Volume 59 · Supplement 1 · 2009

Volume 59 · Supplement 1 · 2009

International Scientific Program Committees (ISPC) ISPC Chair Yoshihisa Kurachi Vice Chair Ole Petersen ISPC from IUPS Council Akimichi Kaneko (IUPS President) Irene Schulz (IUPS Vice President) Pierre Magistretti (IUPS Vice President) Malcolm Gordon (IUPS Treasurer)

ISPC IUPS2009 Members and Associated Members Commission I Locomotion Hans Hoppeler, Masato Konishi, Hiroshi Nose Commission II Circulation/Respiration Yung Earm, Makoto Suematsu, Itsuo Kodama Commission III Endocrine, Reproduction & Development Caroline McMillen, Yasuo Sakuma, Toshihiko Yada

Commission VII Comparative Physiology: Evolution, Adaptation & Environment Malcolm Gordon, Ken-ichi Honma, Kazuyuki Kanosue Commission VIII Genomics & Biodiversity David Cook, Hideyuki Okano, Gozoh Tsujimoto

Commission IV Neurobiology Quentin Pittman, Harunori Ohmori, Megumu Yoshimura

Commission IX Others Ann Sefton, Peter Hunter, Osamu Matsuo, Fumihiko Kajiya, Tadashi Isa, Tadaharu Tsumoto, Jun Tanji

Commission V Secretion & Absorption Irene Schulz, Miyako Takaki, Yoshikatsu Kanai

Local Executives Yasuo Mori, Ryuji Inoue

Commission VI Molecular & Cellular Biology Cecilia Hidalgo, Yoshihiro Kubo, Katsuhiko Mikoshiba, Masahiro Sokabe, Yukiko Gotoh

Volume 59 · Supplement 1 · 2009 · pp 1–XX

The XXXVI International Congress of Physiological Sciences (IUPS2009)

Proceedings of the XXXVI International Congress of Physiological Sciences (IUPS2009) Function of Life: Elements and Integration July 27–August 1, 2009, Kyoto, Japan

FAMILIAL ISOLATED CARDIAC CONDUCTION DEFECT ASSOCIATED WITH A MUTATION IN THE CONNEXIN40 GENE GJA5 Naomasa Makita1, Naokata Sumitomo2, Akiko Seki3, Nobuhisa Hagiwara3, Jean-Jacques Schott4, Hiroyuki Tsutsui1 1

Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Japan, 2Department of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan, 3Department of Cardiology, Tokyo Women’s Medical University, Tokyo, Japan, 4INSERM U915, l'institut du thorax, Nantes, France Isolated cardiac conduction defect (ICCD) is a hereditary lethal arrhythmia, characterized by slow conduction in the specialized conduction system without underlying structural heart diseases. We have genetically screened gap junction (GJ) genes for 139 ICCD probands. In one ICCD family with two sudden death victims, we found a missense mutation Q58L in connexin40 (Cx40), a GJ predominantly expressed in the atrium and His-Purkinje system. The mutation carriers showed identical ECG of idioventricular rhythm and complete left bundle branch block. GFP-tagged Q58L Cx40 transfected in GJ-deficient N2A cells showed predominant expression in the intracellular space and impaired GJ formation. Intracellularly applied dye Lucifer yellow was readily transferred to the neighboring cells in wild type (WT), but its transfer was delayed in the Q58L. Furthermore, junctional conductance measured by the dual whole-cell patch clamp was severely impaired in Q58L cell pairs (12.9±5.8 nS for WT (n=4) vs. 1.2±0.7 nS for Q58L (n=5); p30 s) significantly increased from 22/73 to 53/67 after CBX, and average VT cycle length significantly increased from 132±12 ms to 149±23 ms (n=25, p p38 MAPK -> PLA2 signaling axis has a crucial role in caspase-independent cell death induced by hypoxia/low glucose stress.

P1AM-18-9

P1AM-18-10

Aysegul Kucuk1, M.Kenan Kinaci2, Tulay Koken3, Murat Tosun4, Deniz Uren5, Nilufer Erkasap6

Jong-Shyan Wang

EFFECTS OF QUERCETIN ON APOPTOSIS AND iNOS GENE EXPRESSION ACCOMPLISHED WITH REAL TIME PCR ON RAT KIDNEY 1

Department of Physiology, Dumlupinar University, Turkey, 2Department of Physiology, Eskisehir Osmangazi University, Turkey, 3Department of Biochemistry, Afyon Kocatepe University, Turkey, 4Department of Histology, Afyon Kocatepe University,Turkey, 5ATQ Biotechnology,Turkey, 6Department of Physiology, Eskisehir Osmangazi University,Turkey The aim of this study is to evaluate the effects of quercetin on apoptosis and iNOS gene expression on kidney in I/R induced rats. 42 Sprague-Dawley rats were divided in 3 groups. Control group, I/R group(2 hours ischemia-6 hours reperfusion) and Quercetin+I/R group (50 mg/kg quercetin, i.p, 1 hour before the ischemia). MDA and GSH levels were analyzed by biochemical methods. MDA levels were significantly decreased in quercetin group compaired to the I/R group, however GSH levels were increased with quercetin treatment according to the I/R group. Histological evaluation of hematoxylene eosine stained tissue sections in the I/R group showed edema vascularisations and local areas of inflammatory cell infiltration. The number of apoptotic cells in the Quercetin+I/R group was determined to be less than the apoptotic cells in the I/R group. iNOS gene expression analysis by RT- PCR showed that the expression of iNOS gene (target gene) was increased in the I/R group, but when the concentration was calculated relative to the GAPDH (reference gene), the differences were not statistically significant. Quercetin, decreased apoptotic cells according to I/R group, so these data revealed that quercetin has protective effects on renal tissue I/R injury.

