggested that there
might be heterogenious types of MOB cells working in different combinations to
process various kinds of scents. [09 Brain Frontier Grant to HCSHIN]
Key Word : Olfaction, Odor discrimination, Main Olfactory Bulb, Single Neuron,
Olfactory System
저자 : 함형걸, 김설매, 임창균, 랑이란, 이현주, 신형철
소속 : 한림대학교 의과대학 생리학교실