The Journal of Physiological Sciences (Formerly The Japanese Journal of Physiology) Official Journal of The Physiological Society of Japan The Journal of Physiological Sciences publishes peer- JPS Chief Editor reviewed original papers, reviews, short Yoshihiro Ishikawa communications, technical notes, and letters to the editor, based on the principles and theories of modern JPS Associate Editors physiology and addressed to the international Harumi Hotta scientific community. All fields of physiology are Yoshinori Marunaka covered, encompassing molecular, cellular and Hironobu Morita systems physiology. The emphasis is on human and vertebrate physiology, but comparative papers are also Volume 65 ∙ Supplement 2 ∙ 2015 considered. The process of obtaining results must be ethically sound. Chief Editor Wattana B. Watanapa Fields covered: Adaptation and environment Editors Autonomic nervous function Panaree Busarakumtragul Biophysics Narattaphol Charoenphandhu Cell sensors and signaling Santipongse Chatchavalvanich Central nervous system and brain sciences Nipon Chattipakorn Endocrinology and metabolism Chatsri Deachapunya Excitable membranes and neural cell physiology Suwattanee Kooptiwut Exercise physiology Suchinda Malaivijitnond Gastrointestinal and kidney physiology Phornphop Naiyanetr Heart and circulatory physiology Punnee Nusuetrong Molecular and cellular physiology Narawut Pakaprot Muscle physiology Sutthasinee Poonyachoti Physiome/systems biology Thamolwan Suanarunsawat Respiration physiology Roongtawan Supabphol Senses Sompol Tapechum Watchareewan Thongsaard Kanokwan Tilokskulchai Assistants to Editors Thanaporn Kaewpaleuk Pimchanok Nambundit Kitinat Rodthongdee Katesirin Ruamyod Patcharaporn Taokum Wuttinan Theerathananon Kritsana Tipcome The Journal of Physiological Sciences Proceedings of The 8th Congress Federation of the Asian and Oceanian Physiological Societies November 22-25, 2015, Bangkok, Thailand CONTENTS Original Articles GluN2A/B ratio elevation induced by cortical spreading depression: electrophysiological and quantitative studies of the hippocampus Hansrivijit P, Vibulyaseck S, Maneepark M, Srikiatkhachorn A, Bongsebandhu-phubhakdi S .............................................................................................................. S-3 Low gamma wave oscillations in the striatum of mice following morphine administration Reakkamnuan C, Hiranyachattada S, Kumarnsit E ........................................................................ S-11 Gamma wave oscillation and synchronized neural signaling between the lateral hypothalamus and the hippocampus in response to hunger Samerphob N, Cheaha D, Chatpun S, Kumarnsit E ....................................................................... S-17 Antinociceptive effects of Rhus coriaria L. extract in male rats Mohammadi S, Zarei M, Zarei MM ................................................................................................ S-23 The estrous cycle modulates voltage-gated ion channels in trigeminal ganglion neurons Saleeon W, Jansri U, Srikiatkhachorn A, Bongsebandhu-phubhakdi S .......................................... S-29 Abstracts of the 8th FAOPS Congress .................................................................... S-A1 Author Index .............................................................................................................................. S-A209 J Physiol Sci (2015) 65 Suppl 2: S-3 – S-10 ORIGINAL PAPER GluN2A/B ratio elevation induced by cortical spreading depression: electrophysiological and quantitative studies of the hippocampus Panupong Hansrivijit • Suteera Vibulyaseck • Montree Maneepark • Anan Srikiatkhachorn • Saknan Bongsebandhu-phubhakdi © The Journal of Physiological Sciences 2015 Abstract Cortical spreading depression (CSD), an subunits. This ratio was demonstrated to be associated underlying mechanism of migraine aura, propagates to with synaptic plasticity of the hippocampus in numerous the hippocampus, and might explain hippocampus- studies. In conclusion, we showed that CSD increased associated symptoms during migraine attack. We hypo- GluN2A/B ratio, in turn, would result in altered synaptic thesised that this process is, some parts, mediated by plasticity. Our findings provide a probable implication on NMDA receptors. By using a rat model, CSD was the correlation of migraine aura and hippocampus- elicited by solid KCl for 45 minutes prior to electrophy- associated symptoms. siological and quantitative analyses. The result from elec- trophysiological study was the ratio of glutamate NMDA Keywords NMDA receptors • migraine aura • transient receptor 2A and 2B subunits (GluN2A/B). Total NMDA global amnesia (TGA) • hippocampal spreading depres- receptor response was isolated