IUPS 2009 July 27 - August 1, 2009 in Kyoto

HYPOXIA PROMOTES EXERCISE-MEDIATED ANTITUMOR CYTOTOXICITY OF NATURAL KILLER CELL Graduate Institute of Rehabilitation Science and Center for Healthy Aging Research, Chang Gung University, Taiwan This study was to investigate how hypoxic exercise affects natural killer cell (NK) subset mobilization and anti-nasopharyngeal carcinoma (NPC) cytotoxicity of NK. Fifteen sedentary males randomly engaged in two normoxic exercise [i.e., strenuous exercise (SE) and moderate exercise (ME)] and two hypoxic exercise (i.e., ME while exposed to 12%O2 and 15%O2), as well as, exposed to two hypoxic conditions (i.e., resting while exposed to 12%O2 and 15%O2). Results showed that normoxic SE, but not ME, elicited a large mobilization of senescent/activated NKs into the blood, whereas NK count and perforin/granzyme B/interferon-gamma levels, NK-NPC binding and NK-induced CD95 expression and PS exposure on NPC were enhanced in response to the SE. Exposure to 15%O2 or 12%O2 did not induce a redistribution of blood NK subset populations, and the two hypoxic exposures also unaltered in terms of NK-induced NPC apoptotic responses. However, both 15%O2 and 12%O2 hypoxic ME increased NK cytotoxic protein levels, NK-NPC binding and anti-NPC cytotoxicity of NKs, whereas only 12%O2 hypoxic ME simultaneously enhanced senescent/activated NKs mobilization into the bloodstream. We conclude that severe hypoxia simultaneously increases NK subset mobilization and anti-NPC cytotoxicity of NK during exercise.

159

Poster Session

P1AM-18-5

P1AM-18-11

P1AM-18-12

Vladimir Strbak1, Zuzana Bacova1, Jana Galcikova2, Jana Matejikova2, Martina Orecna1, Roman Hafko1, Tana Ravingerova3

Mi-Young Kim1, Eun Ji Seo1, Dong Ha Lee1, Young-Ae Kim1, Eun Joo Kim2, Hye Soo Kim3, Hea-Young Cho3, Eun Yong Chung3, Chang-Hyun Moon1, Soo Hwan Lee1, Eun Joo Baik1, Yi-Sook Jung1

POSSIBLE PROTECTIVE EFFECT OF CELL SWELLINGINDUCED PEPTIDE SECRETION AGAINST ISCHEMIA REPERFUSION INJURY 1

Dept Neurohumoral Regulations, Institute of Experimental Endocrinology, Slovak Academy of Sciences, Slovakia, 2Institute of Cardiovascular Research, Slovak Academy of Sciences, Bratislava, Slovakia, 3Institute of Cardiovascular Research Slovak Academy of Sciences, Bratislava, Slovakia

PHOSPHORYLATION OF p53 AT Ser15 AND Ser20 INDUCED BY HYPOXIA REGULATES THE GADD45β GENE PROMOTER IN CARDIOMYOCYTES

1

Swelling-induced peptide secretion represents cellular reaction when material stored in secretory vesicles is expulsed from various types of cells. Dynamics of secretion is indistinguishable from that induced by specific secretagogue. It possesses, however, specific features indicating unique signaling pathway: it bypasses Ca2+ involving steps and conventional intracellular signal mediators and is resistant to physiological inhibitors. Pathophysiological implications: shift to anaerobic glycolysis and production of metabolites in ischemia increase intracellular osmolarity producing cell swelling. Products released after swelling could participate in the development of ischemia injury; the others could be mediators of local or remote preconditioning when factors released at the place of ischemia have protective effect. Perfusion of isolated rat heart with hyperosmolar high glucose medium followed by washout with isosmolar medium (relative hyposmotic stress) prior to ischemia substantially decreased postischemic contractile dysfunction and size of myocardial infarction. Protective effect of factors released during washout period might participate in the mechanism of preconditioning. Supported by projects: VEGA 2/6158/26, APVV 0235-06, 2/0173/08, APVV VVCE-0064-07 CENDO and CEKVY.

Department of Physiology, School of Medicine, Ajou University, Korea, 2Korea Institute of Toxicology, KRICT, Yusong, Taejon, Korea, 3Korea Food and Drug Administration, Tongilro, Eunpyeong-gu, Seoul, Korea In this study, we performed DNA microarray to identify patterns of expression changes in genes, especially focusing on apoptotic genes, in both in vivo rat heart and in vitro cardiomyocyte models of transient ischemia/hypoxia, and we found that three apoptotic genes, ATF3, GADD45β and DDIT4, were up-regulated in both in vivo and in vitro models. The results from the transfection of H9c2 cells with Gadd45β siRNA and GADD45β plasmid suggested the potential role of GADD45β as an important mediator of myocardial ischemic injury. To evaluate whether Gadd45β is a transcriptional target of p53, we examined effects of p53 on Gadd45β-Luc, reporter of Gadd45β. Gadd45β-Luc expression in H9c2 cells was enhanced by overexpression of p53 in a dose-dependent manner, but not by transfection with mutant p53, p53(S15A) or p53(S20A). Furthermore, the mRNA and protein levels of Gadd45β were increased by overexpression of p53 in a dose-dependent manner. In conclusion, the present study reveals that the transcriptional factor p53 transactivates downstream effector gene, GADD45β. GADD45β protein products may mediate apoptotic cell death. This work was supported by Brain Korea 21 for Molecular Science and Technology, Ajou University and grant from the Korea Food and Drug Administration.

P1AM-18-13

P1AM-18-14

HYDROGEN-RICH SALINE PROTECTS AGAINST INTESTINAL ISCHEMIA/REPERFUSION INJURY IN RATS

HYDROGEN-RICH WATER THERAPY ON NEONATAL HYPOXIA-ISCHEMIA RAT: SHORT AND LONG-TERM EFFECTS

1

Diving Medicine, Second Military Medical University, China

Xuejun Sun1, Yuan Hongbin2, Mao Yanfei3, Sun Xuejun1

Xuejun Sun, Sun Xuejun, Cai Jian Mei, Kang Zhimin

Hydrogen gas was reported to reduce reactive oxygen species and alleviate cerebral, myocardial and hepatic ischemia/reperfusion (I/R) injuries. We studied the effect of hydrogen-rich saline, which was easier for clinical application, on the intestinal I/R injury. In male Sprague Dawley rats, intestinal injury was induced by clamping the superior mesenteric artery for 45 minutes, followed by 120 min reperfusion. Hydrogen-rich saline or vehicle physiological saline (5 ml/kg) was administered via intravenous infusion 10 minutes before reperfusion, respectively. The intestine damage was detected microscopically and was assessed by Chiu score system after I/R injury. In addition, serum DAO activity, tissue MDA and MPO activity, serum TNF-α, IL-1β and IL-6 levels were all increased significantly by I/R injury. Hydrogen-rich saline reduced these tissue injury markers and relieved morphological intestinal injury. In conclusion, Hydrogen-rich saline protected the small intestine against I/R injury possibly by reduction of inflammation and oxidative stress.

