Yutaka Kirino
Tokushima Bunri University
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Publication
Featured researches published by Yutaka Kirino.
Neuron | 2005
Masayoshi Murakami; Hideki Kashiwadani; Yutaka Kirino; Kensaku Mori
Sensory systems show behavioral state-dependent gating of information flow that largely depends on the thalamus. Here we examined whether the state-dependent gating occurs in the central olfactory pathway that lacks a thalamic relay. In urethane-anesthetized rats, neocortical EEG showed a periodical alternation between two states: a slow-wave state (SWS) characterized by large and slow waves and a fast-wave state (FWS) characterized by faster waves. Single-unit recordings from olfactory cortex neurons showed robust spike responses to adequate odorants during FWS, whereas they showed only weak responses during SWS. The state-dependent change in odorant-evoked responses was observed in a majority of olfactory cortex neurons, but in only a small percentage of olfactory bulb neurons. These findings demonstrate a powerful state-dependent gating of odor information in the olfactory cortex that works in synchrony with the gating of other sensory systems. They suggest a state-dependent switchover of signal processing modes in the olfactory cortex.
Brain Research | 2002
Kaori Takehara; Shigenori Kawahara; Kanako Takatsuki; Yutaka Kirino
We examined the role of the hippocampus in memory retention after trace eyeblink conditioning in mice. After establishing the conditioned response (CR) in the trace paradigm, mice received a bilateral aspiration of the dorsal hippocampus and its overlying neocortex on the next day (1-day group) or after 4 weeks (4-week group). Control mice received a neocortical aspiration on the same schedule as the hippocampal-lesion group. After 2 weeks of recovery, these groups received additional conditioning for 3 days. Frequency of the CR of the 1-day group was as low as spontaneous values on the first day in the post-lesion session and never reached pre-surgical level during the post-lesion sessions, while that of the control group did reach pre-surgical level during the post-lesion sessions although there was a transient decline just after lesion. In contrast to the 1-day group, the 4-week-hippocampal lesion group retained the CR and showed a further increase, without significant difference from the control group. The temporal pattern of the CR also was unchanged by the hippocampal lesion 4 weeks after learning. These results suggest a time-limited role for the hippocampus in memory retention after trace conditioning in mice: the CR acquired recently requires an intact hippocampus for its retention, but the CR acquired remotely does not. This is similar to the result reported in rabbits. Therefore, the mechanism and time course of memory consolidation after trace eyeblink conditioning may be similar in mice and rabbits.
The Journal of Neuroscience | 2006
Kaori Takehara-Nishiuchi; Kazuhito Nakao; Shigenori Kawahara; Norio Matsuki; Yutaka Kirino
The importance of the hippocampus in declarative memory is limited to recently acquired memory, and remotely acquired memory is believed to be stored somewhere in the neocortex. However, it remains unknown how the memory network is reorganized from a hippocampus-dependent form into a neocortex-dependent one. We reported previously that the medial prefrontal cortex (mPFC) is important for this neocortex-dependent remote memory in rat trace eyeblink conditioning. Here, we investigate the involvement of NMDA receptors in the mPFC in this reorganization and determine the time window of their contribution using chronic infusion of an antagonist into the mPFC, specifically during the postlearning consolidation period. The rats with blockade of the mPFC NMDA receptors during the first 1 or 2 weeks after learning showed a marked impairment in memory retention measured 6 weeks after learning, but relearned normally with subsequent conditioning. In contrast, the same treatment had no effect if it was performed during the third to fourth weeks or during the first day just after learning. The specificity of NMDA receptor blockade was confirmed by the reduced long-term potentiation in the hippocampal-prefrontal pathway in these rats. These results suggest that successful establishment of remotely acquired memory requires activation of NMDA receptors in the mPFC during at least the initial week of the postlearning period. Such NMDA receptor-dependent processes may mediate the maturation of neocortical networks that underlies permanent memory storage and serve as a way to reorganize memory circuitry to the neocortex-dependent form.