using an AMPA antagon- sion • long-term potentiation (LTP) • AMPA receptors ist, prior to a GluN2B receptor antagonist. The GluN2A/B ratio was calculated by dividing the remain- ing NMDA-mediated field-excitatory synaptic potentials Introduction (fEPSP) with the subtracted difference of NMDA- mediated fEPSP. Western blot analysis of the hippocam- Various cerebral insults (e.g. epileptic crises, trauma, pus was performed to confirm the quantitative change of ischemia, haemorrhage, and migraine) were shown to GluN2A/B ratio. In hippocampal slice study (n = 12), the produce a transient disturbance in cortical activity, so- GluN2A/B ratio of hippocampal fEPSP was significantly called cortical spreading depression (CSD). Cortical increased in CSD group. Western blot analysis (n = 30) spreading depression is caused by massive redistribution revealed an increase in GluN2A subunits and a decrease of ions, particularly potassium and hydrogen ions in GluN2B subunits in the hippocampus ipsilateral to the between intracellular and extracellular compartments [1] CSD induction. Our current study revealed that resulting in cortical depolarisation that can spread to the GluN2A/B ratio was shown to be elevated following adjacent areas. By adopting a model of migraine with CSD stimulation by increasing the total number of aura, spreading depression (SD) in each cortical area is GluN2A while reducing the total number of GluN2B accountable for different clinical manifestations seen in the patients. For instance, CSD in the occipital cortex can P. Hansrivijit • S. Vibulyaseck • M. Maneepark • cause visual metamorphopsia [2, 3], whereas those occur A. Srikiatkhachorn • S. Bongsebandhu-phubhakdi () in the somatosensory cortex result in paraesthesia or Department of Physiology, Faculty of Medicine, Chulalongkorn hemi-anaesthesia [4]. University, Bangkok, Thailand Spreading depression propagated to the hippocampus e-mail: [email protected] is believed to cause amnesia, emotional and behavioural S. Vibulyaseck changes (e.g. hyperactivity, yawning) during migraine Medical Research Institute, Tokyo Medical and Dental University, attack [5]. In case of acute amnesia, it seems to be Tokyo, Japan transient (4-8 hours in duration) and may impair both anterograde and retrograde memory. Long-term M. Maneepark association of migraine and amnesia was also Department of Biology, Faculty of Science, Srinakharinwirot Uni- versity, Bangkok, Thailand demonstrated in a retrospective cohort study suggesting that migraine is a risk factor of developing transient 8th FAOPS Congress, November 22-25, 2015, Bangkok, Thailand S-4 J Physiol Sci (2015) 65 Suppl 2: S-3 – S-10 global amnesia (TGA) [6]. For decades, Olesan and The animals were acclimatised to the housing facility for Jorgensen proposed that the association between at least seven days prior to the experiments. The study migraine and TGA may be explained by presence of was conducted according to the guideline for spreading depression in the hippocampus [7]. The experimental animals suggested by the National Research hypothesis was later proven by groups of ex vivo and in Council of Thailand. The study protocol was approved vitro experiments showing that CSD propagated to the by the Ethics Committee of the Faculty of Medicine, hippocampus. Limited studies were published regarding Chulalongkorn University (No.012/2553). the presence of SD in the in vivo hippocampus following CSD except in familial hemiplegic migraine type 1 Animal preparations (FHM1) mutant mice [8]. Although the molecular mechanisms underlying the correlation of migraine and Each rat was anaesthetised with 60 mg/kg of sodium TGA are still unclear, existing evidence suggested that pentobarbital (Ceva Sante Animale, Libourne, France) the process may involve actions of glutamatergic intraperitoneally. We avoided using inhaled isoflurane or receptors [9]. IV dexmedetomidine as surgical anaesthetics due to their Glutamatergic transmission is known to play an effects on suppressing CSD frequency [14]. important role in inducing plastic change in the Physiological parameters were monitored and only hippocampal synapse. Repetitive activation of the animals that were in stable condition throughout the hippocampal synapse can result in a long-lasting change preparation were included in the experiment. All in synaptic activity known as long-term potentiation anatomical landmarks guided by Paxinos & Watson’s (LTP). This process is an important step in the brain atlas [15]. registration and consolidation of new memories. Various classes of glutamatergic receptors are involved in LTP CSD induction development, specifically α-amino-3-hydroxy-5-methyl- 4-isoxazolepropionic acid (AMPA) and N-methyl-D- The rat’s head was fitted to a stereotaxic