Cerebral hypoxia/ischemia (HI) represents a major cause of brain damage in the term newborn. This study aimed to examine the short and long-term effect of hydrogen-rich normal saline water therapy in an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 οC). H2 saturated water was administered by peritoneal injection (5 ml/kg) immediately and again 8 h after HI insult. 24 h after hydrogen-rich water treament, the pups were decapitated and brain injury was assessed by2,3,5triphenyltetrazoliumchloride (TTC), Nissl, and TUNEL staining, caspase-3 activity, content of MDA as well as Iba-1 immunochemistry in the brain. 5 w after therapy, the long-term effects were assessed by the function test, Spontaneous activity test, and morris water maze test. The results indicated that proper amount of hydrogen-rich water therapy reduced the infarct ratio and increased the number of survival cells via suppressing the caspase activity, inhibiting oxidation and inflammation. This strategy also improved the long-term function of brain which proved that peritoneal injection of hydrogen-rich water was a good practice in the clinical treatment of HI or other ischemia-related diseases.

P1AM-19-1

P1AM-19-2

Diving Medicine, Second Military Medical University, China, 2Department of Anaesthesiology, Changzheng Hospital, Second Military Medical University, Shanghai, China, 3Department of SICU, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China

EFFECTS OF S-ADENOSYLHOMOCYSTEINE AND HOMOCYSTEINE ON DNA DAMAGE AND CELL VIABILITY IN MURINE HEPATIC AND MICROGLIA CELL LINES

Tsai-Hsiu Yang1, Wen-Yueh Ho2, Kuen-Lin Leu2, Chia-Chyuan Liu2 1

Poster Session

Department of Health and Nutrition, Chia-Nan University of Pharmacy and Science, Taiwan, 2Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, Taiwan The limited research has been performed regarding the s-adenosylhomocysteine (SAH)-evoked cell damage in hepatic and neuronal cells. In this study we assessed effects of SAH or homocysteine (Hcy) in hepatic and neuronal cells on cell viability and DNA damage, and attempted to find the underlying influences. Cell viability and DNA damage were evaluated in BNL CL.2 cell line and BV-2 cell line with SAH or Hcy treatment for 48 hours. Effects of SAH or Hcy on lipid peroxidation and DNA methylation were also measured in both cell lines. SAH or Hcy dose dependently inhibited cell viability and enhanced DNA damage in both types of cells. Furthermore, SAH treatment markedly increased intracellular SAH levels and DNA hypomethylation, the effect of SAH was much stronger than that of Hcy. The findings were also obtained that Hcy significantly induced lipid peroxidation. Results show that SAH might cause cellular DNA damage in hepatic and microglia cells by DNA hypomethylation, further resulting in irreversible DNA damage and decrement of cell viability. Additionally, higher Hcy could induce cellular DNA damage through increased lipid peroxidation and DNA hypomethylation. We suggest that SAH is more informative to cell damage than that of Hcy in hepatic and microglia cells.

160

BEHAVIOR OF INTRACELLULAR VESICLE AND CYTOSKELETON AFTER AMPHOTERICIN B TREATMENT Masao Miyake, Akihiro Hazama

Department of Cellular and Integrative Physiology, Fukushima Medical University School of Medicine, Japan

The sodium ionophore, amphotericin B (amB) causes HeLa cells to appear necrosis with morphological change after two-hour incubation. We visualized this cell death with propidium iodide (PI), and showed that the ion replacement of extracelluar fluid and ion channel blockers could suppress necrosis. However, PI can detect cells which has cracked cell membrane only, there was less information about what was going on during the morphological change after amB treatment. In this study, we visualized intracellular vesicles with acridine orange, lysotracker and lysosensor to measure vesicular pH level. Incubation with amB neutralized lysosomal pH, same as that with Bafilomycin A1. At the same time, vesicles moved vigorously after 20 minutes incubation with amB. And this vesicle fluidization occurred in dose-dependent manner with amB. When Cl- was replaced to Gluconate - in extracellular fluid, vesicle neutralization and fluidization were inhibited effectively, as a result, necrotic cell death was suppressed. Accordingly, we report behavior of cytoskeleton and membrane trafficking with fluorescent probe here, because their failure might contribute to realize amB-induced necrosis.

IUPS 2009 July 27 - August 1, 2009 in Kyoto

P1AM-20-1

P1AM-20-2

AKIN ABDUL-RAZAQ ALADA, GRACE OLUFUNMILAYO ISEHUNWA

Hoda Metwaly Nasr

PHYSIOLOGY, UNIVERSITY OF IBADAN, Nigeria

TOXICOLOGICAL AND PHYSIOLOGICAL EFFECTS OF SOME PESTICIDES ON LARVAL STAGES OF SILK WORM Department of Pest control and environmental protection, Faculty of Agriculture, Alexandria University, Damanhour branch, Egypt

The effects of adrenaline, cortisol, and glucagon on the blood glucose, liver and muscle glycogen during the rainy and dry seasons were studied on fasted adult toads. The toads were administered adrenaline, cortisol, glucagon, or amphibian saline respectively. Blood glucose, liver and muscle glycogen were determined using glucose oxidase and anthrone reagent methods respectively. Data were analyzed for statistical significance using Student t test. The basal blood glucose 61.8±1.4 mg per dl, during the rainy season was significantly higher than 51.6±0.8 mg per dl in the dry season. Basal liver glycogen 325.3±27.3 mg per 100 g, and muscle glycogen, 165.5±13.7 mg per 100 g, during rainy season were significantly less than the basal liver glycogen 757.5±89.2 mg per 100 g, and muscle glycogen 265.3±36.5 mg per 100 g in the dry season. Adrenaline, cortisol and glucagon produced greater hyperglycemia during rainy season than the dry season. The liver and muscle glycogen contents of 250.5± 13.20 to 376.10± 15.46 in response to the hormones during the rainy season were lower than 567.12± 23.12 to 840. 6± 17.3 in dry season. The study showed that seasonal conditions affect hormonal actions on carbohydrate metabolism in toads.