European Journal of Neuroscience | 2001
Yasushi Kishimoto; Shigenori Kawahara; Ryoko Fujimichi; Hisashi Mori; Masayoshi Mishina; Yutaka Kirino
Mice lacking the glutamate receptor subunit δ2 (GluRδ2) are deficient in cerebellar long‐term depression (LTD) at the parallel fibre–Purkinje cell synapses. We conducted delay and trace eyeblink conditioning with these mice, using various temporal intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). During trace conditioning in which a stimulus‐free trace interval (TI) of 250, 100 or 50u2003ms intervened between the 352‐ms tone CS and 100‐ms US, GluRδ2‐mutant mice learned as successfully as wild‐type mice. Even in the paradigm with TIu2003=u20030u2003ms, in which the end of CS and onset of US are simultaneous, there was no difference between the GluRδ2‐mutant and wild‐type mice in their acquisition of a conditioned response. However, in the delay paradigm in which the 452‐ms CS overlapped temporally with the coterminating 100‐ms US, GluRδ2‐mutant mice exhibited severe learning impairment. The present study together with our previous work [Kishimoto, Y., Kawahara, S., Suzuki, M., Mori, H., Mishina, M. & Kirino, Y. (2001) Eur. J. Neurosci.,13, 1249–1254], indicates that cerebellar LTD‐independent learning is possible in paradigms without temporal overlap between the CS and US. On the other hand, GluRδ2 and cerebellar LTD are essential for learning when there is CS–US temporal overlap, suggesting that the cerebellar neural substrates underlying eyeblink conditioning may change, depending on the temporal overlap of the CS and US.
European Journal of Neuroscience | 2002
Yasushi Kishimoto; Ryoko Fujimichi; Kenji Araishi; Shigenori Kawahara; Masanobu Kano; Atsu Aiba; Yutaka Kirino
In metabotropic glutamate receptor‐subtype 1 (mGluR1)‐null (mGluR1–/–) mice, cerebellar long‐term depression (LTD) and several forms of memory are impaired. However, because mGluR1 is expressed in various brain regions in wild‐type mice, it has been difficult to identify which type of memory depends on mGluR1 expressed in a given brain region. Furthermore, severe ataxia in mGluR1–/– mice complicated interpretation of the data from non‐cerebellum‐dependent tasks. We have generated mGluR1‐rescue mice, which express mGluR1 only in Purkinje cells (PCs) of their cerebellum, by introducing the mGluR1α transgene into mGluR1–/– mice under the control of a PC‐specific promoter. The mGluR1‐rescue mouse has normal LTD and displays no apparent ataxia. Therefore, this mouse is the first animal model in which effects of mGluR1 deficiency outside PCs can be studied without cerebellar dysfunction. We used three eyeblink conditioning paradigms with different temporal specificities between conditioned stimulus (CS) and unconditioned stimulus (US). Delay conditioning, in which CS and US coterminate, was impaired in mGluR1–/– mice but normal in mGluR1‐rescue mice. However, both strains of mice displayed severe impairment in trace conditionings, in which a stimulus‐free interval of 250 or 500u2003ms intervened between CS and US. We also examined social transmission of food‐preference and novel‐object‐recognition memory tests. In these tasks, mGluR1‐rescue mice showed normal short‐term but impaired long‐term memory. We conclude that mGluR1 in PCs is indispensable for normal learning of association of temporally contiguous stimuli in associative conditioning. In contrast, mGluR1 in other cell types is required for associating discontiguous stimuli and long‐term memory formation in nonspatial hippocampus‐dependent learning.
The Journal of Neuroscience | 2006
Yasushi Kishimoto; Kazu Nakazawa; Susumu Tonegawa; Yutaka Kirino; Masanobu Kano
Classical conditioning of the eyeblink reflex is a simple form of associative learning for motor responses. To examine the involvement of hippocampal CA3 NMDA receptors (NRs) in nonspatial associative memory, mice lacking an NR1 subunit selectively in adult CA3 pyramidal cells [CA3-NR1 knock-out (KO) mice] were subjected to eyeblink conditioning paradigms. Mice received paired presentations of an auditory conditioned stimulus (CS) and a periorbital shock unconditioned stimulus (US). With repeated presentation of the CS followed by the US, wild-type mice learned to blink in anticipation of the US before its onset. We first confirmed that wild-type mice require an intact hippocampus in the trace version of eyeblink conditioning in which the CS and US do not overlap, creating a stimulus-free time gap of 500 ms. Under the same condition, CA3-NR1 KO mice successfully acquired conditioned responses (CRs) during the 10 d acquisition sessions, whereas the extinction of CRs was impaired on the first day of extinction sessions. Importantly, CA3-NR1 KO mice were impaired in the formation of an adaptively timed CR during the first five trials in the daily acquisition sessions. The aberrantly timed CR was also observed in the extinction sessions in accordance with the impaired extinction of CRs. These results indicate that CA3-NR1 KO mice are unable to rapidly retrieve adaptive CR timing, suggesting that CA3 NRs play a crucial role in the memory of adaptive CR timing in trace conditioning.