Toxicity of selected pesticides was tested against third instars larval stages of Bombyx mori, series of concentration were prepared according to the recommended and half recommended doses of pesticides. Mortality Percent was calculated after 24 and 48 hrs of treatment. The fresh mulberry leaves were treated with the tested pesticides. The third larval instars were fed on the treated leaves one time during its life duration. Results showed that AChE and phenoloxidase activities were inhibited in vivo and inhibition was calculated for the survived larval. Percentage of pupation and cocoons shells were determined. Results indicated that diazinon was the most effective one on the percent of mortality after 24 and 48 hrs from treatment followed by chloropirifos and kingbo (diazinon was 97% , 99% ,chloropirifos was 91% , 86% while kingbo was 59% , 63% ). Chloropirifos was the most effective one inhibited AChE followed by Diazinon and kingbo. Inhibition percentage was 92%, 89% and 61%, respectively. On the other hand, kingbo caused a higher percentage of phenoloxidase inhibition followed by chloropirifos and diazinon (85%, 68% and 65%, respectively). In conclusion, most parameters were in agree with mode of action of tested pesticides and were discussed through the results.

P1AM-20-3

P1AM-20-4

EFFECT OF INTERMEDIATE-FREQUENCY MAGNETIC FIELD ON SEED GROWTH RATE Isao Kayano, Seiichi Mochizuki

Department of Medical Engineering, Kawasaki University of Medical Welfare, Japan

THE OXIDATIVE STRESS STATUS OF NINE DIFFERENT BIRD SPECIES Mirella Mariia Kanerva, Miia Koivula, Tapio Eeva, Mikko Nikinmaa Department of Biology, University of Turku, Finland

In our preliminary studies, it was suggested that exposure to an intermediatefrequency magnetic field accelerate the growth of seeds. However, no detailed studies have been performed on effects of magnetic-flux density as well as exposure time on seed-growth promotion. Here, we thus aimed at investigating effects of these factors on the growth of seeds. White daikon radish sprouts seeds were used for hydroponic cultivation under exposure to the 25 kHz magnetic field (10 or 20 μT), generated by a Helmholtz coil. Three groups were studied: 1) ‘pre-sprout exposure’ group was exposed to the magnetic field for 48 hours from the beginning, 2) ‘post-sprout exposure’ group started to be exposed after 48 hours, and 3) ‘control’ group was without any exposure (n=58 in each group). The average growth rates between 48 and 78 hours were calculated and compared among these groups. The growth rates in the ‘pre-sprout exposure’ group were significantly higher (1.43±0.58 mm/h, mean±SD; p3 times) of mGluR-dependent LTD led to the long-lasting reduction in synaptic strength as well as synapse density in CA3-CA1 pathway in cultured hippocampal slices. We call this phenomenon LOSS (LTD-repetition-Operated Synaptic Suppression) to distinguish it from LTD itself. We found that LOSS depended on new protein synthesis in response to LTD-inducing stimuli, having a limited time window for the synthesis. These findings endorse LOSS as a good in vitro model system for the analysis of structural plasticity (as well as RISE, repetitive-LTP-induced synaptic enhancement, an apparently mirror-image phenomenon of LOSS). Since proBDNF-p75NTR (low-affinity neurotrophin receptor) signaling is suggested to be involved in apoptosis and synaptic plasticity including LTD, we hypothesized its involvement in LOSS. We performed quantitative analyses on the expression levels of mature BDNF, proBDNF, TrkB and p75NTR with special respect to the times of mGluR activation. The results were largely consistent to the hypothesis.

P1PM-9-7

P1PM-9-8

Arif Aliovsad Mekhtiev

Sayyed Alireza Talaei Zavareh, Mahmoud Salami

TWO NOVEL SEROTONIN-MODULATING PROTEINS INVOLVED IN MEMORY FORMATION IN OPPOSITE WAY Department of Ecological Physiology & Toxicology, Institute of Physiology, Azerbaijan

LIGHT DEPRIVATION IMPROVES MELATONIN RELATED SUPPRESSION OF HIPPOCAMPAL PLASTICITY Department of Physiology, Kashan University of Medical Sciences, Iran

The novel serotonin-modulating SMP-69 protein (Mr 69 kDa and pI 6,0) was purified from the rat brains. Its inactivation by the antibodies leads to a significant impairment of memory consolidation in the conditioned passive avoidance model in rats, if they had been injected 24 h prior to the learning session. Administration of the anti-SMP-69 antibodies brought to significant increase in the total RNA and protein synthesis in the rat brain cortex on 37% and 30%, correspondently. Electrophoresis fractionation of the water-soluble proteins of the rat brain cortex revealed approximately twotimes upregulation of the 28th protein's fraction content under the influence of anti-SMP-69 antibodies. This protein fraction was purified from the rat brains and appeared to consist of two subunits of Mr 60 and 126 kDa. Intracerebral administrations of the purified protein into the rats 24 h prior to learning sessions in the passive avoidance model leads to memory processes impairment ("anticonsolidation protein"). On the basis of these data the existence of the "switch off" molecular mechanism in which SMP-69 protein induces memory formation, while anticonsolidation protein, in opposite, blocks memory consolidationfor memory consolidation, is proposed.

In early postnatal life sensory inputs influence development and function of the brain.long-term potentiation (LTP), is affected by sensory deprivation in neocortex. This study is devoted to assess if dark rearing and melatonin influence LTP in the hippocampus. experiments were carried out on 2 groups of 45 days old male Wistar rats kept in standard light/dark condition (Light reared-LR) or in complete darkness (Dark reared- DR) since birth to testing. Each group, in turn, was divided to two, vehicle- and melatonin-treated, groups. Stimulating the Schaffer collaterals of CA3 area of hippocampus extracellular postsynaptic potentials (EPSPs) were recorded in the CA1 area. then, the hippocampus was perfused by either saline or 2 micrograms melatonin and EPSPs were recorded and LTP Induced. The light deprivation resulted in a significant augmentation in the amplitude of baseline responses. Also, melatonin-induced increase in amplitude of the baseline recordings in either LR or DRs. Tetanic stimulation elicited LTP of EPSPs in both groups, robustly in the former. melatonin inhibited the production of LTP in the two groups especially in the LR animals. concluded that higher level of neuronal activity in the DR rats give rise to a lower level of LTP.

P1PM-9-9

P1PM-9-10

MELATONIN ATTENUATES LONG-TERM POTENTIATION VIA INHIBITION OF NITRIC OXIDE SIGNALING PATHWAY IN RAT HIPPOCAMPUS Yoshiyuki Takahashi1, Takashi Okada2 1

Graduate School of Human Sciences, Sophia University, Japan, Department of Psychology, Faculty of Human Sciences, Sophia University, Japan Hippocampal long-term potentiation (LTP) is considered one of the candidate physiological bases of memory, and some recent studies have tried to identify the endocrine substances involved in the regulation of LTP. It is thought that a pineal hormone, melatonin, may regulate LTP with circadian rhythm, because the secretion pattern of melatonin shows a circadian rhythm, and because melatonin receptors reportedly exist in the hippocampus. In this study, we examined the effects of melatonin on LTP and the affected signaling cascade at the CA1 region in rat hippocampal slices electrophysiologically. Melatonin (50 μM) attenuated the degree of LTP irrespective of the time that hippocampal slices were prepared. Then we investigated the effects of melatonin on the nitric oxide (NO) signaling pathway, which is important for LTP induction. Although melatonin (100 nM) attenuated LTP and application of NO synthase (NOS) inhibitor (L-NAME, 100 μM) for blockade of NO signaling pathway also attenuated LTP, the attenuating effects of melatonin and L-NAME were not additive. NO donor, DEA/NO (3 μM), rescued the attenuating effects of melatonin and L-NAME on LTP. These findings suggest that melatonin attenuates hippocampal LTP through inhibition of the NO signaling pathway. 2

Poster Session

186

DOPAMINE D1 AGONIST FACILITATES INDUCTION OF LONG TERM DEPRESSION BY CALLOSAL LOWFREQUENCY STIMULATION, IN RAT ANTERIOR CINGULATE CORTEX Sokichi Sakuragi

Department of School Nursing and Health Education, Aichi University of Education, Japan To test whether dopamine have some effects on synaptic plasticity in emotion processing areas, I examined callosally evoked field potentials in coronal slices of rat anterior cingulate cortex, when low-frequency stimulation (LFS) was applied to corpus callosum as a conditioning stimulus. Neither dopamine nor D2 agonist had significant effect on the synaptic plasticity, while D1 agonist, SKF-38393, facilitated long term depression (LTD) induction. This facilitating effect of SKF on the LTD induction was completely blocked by D1 antagonist, SCH-23390. The LFS induced LTD was not blocked by application of metabotropic glutamatergic receptor antagonist, MCPG, or voltage gated calcium channel blocker, nifedipine, but blocked by application of NMDA receptor antagonist, APV. The facilitating effect of SKF on LTD induction was not mimicked by forskolin, but partially mimicked by phorbol 12,13-didecanoate, which is known to activate intracellular PKC pathway. These results suggest that LTD in ACC would be induced via NMDAR, and facilitated by D1 agonist at least partially via PKC related intracellular pathway. This type of facilitation of LTD induction might have some contribution to the pathogenesis of schizophrenia or major depression, in which frontal lobe hypofunction was indicated.

IUPS 2009 July 27 - August 1, 2009 in Kyoto

P1PM-9-11

P1PM-9-12

Masashi Kondo1, Yasuhiro Hukushima2, Minoru Tsukada2, Takeshi Aihara1

Mayumi Shindou, Tomomi Shindou, Jeffery R Wickens

1

Faculty of Engineering, Tamagawa University, Japan, 2Brain Science institute, Tamagawa University, Tokyo, Japan

DOPAMINE MODULATES SPIKE-TIMING DEPENDENT SYNAPTIC PLASTICITY IN D1 RECEPTOR-POSITIVE SPINY NEURONS IN THE NEOSTRIATUM OF ADULT MICE Neurobiology Research Unit, Okinawa Institute of Science Technology, Japan

It is found that the profiles of spike-timing dependent synaptic plasticity (STDP) were classified into two types, depending upon layer specific location along the dendrite in the CA1 area of a hippocampal slice. However, the interaction between information processing on different dendritic locations is not clear. In this study, to investigate how the temporal information of inputs to the proximal dendrite have an influence on information processing, STDP, at the distal dendrite, stimulation was applied at the proximal dendrite during STDP protocol at the distal dendrite. As the results, the information processing at the distal dendrite was influenced depending on the relative timing of BPAP and the input to the proximal dendrite. It is considered that there is a causality delivered by BPAP as a carrier of temporal information on a dendrite. This may be due to an effect on the coding process at the distal dendrite and could support the basis for a novel learning rule in the brain.

Recent evidence suggests that spike-timing dependent plasticity (STDP) exists in the corticostriatal pathway. In addition, dopamine (DA) has been suggested to play a crucial role in corticostriatal synaptic plasticity. Here we studied STDP of corticostriatal synapses in brain slices of adult mice (2-5 month-old). Whole cell recordings were obtained from spiny projection neurons and synaptic responses were measured in response to stimulation of the subcortical white matter. We found that long-term depression (LTD) was induced by three action potentials occurring 10 msec after the EPSP (pre-post protocols), but post-pre protocols caused little change. We also examined effects of DA on STDP. The LTD evoked by pre-post protocols was reversed by a D1 receptor agonist but not a D2 agonist. Modulation by the D1 agonist only occurred if it was applied during the induction protocol. Furthermore, this LTD was observed in the D1-expressing spiny neurons but not the D2-expressing spiny neurons. We suggest that the timing of DA receptor activation is important for modulation of corticostriatal STDP, especially in the D1-expressing spiny neurons.

P1PM-9-13

P1PM-9-14

THE NEURON SPECIFIC NF1 EXON 9a IS ESSENTIAL FOR THETA-FREQUENCY LTP AND LEARNING Mohammad reza Hojjati1, Geeske M. Van Woerden2, Alcino J. Silva3, Ype Elgersma2 1

Department of Physiology, Shahrekord University of Medical Sciences, Iran, 2Department of Neuroscience, Erasmus University Medical Center, The Netherlands, 3Department of Neurobiology, Psychiatry and Psychology, University of Carolina, USA

Neurofibromatosis type 1 (NF1) is one of the most common inherited singlegene disorders affecting cognitive function. The NF1 gene encodes a large amino acid protein called neurofibromin, which functions as a Ras GTPase activating protein (GAP). Although NF1 is expressed in all cells of the brain, expression of NF1 containing the small alternatively spliced exon 9a is restricted to neurons, and this isoform is particularly high expressed in the forebrain. This exon is not part of the GAP domain and its function is unknown. To study the role of the NF1-Ex9a isoform in cognitive function, we created a mouse lacking the NF1-Ex9a isoform. Here we show that mice lacking NF1 exon 9a demonstrate spatial learning deficits in the Morris water maze task and impaired LTP induced at theta frequency. Our finding suggest that exon 9a is essential for the function of NF1 in spatial learning and hippocampal plasticity, and that the role of NF1 in neuronal function is not restricted to its function as a GAP protein.