Learning & Memory | 2008
Satoshi Watanabe; Yutaka Kirino; Alan Gelperin
Various non-mammalian model systems are being explored in the search for mechanisms of learning and memory storage of sufficient generality to contribute to the understanding of mammalian learning mechanisms. The terrestrial mollusk Limax maximus is one such model system in which mammalian-quality learning has been documented using odors as conditioned stimuli. The Limax odor information-processing circuits incorporate several system design features also found in mammalian odor-processing circuits, such as the use of cellular and network oscillations for making odor computations and the use of nitric oxide to control network oscillations. Learning and memory formation has been localized to a particular central circuit, the procerebral lobe, in which selective gene activation occurs through odor learning. Since the isolated Limax brain can perform odor learning in vitro, the circuits and synapses causally linked to learning and memory formation are assessable for further detailed analysis.
Neuropharmacology | 2001
Kanako Takatsuki; Shigenori Kawahara; Kaori Takehara; Yasushi Kishimoto; Yutaka Kirino
N-methyl-D-aspartate (NMDA) receptors are involved in synaptic plasticity and play a critical role in learning and memory. We investigated the effects of the noncompetitive NMDA receptor antagonist (+)MK-801 on classical eyeblink conditioning of mice, using various interstimulus intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). A tone was used for the CS and a periorbital shock was used for the US. In the delay paradigm, in which the US coterminated with the CS or started immediately after CS offset, the effect of (+)MK-801 (0.1mg/kg, i.p.) was a slight impairment in the acquisition of the conditioned response (CR). During subsequent CS-alone trials, the responses of (+)MK-801-injected mice were extinguished as easily as those of saline-injected mice. In the trace paradigm, (+)MK-801 impaired acquisition of the CR with a trace interval of 250 ms more than it did with a trace interval of 100 ms, and more than in the delay paradigm. (+)MK-801 injected after acquisition of 250-ms trace conditioning did not impair expression or extinction of the CR. These results suggest that NMDA receptors are involved in acquisition of the CR during longer trace interval conditioning more than during shorter trace interval conditioning or delay conditioning, and that their contribution to extinction is much smaller than their contribution to acquisition in mouse eyeblink conditioning.
Neuroreport | 2001
Yasushi Kishimoto; Michiyuki Suzuki; Shigenori Kawahara; Yutaka Kirino
The age effect on classical eyeblink conditioning in unrestrained mice (C57BL/6J strain) was evaluated. Mice were trained at one of three age periods (8, 45–50 or 85–90 weeks). In the delay paradigm, significant learning deficits were evident in the 85–90 week-old group, but no deficits were observed in the behavior of the 45–50 week-old group. On the other hand, in the trace paradigm with a stimulus-free trace interval of 500 ms, significant deficits became apparent at the age of 45–50 weeks. These results indicate that trace eyeblink conditioning is more susceptible to age-related deterioration of memory in mice than delay eyeblink conditioning.
Brain Research | 2003
Sadaharu Kotani; Shigenori Kawahara; Yutaka Kirino
During classical eyeblink conditioning, animals acquire adaptive timing of the conditioned response (CR) to the interstimulus interval (ISI) between the conditioned stimulus (CS) and the unconditioned stimulus (US). To investigate this coding of the timing by the cerebellum, we analyzed Purkinje cell activities during acquisition of new timing after we shifted the ISI. Decerebrate guinea pigs were conditioned to an asymptotic level of learning using a delay paradigm with a 250-ms ISI. A 350-ms tone and a 100-ms electrical shock were used as the CS and US, respectively. As reported previously in other species, Purkinje cells in the simplex lobe exhibited three types of responses to the CS: excitatory, inhibitory, or a combination of the two. After we increased the ISI to 400 ms, the frequency of the CR stayed at an asymptotic level, but the latency of the CR peak became gradually longer. Two types of cells were observed, based on changes in the nature of their response to the CS; one changed its type of response in parallel with learning the new timing, while the other did not. There was no correlation between the type of response before and after we changed the ISI. In some cells, the peak latency of activities became longer or shorter, while the type of response did not change. These results suggest that some Purkinje cells code the timing of the CR, but do not play a consistent role in shaping the CR over a range of ISIs.