P1PM-9-15

INVESTIGATION OF MODULATORY EFFECTS ON LTP USING MULTIELECTRODE ARRAY (MEA) SYSTEM Ji-Ho PARK1, Jung-A Shin1, Se-Ra Yang1, Min-Sook Son1, GunHoon Choi1, Do-Hyoung Kim2 1 2

Department of Medical Science, Kyung Hee University, Korea, Department of Biomedical Engineering, Hanyang University, Korea

In this study, a reliable and acceptable electrophysiological system was established for screening LTP modulatory potential materials in rat hippocampal slice using MEA systems. An organotypic slice culture was also adapted to meet better accuracy rather than acute slice. As the results, there were three different modulatory effects on LTP. Firstly, additional treatment of Cassia tora extract increased fEPSP amplitude compare to the baseline of tetanic bust induced LTP. It may relate to an improvement of memory as other researchers reported. Secondly, a slow declining post tetanic and inhibitorylike potential was appeared with treatment of ESP-102 (a novel extracts). This data was similar to NMDA receptor antagonists treatment. Finally, there was fast post-tetanic and inhibitory potential with a compound (a novel extracts) treatment which may be related with elevation of the concentration. Furthermore, it was investigated that NGF-induced the spatiotemporal LTPLike neuronal activity changes. Taken together, this study tried to establish an accurate monitoring system for screening modulatory compounds on LTP using a spatiotemporal analytic system. We hope it can help to investigate more profound spatiotemporal changes on the synaptic plasiticity.

IUPS 2009 July 27 - August 1, 2009 in Kyoto

ROLE OF ENDOGENOUS CANNABINOID BREAKDOWN INHIBITOR ON HIPPOCAMPAL LTP IN RAT Alireza Komaki1, Siamak Shahidi1, Fatemeh Kazemi1, Abdolrahman Sarihi1, S. Mansour Malakouti1, Parisa Hasanein2, Reza Lashgari3, Abbas Haghparast3 1

Department of Physiology, Hamedan University of Medical Sciences, Iran, Department of Biology, School of Basic Sceinces, Bu-ali Sina University, Hamadan, Iran, 3Neuroscience Research Center, Shaheed Beheshti University of Medical Sciences, Tehran, Iran 2

There is currently debate over the interaction between L-type voltage dependent Ca2+ channels and endocannabinoid system on the synaptic plasticity. In this study we examined the effects of acute administration of URB597, as endocannabinoid breakdown inhibitor, following chronic administration of Verapamil, as Ca2+ channels blocker, on the evoked potentials and LTP induction in the dentate gyrus of hippocampus. Rats (Wistar) were treated i.p. with doses 10, 25, 50 mg/kg Verapamil for 13 days (once daily). Then following surgery, recording and stimulating electrodes were positioned in the granular cells of dentate gyrus and perforant pathway respectively. After ensuring a steady state baseline response, single i.p injection of saline or URB597 (0.1, 0.3 mg/kg) was done. The results show that there is difference between slopes of EPSP and population spikes in the Verapamil and URB597 groups after HFS. Decrease in LTP induction during chronic administration of Verapamil + acute URB597, is greater than other groups. In conclusion, these results indicate that acute administration of endocannabinoid breakdown inhibitor, URB597, disrupt LTP induction in the dentate gyrus of hippocampus in rat. Also, there is an interaction between Ca2+ channels blocker and endocannabinoid system.

P1PM-9-16

LONG-TERM IN VITRO MORPHINE DISAPPEARS ENHANCEMENT OF PAIRED PULSE FACILLITATION (PPF) IN WITHDRAWN SLICES Narges Hosseinmardi1, Yaghoub Fathollahi1, Naser Naghdi2, Mohammad Javan1 1

Department of Physiology, Tarbiat Modares University, Iran, 2Department of Physiology, Pasteur Institute, Iran

Addictive drugs are thought to alter normal brain function and cause the remodeling of synaptic functions in areas important to memory and reward. Given the known effects of opiate on hippocampal function, we investigated the potential effect of chronic morphine treatment on baseline synaptic response and paired pulse index (PPI) at CA1 synapses of rat hippocampal slices. There was no significant difference in the baseline synaptic response of slices taken from control or dependent rats. Also morphine and naloxone had no effect on baseline responses. The mean PPI was 1 for 80 and 200 ms IPIs in both groups. A significant increase in PPI was observed in the dependent slices at 80 ms IPI. This enhancement was disappeared in the present of morphine. In vitro morphine application caused an increase of PPI in 20 ms IPI in dependent slices. These results suggest that chronic morphine treatment alters mechanisms involved in PPF and paired pulse depression (PPD) and this alteration maybe a resetting in CA1 network due to chronic morphine treatment.

187

Poster Session

THE INFLUENCE OF MODULATING THE BACKPROPAGATING ACTION-POTENTIAL ON STDP IN HIPPOCAMPAL CA1 AREA

P1PM-10-1

P1PM-10-2

Taisuke Kawasaki, Hiroki Matsuki, Susumu Jitsuki, Takuya Takahashi

Makoto Sugita1, Yoshiki Shiba2

BRAIN REGIONS RESPONSIBLE FOR THE CROSSMODAL REORGANIZATION OF CORTICAL CIRCUIT Department of physiology, Yokohama City University Graduate School of medicine, Japan

GENETIC TRACING AND CHARACTERIZATION OF THE NEURONS IN THE NUCLEUS OF THE SOLITARY TRACT, RECEIVING SPECIFIC TASTE INPUT 1

PRESTO, JST, and Department of Oral Physiology, Hiroshima University, Japan, 2Department of Oral Physiology, Hiroshima University, Japan

Although sensory deprivation in one modality can lead to the improvement of remaining modalities, neuronal mechanisms underlying cross-modal regulation of primary sensory cortex are poorly understood. Recently, we found that AMPA receptors were delivered into layer4-2/3 synapses in the barrel cortex of adolescent rats (P21-P23) with visual deprivation. Furthermore, this is mediated by the increased secretion of serotonin in the barrel field (Jitsuki et al, preliminary data). However, it remains to be elucidated which brain regions control cross-modal regulation of barrel cortex specific serotonin secretion in animals with visual deprivation. Here we report brain areas responsible for the cross modal regulation of cortical circuit. We monitored the expression of c-Fos in the brain of rats with visual deprivation.

We recently applied a genetic approach to delineate the neuronal circuitries of bitter and sweet/umami taste by selectively expressing the transsynaptic tracer, tWGA-DsRed, in mT2R5- and mT1R3-expressing taste receptor cells, respectively. Locations of the neurons labeled by tWGA-DsRed originating from the specific taste receptor cells revealed segregation of bitter- and sweet-inputs in the gustatory area in the brain. Spatial distribution of the cell somata of tWGA-DsRed-labeled neurons suggested that the gustatory neurons dispersed in the solitary tract nuclei may be organized with sweet/ umami inputs rostral and with bitter inputs caudal. In the present study, the neuronal types and the microstructure of tWGA-DsRed-labeled neurons in the solitary tract nuclei were analyzed by immunohistochemistry and patchclamp recording, and by loading the fluorescent dye, lucifer yellow, in the labeled neurons. Large subsets of the neurons in the solitary tract nuclei, labeled by tWGA-DsRed originating from mT2R5-expressing taste receptor cells, receive glutamatergic synaptic transmission via the non-NMDA glutamate receptor, and are tyrosine hydroxylase-immunoreactive neurons.

P1PM-10-3

P1PM-10-4

Javier Cudeiro, Nelson Espinosa, Jorge Marino, Carmen de Labra, Casto Rivadulla

Kei Igarashi1, Yukie Yamaguchi1, Myungho An1, Nao Ieki1, Shin Nagayama2, Nian Liu3, Ko Kobayakawa4, Reiko Kobayakawa4, Yoshihiro Yoshihara5, Manabu Tanifuji5, Hitoshi Sakano4, Wei R Chen2, Kensaku Mori1

THE WAY V1 FEEDBACK INFLUENCES SPATIOTEMPORAL RESPONSES IN LGN. A TMS STUDY

Medicine-NEUROcom, University of A Coruna, Spain We have shown that sustained responses to flashed spots on X and Y lateral geniculate nucleus (LGN) cells were reduced after application of Transcranial Magnetic Stimulation (TMS) at 1Hz on primary visual cortex (V1). Transient responses were largely unaffected. Here we show, using a different experimental approach, that TMS at 1Hz induces subtle effects on transient responses depending on cell type. Experiments were performed in anesthetized and paralyzed adult cats.Visual stimulation (flashed bright and dark bars) was used to build the spatiotemporal receptive fields of LGN neurons extracellularly recorded, both under control conditions and during the simultaneous application of TMS on V1. X cells (n = 18) did show an increase in the latency to maximal response (mean = 1 msec, p < 0.05) and a decrease of firing rate (mean = 10 %, p < 0.005). Analysis of the receptive field shapes suggests that these changes were due to an increase in the rate between peripheral and central amplitudes. Y cells (n = 25) showed no changes regarding the spatiotemporal structure. Subsequent intervalogram analysis confirmed the results. These results indicate the existence of different cortical effects on X and Y cells transient response. Supported by MEC and Conselleria de Educacion (Galicia)

P1PM-10-5

PROCESSING OF FOOD ODOR INFORMATION IN THE RAT OLFACTORY CORTEX Ikue Yoshida, Kensaku Mori

Department of Physiology, the University of Tokyo, Japan

Poster Session

Exploration, detection and evaluation of foods are behaviors that all necessary for appeasing animal’s appetite, and these behaviors are controlled by olfactory cues. However, it is not known about how olfactory signals trigger or modulate these eating related behaviors. We previously reported that neurons in the dorsal part of the anterior piriform cortex (APC) of rats were tuned to specific odorant category profiles of fruits or vegetables. Although the result suggests that APC neurons integrate signals from distinct odorant categories to detect food odors, it is not well understood how food odor-responsive APC neurons integrate signals from multiple component odorants. Using single-unit recording methods, we here examined the odorant selectivity of rat APC neurons that responded to fruits odor. Each fruits odor responsive neurons showed excitatory responses to its component odorants. 71% of 21 watermelon responsive neurons responded to multiple component odorants. In addition to fruits odor responsive neurons, we examined odorant selectivity of rat food pellet responsive neurons. Some of these neurons responded to multiple components. Present result suggests that integration of diverse component odorants in the APC is a common way of processing food odors.

188

AXON PROJECTION MAPS OF FOX-ODORRESPONSIVE MITRAL/TUFTED CELLS IN THE MOUSE OLFACTORY CORTEX

1

Department of Physiology, Graduate School of Medicine, University of Tokyo, Japan, 2Dept Neurobio&Anatomy, U Texas Med Sch, USA, 3Dept Neurobio, Yale Univ Med Sch, USA 4Dept Biochem&Biophys, Grad Sch Sci, Univ Tokyo, Japan, 5 RIKEN BSI, Japan The glomerular sheet of the olfactory bulb (OB) forms odorant receptor maps. We have previously shown that glomeruli in the dorsal (D) zone of the OB are required for innate aversive response to predator odors. Here we report the axonal projection pattern to the olfactory cortex (OC) of individual mitral/tufted (M/T) cells associated with D-zone glomeruli and responding to TMT (a compent of fox’s predator odor). TMT-responsive M/T cells were juxtacellularly labeled and then labeled axons were histochemically visualized and 3D-reconstructed. The results showed that individual M/T cells extended axon collaterals to multiple areas of the OC, including the anterior olfactory nucleus (AON), piriform cortex (PC), olfactory tubercle, tenia tecta, amygdaloid cortex, and lateral entorhinal cortex. Axon collaterals formed several high-density clusters at the stereotypical positions in the AON and anterior PC, while they were distributed relatively widely in the posterior PC. These results provide initial steps toward understanding how the fox-odor TMT signals are sent to specific regions of the OC to induce innate aversive behavioral responses. Distinct distribution patterns of axons for different cell types and for cells located in different domains in D-zone will be discussed.

P1PM-10-6

ROLES OF PHASE-LOCKED INHIBITION FOR PROCESSING INTERAURAL TIME DIFFERENCE CUE IN THE NUCLEUS LAMINARIS OF BIRDS Rei Yamada, Hiroko Okuda, Eri Nishino, Hiroshi Kuba, Takahiro Ishii, Harunori Ohmori Department of Physiology, Faculty of Medicine, Kyoto University, Japan

Interaural time difference (ITD) is a cue for sound source localization and first processed in nucleus laminaris (NL) in birds. NL neurons act as a coincidence detector of bilateral phase-locked excitatory inputs and encode ITD. Relatively large temporal jitter is observed in the firing of low frequency auditory nerves, and the jitter should broaden the ITD tuning. In mammals that use low frequency sound for ITD coding, a phase-locked inhibition is proposed to increase the sharpness of ITD tuning. In contrast in birds, NL receives sound level dependent inhibition from superior olivary nucleus (SON) but this inhibition is poorly phase-locked. A presence of GABAergic interneurons around NL is reported, but their roles are not known. In this study, we found polysynaptic IPSC that followed EPSC with 1~2 ms latency in the low characteristic frequency (CF) NL neurons. IPSC was elicited even when SON was dissected out. This suggests that the low CF NL neurons also receive phase-locked inhibition from some interneurons located near NL. Consistently, GABA positive neurons were found concentrated in the low CF NL region and, their projection to NL was confirmed by photo-activation of caged glutamate. We will examine the roles of phase-locked inhibition in NL.

IUPS 2009 July 27 - August 1, 2009 in Kyoto

GAMMA BAND RESPONSES TO AM SOUNDS AT THE AUDITORY CORTEX OF CONSCIOUS RATS Wan-Chun Liao, Paul W Poon

Department of Physiology, National Cheng Kung University, Taiwan

P1PM-10-8

DIFFERENTIAL EFFECTS OF THE ACTIVITY OF AI TO THE BELT FIELDS IN THE GUINEA PIG AUDITORY CORTEX OBSERVED BY OPTICAL IMAGING Ryota Numata, Shunji Sugimoto, Junsei Horikawa

Evoked gamma band activity (viz., 30-200 Hz) is generally considered to reflect local fast synaptic and spike potentials related to cortical processing of stimuli. Sound-evoked gamma activity is known to vary depending on stimulus parameters, brain structures and animal species. It remains poorly understood whether the pattern of gamma response could be related to the time-varying features of sounds, which are important building blocks of speech signals. Here we studied gamma responses at the cerebral cortex of conscious rats to sound stimuli with different time-varying or more specifically amplitude modulated (AM) feature. Chronic epi-dural electrodes were first implanted surgically at the auditory fields on the rat cortex. After recovery from surgery, sound-evoked electro-corticograms to AM stimuli were recorded. We presented at random intervals AM bursts amplitude modulated systematically from 20 to 200 Hz. Gamma responses were computed in the form of event-related-spectral-perturbation and displayed using EEGLAB and MATLAB programs. Results showed an apparent demodulation of the AM time-profiles in the frequency range from 30 to160 Hz, which may or may not correlate with phase-locked evoked responses in the averaged time waveform.

Department of Knowledge-Based Information Engineering, Toyohashi University of Technology, Japan

P1PM-10-9

P1PM-10-10

Akihisa Kimura, Hiroki Imbe, Tomohiro Donishi

Tomohiro Donishi, Akihisa Kimura, Hiroki Imbe

EFFERENT CONNECTIONS OF AN AUDITORY AREA IN THE INSULAR CORTEX: ANATOMICAL NODES FOR AUDITORY, SOMATOSENSORY AND VISCERAL PROCESSING Department of Physiology, Wakayama Medical University, Japan

Functional connections between the dorsal (AId) and middle (AIm) parts of AI and the belt fields of the guinea pig auditory cortex were investigated using optical imaging and local cortical inhibition by muscimol (GABA A agonist) and activation by bicuculline (GABAA antagonist). The auditory cortex of a guinea pig under anesthesia was exposed and stained with a voltage-sensitive dye. The flouresonent signals were recorded using a 100× 100 CMOS camera. Pure tones (2-16 kHz, 200-ms long, 5-ms cosine ramps) were used for stimuli. After inhibition of AId by muscimol, the activities of the dorsocaudal field (DC), the dorsocaudal belt (DCB) and the posterior belt (P) were decreased, and they were increased after activation of AId by bicuculline. The activities of DCB and P were increased after inhibition of AIm and were decreased after activation of AIm. These results suggest that AId activity has excitatory effects to DC, DCB and P and AIm activity has inhibitory effects to DCB and P. The activities of AIm and AIv remained after inhibition of AId. The activities of AId and AIv remained after inhibition of AIm. These results suggest that AI has the three regions receiving independent inputs from the thalamus.

TEMPORAL INTERACTIONS BETWEEN AUDITORY AND SOMATOSENSORY INPUTS IN AUDITORY THALAMIC NUCLEI OF ANESTHETIZED AND AWAKE RATS Department of Physiology, Wakayama Medical University, Japan

We electrophysiologically delineated an auditory area in the caudal part of the granular insular cortex of the rat and determined its efferent connections based on axonal labeling with biocytin. The auditory area projected to the rostral agranular insular cortex (r-AI), which plays a pivotal role in nociceptive processing. It also projected to the caudal end of the agranular insular cortex and sent feedback projections to cortical layer I of the primary and secondary somatosensory areas. Corticofugal projections terminated in the medial division of the medial geniculate body (MG), somatosensory and visceral thalamic nuclei, and the rostral end of the auditory sector in the thalamic reticular nucleus that overlaps with the somatosensory and visceral sectors. The ventral part of the caudate putamen and the external cortex of the inferior colliculus were also the main targets. The projection to the r-AI (the lateral part of the prefrontal cortex) is thought to constitute the main stream of cortical auditory processing that originates from ventral auditory area, the secondary auditory area receiving non-lemniscal thalamic inputs from the dorsal division of the MG. The auditory area is considered pivotal for cortical and thalamic integration of auditory, somatic and visceral inputs.

We determined how somatosensory inputs affect auditory thalamic cell activity in anesthetized and awake rats. Under equithesin anesthesia, electrical stimuli or mechanical pinches on the hind paw increased and/or decreased unit discharges elicited by noise bursts in the medial geniculate body (MG), most notably those recorded in the ventral division (MGV) of the MG. The effects were likely related with the time intervals between preceding electrical stimuli and noise bursts. In most cases decrease was observed at short intervals (